Iliopsoas involvement complicating longstanding nephrolithiasis with chronic infection: a three-patient case series reconsidering “malignant lithiasis”

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This phenotype may extend beyond the collecting system, resulting in extensive retroperitoneal infection with extrarenal extension, irreversible renal functional loss, and, in rare instances, occult malignancy. Reconsidering the historical descriptor “malignant lithiasis” may help frame this aggressive clinical trajectory, particularly in patients with delayed presentation or limited access to timely care. Case presentation: We report three cases of longstanding nephrolithiasis with chronic infection with iliopsoas involvement. Case 1 was a 50-year-old woman with perinephric and iliopsoas abscesses, with inferior tracking along the iliopsoas compartment into the obturator region. Case 2 was a 53-year-old man with perinephric and iliopsoas abscesses and inflammatory involvement extending to the colon. Case 3 was a 59-year-old man with a large renal abscess who underwent nephrectomy to achieve definitive source control for uncontrolled infection, revealing an incidental diagnosis of renal pelvic squamous cell carcinoma. Across cases, infection was recurrent or refractory, temporizing measures (e.g., percutaneous drainage and/or nephrostomy) did not achieve sustained definitive source control, and two patients developed non-functioning kidneys requiring nephrectomy after infection control. Conclusions These cases illustrate an aggressive phenotype of longstanding nephrolithiasis with chronic infection, consistent with “malignant lithiasis” as a marker of clinical severity rather than malignant histology. Recognizing red flags—recurrent or refractory infection, imaging evidence of extrarenal extension (e.g., iliopsoas and perinephric involvement), and progressive functional decline—may support timely escalation to definitive source control. Routine histopathology of nephrectomy specimens is critical to minimize missed malignancy in stone-related non-functioning kidneys. malignant lithiasis nephrolithiasis nephrolithiasis with chronic infection perinephric abscess iliopsoas abscess extrarenal extension renal squamous cell carcinoma nephrectomy Figures Figure 1 Figure 2 Figure 3 Figure 4 Figure 5 Background Nephrolithiasis is a common chronic condition with a high recurrence rate and a substantial global health burden. Approximately 11% of the global population is affected by urolithiasis, with marked geographic variation in prevalence [ 1 ]. Although minimally invasive techniques have improved stone clearance, recurrence remains common and long-term prevention and follow-up are often required [ 2 ]. In regions with large populations and uneven access to healthcare, nephrolithiasis-related complications—including severe infection and secondary malignancy—continue to be encountered in routine clinical practice [ 3 ]. In the era of open surgery, complex staghorn calculi associated with persistent infection and a destructive clinical course were described as “malignant lithiasis” (also termed “malignant nephrolithiasis” in historical reports) to convey clinical severity and poor outcomes rather than malignant histology [ 4 ]. Despite continuing advances in endourology, similar high-risk phenotypes persist, particularly in patients with longstanding stone disease complicated by chronic infection, delayed presentation, or inadequate follow-up, in whom recurrent or refractory infection, progressive stone growth, and renal functional decline may still occur. In this context, reconsidering this historical descriptor may help reinforce clinical vigilance and support risk stratification and timely escalation to definitive source control. However, contemporary reports that systematically characterize this aggressive phenotype—namely, longstanding nephrolithiasis with chronic infection complicated by extensive extrarenal extension with retroperitoneal abscess formation and/or occult malignancy—remain limited. Case presentation Case 1 A 50-year-old woman was admitted on 27 July 2020 with recurrent right flank pain for 2 years, worsened over the preceding 3 months, with right lower-limb distension and pain and no recent fever. She had a 10-year history of right renal calculi without structured follow-up and denied tuberculosis exposure. At an outside hospital, contrast-enhanced CT excluded an overt renal malignant lesion but raised suspicion of genitourinary tuberculosis (GU-TB); empiric anti-tuberculous therapy for 2 months produced no improvement. On admission, temperature was 36.2 °C. Examination showed right costovertebral angle tenderness and a firm, tender mass extending from the right lower abdomen to the right inguinal region and medial thigh. Laboratory tests showed WBC 13.20 × 10^9/L, hemoglobin 96 g/L, and serum creatinine 72 µmol/L. Urine culture and cytology were negative; interferon-γ release assay (IGRA) and serum anti-Mycobacterium tuberculosis IgG were negative. Non-contrast CT (NCCT) demonstrated multiple right renal calculi with extensive perinephric inflammatory change and abscess formation, tracking inferiorly through the inguinal canal to the proximal thigh near the obturator region (Fig. 1). No adjacent organ involvement was reported, and GU-TB could not be excluded initially. Aspiration from the inguinal abscess was negative for Mycobacterium tuberculosis by quantitative polymerase chain reaction (PCR) and smear microscopy, whereas culture grew Proteus mirabilis , excluding GU-TB. Incision and drainage (I&D) of the inguinal abscess was performed, followed by right percutaneous nephrostomy (PCN). One month later, the nephrostomy drained 5–15 mL/day of turbid yellow pus and the inguinal drain produced 50–80 mL/day of purulent fluid. Repeat CT showed only slight reduction of the iliac collection, with no significant change in the perinephric, psoas major, or iliopsoas lesions. Given inadequate response to drainage and antibiotics, percutaneous nephrolithotomy (PCNL) was performed to reduce stone burden and improve drainage for source control. Intraoperatively, a large staghorn calculus occupied the renal pelvis and calyces with copious pus and necrotic tissue; the renal pelvic outlet could not be identified, and both antegrade and retrograde ureteral stent placement failed, suggesting complete obstruction. On postoperative day 1, she developed fever and hypotension consistent with urosepsis and septic shock, which improved with intensive supportive care. Infrared spectroscopic analysis confirmed a struvite (magnesium ammonium phosphate) stone. She was discharged with the nephrostomy tube in situ. She was readmitted on 19 April 2021. Contrast-enhanced CT on 20 April 2021 showed marked right renal atrophy with residual calculi and substantial regression of prior extrarenal extension (Fig. 2). Renal dynamic scintigraphy showed left GFR 88.65 mL/min and right GFR 6.36 mL/min, consistent with a non-functioning right kidney. After infection control, open right nephrectomy with retroperitoneal abscess debridement was performed on 25 April 2021. Histopathology showed chronic inflammation and necrosis; periodic acid–Schiff (PAS) and acid-fast stains were negative. She was discharged 2 weeks postoperatively and remained clinically well at approximately 5-year follow-up, with normal serum creatinine. Case 2 A 53-year-old man was admitted on 19 February 2024 with persistent left flank pain for 1 month and no recent fever. He had untreated left renal calculi diagnosed approximately 30 years earlier and denied tuberculosis exposure. Temperature was 36.3 °C, and examination showed left costovertebral angle tenderness. Laboratory tests showed WBC 7.66 × 10^9/L, hemoglobin 119 g/L, platelets 439 × 10^9/L, and serum creatinine 96 µmol/L. Urinalysis and urine culture were negative; repeated urine cytology was negative. IGRA and serum anti-Mycobacterium tuberculosis IgG were negative. NCCT demonstrated multiple left renal calculi with marked renal atrophy and a perinephric abscess involving the ipsilateral psoas major muscle, abutting the splenic flexure of the colon (Fig. 3). Concomitant non-obstructing right renal calculi were present. Contrast-enhanced CT showed no definite renal malignant lesion, and GU-TB remained in the differential diagnosis. Ultrasound-guided perinephric drainage yielded 5–20 mL/day of purulent fluid. Quantitative PCR and smear microscopy for Mycobacterium tuberculosis were negative, whereas culture grew Bacteroides fragilis , excluding GU-TB. Targeted antimicrobial therapy was initiated with symptomatic improvement; drainage output gradually ceased and the catheter dislodged spontaneously without complication. On 17 June 2024, he was readmitted with anorexia and progressive anemia (hemoglobin 86 g/L), without fever or urinary symptoms. Renal dynamic scintigraphy showed right GFR 63.24 mL/min and left GFR 6.32 mL/min, consistent with a non-functioning left kidney. Repeat CT on 19 June 2024 showed no meaningful reduction in the perinephric or psoas collections. After multidisciplinary discussion, open left nephrectomy with retroperitoneal abscess debridement was performed on 25 June 2024; dense adhesions at the splenic flexure necessitated partial colectomy. Histopathology was consistent with a calculous renal abscess. He recovered uneventfully and was discharged 10 days postoperatively. One month later, he underwent holmium laser lithotripsy for right renal calculi. At approximately 18 months postoperatively, he remained clinically well without recurrent pain; serum creatinine was normal and there was no recurrence of right renal stones. Case 3 A 59-year-old man was admitted on 11 October 2024 with intermittent right flank pain for 6 months, worsened over the preceding month, with purulent urine and abdominal distension, without recent fever. He had a >20-year history of nephrolithiasis with multiple prior stone-related procedures and residual right renal calculi; he denied tuberculosis. Temperature was 36.3 °C. Laboratory tests showed WBC 9.27 × 10^9/L, hemoglobin 109 g/L, platelets 419 × 10^9/L, and serum creatinine 169 µmol/L. Urinalysis showed RBC 86/µL and WBC 19,477/µL. Urine culture grew Pseudomonas aeruginosa , and repeated urine cytology was negative. Renal dynamic scintigraphy showed impaired bilateral renal function, predominantly affecting the right kidney (right GFR 10.92 mL/min; left GFR 29.42 mL/min). Non-contrast and contrast-enhanced CT urography demonstrated multiple right renal calculi with severe hydronephrosis and pyonephrosis, with suspected involvement of the right psoas major muscle (Fig. 4A–D). Percutaneous nephrostomy (PCN) was performed; because the renal pelvis was small with markedly dilated calyces, two nephrostomy tubes were placed (upper calyx and mid-to-lower calyces) to optimize drainage. Despite drainage and targeted antimicrobial therapy, symptoms worsened, and repeat imaging showed persistent infection with suspected pyonephrosis and progressive retroperitoneal spread (Fig. 4E–G). Open right nephrectomy with psoas abscess resection/debridement was therefore performed to achieve definitive source control for uncontrolled infection. Unexpectedly, histopathological examination of the nephrectomy specimen demonstrated a moderately to poorly differentiated squamous cell carcinoma (SCC) of the renal pelvis/upper urinary tract (Fig. 5). According to the final pathology report, the tumor invaded the renal sinus fat and perirenal adipose tissue with vascular tumor emboli, and metastatic carcinoma was present in 4 of 7 regional lymph nodes (pathological stage pT3N2Mx). Additional findings in the final pathology report not shown in Fig. 5 included focal sarcomatoid change, negativity for PAX8 and GATA3, and a high Ki-67 proliferation index (approximately 50%). He was discharged 2 weeks postoperatively but experienced rapid systemic progression and died 1 month later due to widespread metastases and multiorgan dysfunction. Table 1. Clinical characteristics, interventions, and outcomes of three patients Key elements Case 1 Case 2 Case 3 Age / Sex 50 / Female 53 / Male 59 / Male History 10-year renal calculi; no structured follow-up ~30-year left renal calculi; untreated >20-year; multiple prior procedures Extrarenal extension (CT) Abscess tracking to inguinal canal and proximal thigh Perinephric abscess involving ipsilateral psoas major; abutting splenic flexure Suspected pyonephrosis and progressive retroperitoneal spread Microbiology Abscess: P. mirabilis Abscess: B. fragilis Urine: P. aeruginosa Key interventions I&D; PCN; PCNL → Open nephrectomy + debridement Drainage → Open nephrectomy + debridement (partial colectomy) PCN → Open nephrectomy + psoas abscess debridement Split function (GFR, mL/min) Right: 6.36; Left: 88.65 Right: 63.24; Left: 6.32 Right: 10.92; Left: 29.42 Pathology Chronic inflammation/necrosis Calculous renal abscess Squamous cell carcinoma (SCC) Outcome Recovered; ~5-year follow-up Recovered; ~18 months follow-up Died 1 month postoperatively Abbreviations: CT, computed tomography; GFR, glomerular filtration rate; I&D, incision and drainage; PCN, percutaneous nephrostomy; PCNL, percutaneous nephrolithotomy; SCC, squamous cell carcinoma. Discussion Across our three patients, longstanding nephrolithiasis with chronic infection followed a destructive trajectory: persistent stones complicated by infection; recurrent or smoldering infection; radiographically evident extrarenal extension; and progressive loss of renal function ultimately necessitating nephrectomy. In one case, systematic histopathological evaluation of the nephrectomy specimen revealed occult squamous cell carcinoma. These cases foreground three practical red flags that should trigger timely escalation of evaluation and management: (1) recurrent or refractory infection; (2) imaging evidence of extrarenal extension; and (3) progressive decline in split renal function. In this context, we reconsider “malignant lithiasis” as a historical descriptor of a high-risk clinical course rather than a diagnostic label implying malignant histology. Urolithiasis is increasingly recognized as a chronic condition with a notable global health burden that requires long-term prevention and follow-up [1–2]. Despite advances in minimally invasive techniques, recurrence remains common, and severe infectious complications and renal destruction still occur in a subset of patients. In this report, we use “nephrolithiasis with chronic infection” to describe longstanding stones complicated by persistent or recurrent infection, regardless of stone composition; infection-related (struvite) stones are a common, but not exclusive, substrate for this phenotype. Clinically, this phenotype can be operationally suspected when a prolonged stone history coexists with the red flags above—recurrent or refractory infection, imaging evidence of extrarenal inflammatory extension (e.g., perinephric or iliopsoas involvement), and/or progressive loss of ipsilateral renal function—prompting timely progression from temporizing measures to definitive source control. Historically, in the era of open surgery, complex staghorn calculi associated with chronic infection were described as “malignant lithiasis” to convey clinical severity and poor prognosis rather than malignant histology [4]. Martínez-Piñeiro et al. emphasized the close association between staghorn calculi and infection, including a high likelihood of recurrence and progressive stone growth in the presence of persistent bacteriuria—features that can drive repeated infectious episodes and progressive renal damage when management is delayed or incomplete [4]. Subsequent work and contemporary reviews continue to underscore this infection–recurrence–progression paradigm and the risk of renal functional decline when definitive management is delayed or incomplete, supporting the ongoing clinical relevance of this historical descriptor even in the modern era [5]. In a related context, Pagano et al. used “malignant lithiasis” to describe cases with severely compromised renal function and heterogeneous postoperative renal functional trajectories, reinforcing that this label captured a function-threatening course rather than malignant histology [6]. Cystine stones, characterized by frequent recurrence and rapid progression, have also been discussed under this descriptor as a marker of a high-risk course rather than malignant histology [7]. More broadly, infection-related stones constitute a high-risk subtype, often characterized by rapid growth, persistent bacterial colonization, frequent recurrence, and an increased risk of functional decline or nephrectomy if definitive management is delayed [8–10]. Inadequate treatment may progress to recurrent pyelonephritis, urosepsis, and even death [11,12]. Infection/struvite stones have also been associated with increased postoperative sepsis after endourological stone surgery; these findings align with evidence linking positive stone culture to higher postoperative sepsis rates, supporting the concept that stone-associated bacterial reservoirs can amplify infectious risk [13,14]. Together, these data reinforce the value of recognizing high-risk phenotypes consistent with the historical concept of “malignant lithiasis” as a descriptor of destructive stone disease with potential irreversible renal functional loss. Although nephrolithiasis is often perceived as benign, the mortality risk—while overall low—is real in severe or complicated disease. A systematic review spanning the past two decades summarized reported deaths related to kidney stone disease, identified sepsis as the leading cause, and noted that high stone burden and comorbidities were common among fatal cases [15]. These findings reinforce meticulous preoperative optimization and timely definitive management when stone disease is complicated by infection and systemic illness, consistent with guideline-based principles for surgical management of urinary stones [16]. Severe renal infection can be complicated by extensive perinephric/pararenal involvement on CT, and escalation to definitive management may be required [17,18]. In longstanding nephrolithiasis, extrarenal extension can mark one of the most severe trajectories of infection [17,18]. Perinephric infection may extend contiguously beyond the perirenal space into the iliopsoas compartment, resulting in iliopsoas abscesses associated with notable morbidity; mortality has been reported in severe or advanced cases [19,20,23]. Cross-sectional imaging—particularly CT—defines disease extent and guides drainage and surgical planning [18,21]. Because iliopsoas abscesses are frequently secondary to adjacent or distant foci, careful evaluation of potential sources, including genitourinary infection, remains important [23]. Management emphasizes timely source control with appropriate antimicrobial therapy, often combined with image-guided drainage when feasible [18,22,24]. After stabilization, minimally invasive drainage and other source control strategies may be used to control infection and, in selected patients, facilitate subsequent definitive stone management [25]. When the affected kidney is irreversibly damaged, definitive source control may require surgical intervention, and nephrectomy should be considered in selected cases [10,18]. A further concern is the association between longstanding nephrolithiasis and upper urinary tract malignancy, particularly renal pelvic squamous cell carcinoma (SCC) [26–28]. Chronic irritation and infection are recognized drivers of squamous metaplasia and malignant transformation [28], yet preoperative diagnosis remains challenging because stones and inflammation can render clinical and radiological findings nonspecific [27,30]. Upper urinary tract malignancies have been incidentally detected during or after percutaneous nephrolithotomy (PCNL), underscoring that cancer may coexist with stone disease and be missed on preoperative assessment [29,30]. Epidemiological data also suggest an increased risk of upper urinary tract urothelial carcinoma (UTUC)—and, in some cohorts, renal cell carcinoma—in patients with nephrolithiasis [3,26,31]. Tumors with squamous differentiation tend to be high-risk [27], while xanthogranulomatous pyelonephritis or genitourinary tuberculosis can mimic malignancy and further complicate the differential diagnosis [32,36]. Accordingly, European Association of Urology (EAU) guidance supports diagnostic ureteroscopy (preferably without biopsy) when imaging and/or voided urine cytology are insufficient for diagnosis and/or risk stratification [33]. When suspicious upper urinary tract mucosal abnormalities are encountered, targeted biopsy has been advocated to facilitate timely diagnosis in selected high-risk patients [34]. Occult malignancy has also been reported in nephrectomy specimens from stone-related non-functioning kidneys, supporting systematic histopathological assessment in this setting [35]. These challenges may be amplified in socioeconomically disadvantaged settings, where barriers to timely care and fragmented follow-up are more prevalent. Evidence suggests that neighborhood socioeconomic disadvantage is associated with worse urinary risk factors for recurrent urolithiasis and reduced access to medical management, while adherence to guideline-based prevention and follow-up remains suboptimal in diverse low-resource populations [37,38]. Taken together, the clinical trajectory observed in our cases and the supporting literature support a pragmatic, escalation-oriented approach anchored on the three red flags above and operationalized as practical management considerations (summarized in the Practical points section below). Practical points. Risk recognition: Treat longstanding nephrolithiasis with chronic or refractory infection, extrarenal extension (e.g., perinephric abscess), or progressive renal functional decline as a high-risk clinical entity [10,39]. Socioeconomic disadvantage may further increase the likelihood of irreversible complications [37,38]. Early recognition should prompt timely intervention to optimize outcomes [10,16]. Initial source control and exclusion of mimics: After genitourinary tuberculosis has been reasonably excluded [36], prioritize early urinary drainage (retrograde ureteral stenting or percutaneous nephrostomy) and stabilization; defer definitive stone manipulation until sepsis is controlled and infection has been appropriately treated [10]. Definitive management and functional triage: Aim for complete stone clearance where feasible [9]. If clearance is incomplete, counsel patients and ensure structured follow-up, as residual fragments—especially in infection/struvite stone disease—may perpetuate bacteriuria, recurrent infection, and stone regrowth [9,11,40]. Quantify split renal function early (e.g., nuclear renography) and reassess after infection control to guide kidney-preserving versus extirpative surgery [10,40]. Consider timely nephrectomy for stone-related non-functioning kidneys to achieve definitive source control and to exclude occult malignancy, which can be challenging to detect preoperatively [35,40–42]. Operative planning: In advanced infection with extrarenal extension, anticipate dense adhesions, distorted hilar anatomy, and potential adjacent-organ involvement, which may increase procedural complexity and complications [32,42]. Meticulous imaging review, proactive planning, and multidisciplinary collaboration may improve safety [16,40]. Malignancy vigilance: Maintain a high index of suspicion for occult malignancy and perform systematic histopathological evaluation of nephrectomy specimens, particularly in stone-related non-functioning kidneys [26,31,35]. Limitations and future directions. This small case series is subject to selection and referral biases and cannot quantify risk or establish causality between chronic infection, extrarenal extension, renal functional loss, and management decisions. Clinical heterogeneity (patient factors, microbiology, prior interventions, and timing of definitive surgery) may have influenced outcomes. “Nephrolithiasis with chronic infection” is used as a pragmatic clinical construct rather than a validated classification. Multicenter cohorts are needed to refine imaging- and function-based criteria, identify predictors of irreversible damage and extrarenal spread, and evaluate whether earlier escalation to definitive source control improves outcomes. Conclusions Longstanding nephrolithiasis with chronic infection may follow an aggressive, destructive course, leading to extensive retroperitoneal infection, renal functional loss, and, occasionally, occult malignancy [35,40]. Despite improved stone clearance with endoscopic and other minimally invasive approaches, recurrence remains substantial and delayed care continues to contribute to irreversible complications [1,2,10,40]. Reconsidering “malignant lithiasis” as a historical descriptor of a destructive clinical trajectory—rather than a diagnostic label—may help clinicians recognize high-risk presentations earlier, including recurrent or refractory infection, imaging evidence of extrarenal extension, and progressive decline in split renal function, and prompt clinical vigilance, structured follow-up, and timely escalation to definitive source control [4,6,16,40]. Accordingly, in refractory or complex stone disease, timely progression to definitive treatment (including nephrectomy for non-functioning kidneys) and routine histopathology of nephrectomy specimens should be considered to support individualized decision-making and minimize missed malignancy [16,35]. Abbreviations CT: Computed tomography; EAU: European Association of Urology; GFR: Glomerular filtration rate; GU-TB: Genitourinary tuberculosis; I&D: Incision and drainage; PCN: Percutaneous nephrostomy; PCNL: Percutaneous nephrolithotomy; SCC: Squamous cell carcinoma; UTUC: Upper urinary tract urothelial carcinoma. Declarations Acknowledgements The authors sincerely thank the patients in Cases 1 and 2, and the family of the patient in Case 3, for providing consent for publication of this case series. Authors’ contributions DL drafted the manuscript and reviewed the literature. MM and XY acquired the clinical data and contributed to drafting the manuscript. ZB interpreted the imaging findings and reviewed the literature. HX interpreted the pathological findings. CL revised the manuscript for important intellectual content. All authors read and approved the final manuscript. Funding This study received no specific grant from any funding agency in the public, commercial, or not-for-profit sectors. Availability of data and materials No datasets were generated or analysed during the current study. Ethics approval and consent to participate This case series was approved by the Ethics Committee of Haikou Municipal People’s Hospital. Consent for publication Written informed consent was obtained from the patients in Cases 1 and 2 for publication of this case series and any accompanying images. For Case 3, written informed consent for publication (including any accompanying images) was obtained from the patient’s legal next of kin because the patient is deceased. Competing interests The authors declare that they have no competing interests. References Vera-Ponce VJ, Sanchez-Tamay NM, Ballena-Caicedo J, et al. Global prevalence of urolithiasis: a meta-analysis accounting for methodological heterogeneity. Front Urol. 2025; 5:1705953. doi:10.3389/fruro.2025.1705953. 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Eur Urol. 2025;87(6):697–716. doi:10.1016/j.eururo.2025.02.023. Qiao J, Tian C, An L, et al. Application of warning biopsies in percutaneous nephrolithotomy. Transl Androl Urol. 2024;13(8):1455–1462. doi:10.21037/tau-24-91. Yeh CC, Lin TH, Wu HC, et al. A high association of upper urinary tract transitional cell carcinoma with non-functioning kidney caused by stone disease in Taiwan. Urol Int. 2007;79(1):19–23. doi:10.1159/000102907. Naeem M, Zulfiqar M, Siddiqui MA, et al. Imaging manifestations of genitourinary tuberculosis. Radiographics. 2021;41(4):1123–1143. doi:10.1148/rg.2021200154. Ho L, Chehroudi C, Jevnikar B, et al. Neighborhood socioeconomic disadvantage is associated with worse urinary risk factors and access to medical management for urolithiasis. J Endourol. 2025;39(3):314–321. doi:10.1089/end.2024.0384. Hunt ER, Bergeron T, Edelblute B, et al. Physician and patient adherence to kidney stone prevention guidelines in a diverse, low-resource, urban population. Urology. 2025;201:1–7. doi:10.1016/j.urology.2025.02.040. Liu XQ, Wang CC, Liu YB, Liu K. Renal and perinephric abscesses in West China Hospital: 10-year retrospective-descriptive study. World J Nephrol. 2016;5(1):108–114. doi:10.5527/wjn.v5.i1.108. Sharbaugh A, Morgan Nikonow T, Kunkel G, et al. Contemporary best practice in the management of staghorn calculi. Ther Adv Urol. 2019;11:1756287219847099. doi:10.1177/1756287219847099. Zengin K, Tanik S, Sener NC, et al. Incidence of renal carcinoma in non-functioning kidney due to renal pelvic stone disease. Mol Clin Oncol. 2015;3(4):941–943. doi:10.3892/mco.2015.550. Danilovic A, Ferreira TAC, Maia GVA, et al. Predictors of surgical complications of nephrectomy for urolithiasis. Int Braz J Urol. 2019;45(1):100–107. doi:10.1590/S1677-5538.IBJU.2018.0246. Additional Declarations No competing interests reported. Cite Share Download PDF Status: Under Review Version 1 posted Reviewers agreed at journal 05 Mar, 2026 Reviews received at journal 01 Mar, 2026 Reviewers agreed at journal 26 Feb, 2026 Reviewers agreed at journal 26 Feb, 2026 Reviewers agreed at journal 24 Feb, 2026 Reviewers invited by journal 24 Feb, 2026 Editor invited by journal 30 Jan, 2026 Editor assigned by journal 28 Jan, 2026 Submission checks completed at journal 28 Jan, 2026 First submitted to journal 24 Jan, 2026 You are reading this latest preprint version Research Square lets you share your work early, gain feedback from the community, and start making changes to your manuscript prior to peer review in a journal. As a division of Research Square Company, we’re committed to making research communication faster, fairer, and more useful. We do this by developing innovative software and high quality services for the global research community. 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Also discoverable on Platform About Our Team In Review Editorial Policies Advisory Board Help Center Resources Author Services Accessibility API Access RSS feed Manage Cookie Preferences © Research Square 2026 | ISSN 2693-5015 (online) Privacy Policy Terms of Service Do Not Sell My Personal Information {"props":{"pageProps":{"initialData":{"identity":"rs-8688678","acceptedTermsAndConditions":true,"allowDirectSubmit":false,"archivedVersions":[],"articleType":"Case Report","associatedPublications":[],"authors":[{"id":596313457,"identity":"0d559bba-7a39-4dba-938d-bd2c658a7795","order_by":0,"name":"Donghui Li","email":"","orcid":"","institution":"Affiliated Haikou Hospital of Xiangya Medical College, Central South University","correspondingAuthor":false,"prefix":"","firstName":"Donghui","middleName":"","lastName":"Li","suffix":""},{"id":596313458,"identity":"bd6041ff-64e6-4d8d-9c52-c613aadbe0f4","order_by":1,"name":"Meijiang Meng","email":"","orcid":"","institution":"Affiliated Haikou Hospital of Xiangya Medical College, Central South University","correspondingAuthor":false,"prefix":"","firstName":"Meijiang","middleName":"","lastName":"Meng","suffix":""},{"id":596313459,"identity":"af000dc0-49da-432d-9363-983fdc0a8802","order_by":2,"name":"Xianlai Yin","email":"","orcid":"","institution":"Affiliated Haikou Hospital of Xiangya Medical College, Central South University","correspondingAuthor":false,"prefix":"","firstName":"Xianlai","middleName":"","lastName":"Yin","suffix":""},{"id":596313460,"identity":"cdecccac-f838-471c-ba19-c8d8d6b603ad","order_by":3,"name":"Zhiming Bai","email":"","orcid":"","institution":"Affiliated Haikou Hospital of Xiangya Medical College, Central South University","correspondingAuthor":false,"prefix":"","firstName":"Zhiming","middleName":"","lastName":"Bai","suffix":""},{"id":596313461,"identity":"59625dc8-2153-4666-8339-11dcd8c1c643","order_by":4,"name":"Haixia Xu","email":"","orcid":"","institution":"Affiliated Haikou Hospital of Xiangya Medical College, Central South University","correspondingAuthor":false,"prefix":"","firstName":"Haixia","middleName":"","lastName":"Xu","suffix":""},{"id":596313465,"identity":"6feeed5c-a6d1-4eb3-9d4a-d6de81556cd1","order_by":5,"name":"Cai Lv","email":"data:image/png;base64,iVBORw0KGgoAAAANSUhEUgAAAZAAAAAyAQMAAABI0h/eAAAABlBMVEX///8AAABVwtN+AAAACXBIWXMAAA7EAAAOxAGVKw4bAAAAuklEQVRIiWNgGAWjYBACPhCRUCFRz8/MfPgBUVrYwFrOWCRItrOlGRCvhbGtIsHgPI+CBHFaJJIffnhwRiLP+DAPgwFDjU00EVrSjCWAfik2O8x74AHDsbTcBoJaeM4wSCSckWDcdpgvwYCx4TBRWph/JLZJMG5u5jGQIE4Lew+bBFBL4gZm4rW0mVkAHWYscRgYyAnE+AUYg49v/qiok+PvP3z4wYcaG8JaUEECacpHwSgYBaNgFOACAJwZOUK0cVtVAAAAAElFTkSuQmCC","orcid":"","institution":"Affiliated Haikou Hospital of Xiangya Medical College, Central South University","correspondingAuthor":true,"prefix":"","firstName":"Cai","middleName":"","lastName":"Lv","suffix":""}],"badges":[],"createdAt":"2026-01-24 18:38:45","currentVersionCode":1,"declarations":"","doi":"10.21203/rs.3.rs-8688678/v1","doiUrl":"https://doi.org/10.21203/rs.3.rs-8688678/v1","draftVersion":[],"editorialEvents":[],"editorialNote":"","failedWorkflow":false,"files":[{"id":103587040,"identity":"0619891b-d0c6-4329-b6d6-ed13630fcca6","added_by":"auto","created_at":"2026-02-27 11:26:56","extension":"png","order_by":1,"title":"Figure 1","display":"","copyAsset":false,"role":"figure","size":263418,"visible":true,"origin":"","legend":"\u003cp\u003e\u003cstrong\u003eNon-contrast CT (NCCT) demonstrating extensive inferior tracking of perinephric inflammatory change/collection beyond the perinephric space in Case 1 (July 2020).\u003c/strong\u003e\u003cbr\u003e\n(A) Coronal NCCT shows a right staghorn calculus within the collecting system (solid arrow) with marked perinephric inflammatory change and a perinephric collection (arrowhead). The inflammatory change/collection tracks inferiorly along the retroperitoneum toward the pelvic outlet and proximal thigh (dashed arrow, indicating inferior extension).\u003cbr\u003e\n(B) Axial NCCT at the renal level confirms the staghorn calculus (solid arrow) and the multiloculated perinephric collection (arrowhead).\u003cbr\u003e\n(C) Axial NCCT slightly caudal to the renal hilum shows extension of inflammatory change/collection beyond the perinephric space along the iliopsoas compartment (arrowhead).\u003cbr\u003e\n(D) Axial NCCT at the pelvic level demonstrates continued inferior tracking of inflammatory change/collection along the iliopsoas compartment (arrowhead).\u003cbr\u003e\n(E) Axial NCCT at the level of the pelvic outlet/proximal thigh shows further inferior extension into the anteromedial proximal thigh, near the obturator region (arrowhead).\u003c/p\u003e","description":"","filename":"floatimage1.png","url":"https://assets-eu.researchsquare.com/files/rs-8688678/v1/a5d38cd49060b50bda962e5f.png"},{"id":103586845,"identity":"181bd028-3e42-4fa6-bef0-9268f6872b3a","added_by":"auto","created_at":"2026-02-27 11:26:24","extension":"png","order_by":2,"title":"Figure 2","display":"","copyAsset":false,"role":"figure","size":272603,"visible":true,"origin":"","legend":"\u003cp\u003e\u003cstrong\u003eFollow-up contrast-enhanced CT demonstrating marked interval regression of extrarenal extension, with right renal atrophy and residual calculi in Case 1 (April 2021).\u003c/strong\u003e\u003cbr\u003e\n(A) Coronal contrast-enhanced CT shows marked right renal atrophy with residual calculi (solid arrow) and marked interval improvement of perinephric/retroperitoneal inflammatory change/collection (arrowhead), with regression of the previously inferiorly tracking collections toward the pelvic outlet and proximal thigh (dashed arrow, indicating prior inferior extent).\u003cbr\u003e\n(B) Axial contrast-enhanced CT at the renal level shows marked right renal atrophy with residual calculi (solid arrow) and reduced perinephric inflammatory change/collection (arrowhead); an indwelling nephrostomy tube is present (open arrowhead).\u003cbr\u003e\n(C) Axial contrast-enhanced CT slightly caudal to the renal hilum shows improved perinephric inflammation with regression of inflammatory extension along the iliopsoas compartment (arrowhead).\u003cbr\u003e\n(D) Axial contrast-enhanced CT at the pelvic level shows further regression of the prior inflammatory change/collection tracking along the iliopsoas compartment (arrowhead).\u003cbr\u003e\n(E) Axial contrast-enhanced CT at the pelvic outlet/proximal thigh shows marked regression of the prior anteromedial proximal thigh involvement near the obturator region (arrowhead).\u003c/p\u003e","description":"","filename":"floatimage2.png","url":"https://assets-eu.researchsquare.com/files/rs-8688678/v1/ae3c2fd6916fb336b53c2cc8.png"},{"id":103586946,"identity":"26b764c9-a3ea-4813-80f1-7e48aa2edab5","added_by":"auto","created_at":"2026-02-27 11:26:38","extension":"png","order_by":3,"title":"Figure 3","display":"","copyAsset":false,"role":"figure","size":278116,"visible":true,"origin":"","legend":"\u003cp\u003e\u003cstrong\u003eNon-contrast CT findings in Case 2 (February 2024).\u003c/strong\u003e\u003cbr\u003e\n(A) Coronal non-contrast CT demonstrates marked left renal atrophy with multiple intrarenal calculi (solid arrow). Extensive perinephric inflammatory change/collection is present with involvement of the left psoas major, suggestive of abscess formation (arrowhead). The fat plane between the perinephric inflammatory change/collection and the splenic flexure of the colon is indistinct (dashed arrow).\u003cbr\u003e\n(B) Axial non-contrast CT at the renal level shows severe left renal atrophy with intrarenal calculi (solid arrow) and extension of the perinephric collection into the adjacent psoas major compartment (arrowhead).\u003cbr\u003e\n(C) Axial non-contrast CT demonstrates an ill-defined interface between the perinephric inflammatory change/collection and the splenic flexure of the colon (dashed arrow), compatible with contiguous inflammatory involvement; adjacent extrarenal inflammatory change/collection is also present (arrowhead).\u003cbr\u003e\n(D) Axial non-contrast CT at the level of the lower pole demonstrates hyperdense foci compatible with calculi within the adjacent perinephric/psoas collection (solid arrow); the normal fat plane between the left kidney/perinephric inflammatory change/collection and the adjacent colon is near-completely effaced (dashed arrow), suggesting dense inflammatory adhesion.\u003cbr\u003e\n(E) Axial non-contrast CT demonstrates hyperdense foci compatible with calculi within the perinephric/psoas major collection (solid arrow), in keeping with inflammatory disruption and the presence of calculi within the surrounding collection (arrowhead).\u003c/p\u003e","description":"","filename":"floatimage3.png","url":"https://assets-eu.researchsquare.com/files/rs-8688678/v1/5779a641968109e6870909b0.png"},{"id":103586956,"identity":"318d1435-b136-4764-b37c-e504ada29172","added_by":"auto","created_at":"2026-02-27 11:26:41","extension":"png","order_by":4,"title":"Figure 4","display":"","copyAsset":false,"role":"figure","size":314830,"visible":true,"origin":"","legend":"\u003cp\u003e\u003cstrong\u003eImaging findings in Case 3 before and after percutaneous drainage.\u003c/strong\u003e\u003cbr\u003e\n(A) Coronal contrast-enhanced CT demonstrates a markedly enlarged right kidney with multiple calculi and severe hydronephrosis with pyonephrosis (solid arrow), with suspected contiguous involvement of the right psoas major muscle suggestive of abscess formation (arrowhead). No definite enhancing renal soft-tissue mass is identified.\u003cbr\u003e\n(B–C) Axial contrast-enhanced CT images show multiple right renal calculi and a markedly dilated, multiloculated collecting system compatible with pyonephrosis (solid arrows).\u003cbr\u003e\n(D) Axial contrast-enhanced CT demonstrates extension toward/into the right psoas major muscle (arrowhead).\u003cbr\u003e\n(E) Axial non-contrast CT shows interval regression of pyonephrosis in the upper calyx (solid arrow) after placement of a nephrostomy tube (open arrowhead).\u003cbr\u003e\n(F) Axial non-contrast CT shows increased pyonephrosis involving the mid-to-lower calyces (solid arrow) despite an additional nephrostomy tube in situ (open arrowhead), with hyperdense components compatible with hemorrhagic change.\u003cbr\u003e\n(G) Axial non-contrast CT demonstrates further increase of pyonephrosis involving the mid-to-lower calyces (solid arrow) with progression of inflammatory involvement of the right psoas major muscle (arrowhead).\u003c/p\u003e","description":"","filename":"floatimage4.png","url":"https://assets-eu.researchsquare.com/files/rs-8688678/v1/239d2a11398c5db8b349be45.png"},{"id":103587203,"identity":"0c626f3a-98cd-4f1d-ba0e-e628270b06e5","added_by":"auto","created_at":"2026-02-27 11:27:25","extension":"png","order_by":5,"title":"Figure 5","display":"","copyAsset":false,"role":"figure","size":710415,"visible":true,"origin":"","legend":"\u003cp\u003e\u003cstrong\u003eGross and histopathological findings of the resected right kidney in Case 3.\u003c/strong\u003e\u003cbr\u003e\n(A) Gross examination of the nephrectomy specimen reveals a large, cauliflower-like mass (approximately 8 × 6 cm) centered in the renal pelvis region. The cut surface is hemorrhagic and friable, with associated cystic dilatation and renal calculi.\u003cbr\u003e\n(B) Microscopic examination (hematoxylin and eosin staining, ×100) demonstrates irregular nests and sheets of atypical malignant cells infiltrating the stroma. The tumor exhibits moderate-to-poor differentiation, consistent with squamous cell carcinoma of the renal pelvis/upper urinary tract.\u003cbr\u003e\n(C–E) Immunohistochemical staining supports squamous differentiation. The tumor cells show diffuse strong positivity for p63 (nuclear staining, ×100; Panel C), p40 (nuclear staining, ×100; Panel D), and CK5/6 (cytoplasmic/membranous staining, ×40; Panel E).\u003c/p\u003e","description":"","filename":"floatimage5.png","url":"https://assets-eu.researchsquare.com/files/rs-8688678/v1/0d5b8b1b14e62b22c2d4c366.png"},{"id":103587365,"identity":"f18c9407-97b7-43ef-95ad-90726a6af063","added_by":"auto","created_at":"2026-02-27 11:27:49","extension":"pdf","order_by":0,"title":"","display":"","copyAsset":false,"role":"manuscript-pdf","size":2701791,"visible":true,"origin":"","legend":"","description":"","filename":"manuscript.pdf","url":"https://assets-eu.researchsquare.com/files/rs-8688678/v1/b7138b19-9057-4f83-9673-3684d0735df8.pdf"}],"financialInterests":"No competing interests reported.","formattedTitle":"Iliopsoas involvement complicating longstanding nephrolithiasis with chronic infection: a three-patient case series reconsidering “malignant lithiasis”","fulltext":[{"header":"Background","content":"\u003cp\u003eNephrolithiasis is a common chronic condition with a high recurrence rate and a substantial global health burden. Approximately 11% of the global population is affected by urolithiasis, with marked geographic variation in prevalence [\u003cspan citationid=\"CR1\" class=\"CitationRef\"\u003e1\u003c/span\u003e]. Although minimally invasive techniques have improved stone clearance, recurrence remains common and long-term prevention and follow-up are often required [\u003cspan citationid=\"CR2\" class=\"CitationRef\"\u003e2\u003c/span\u003e]. In regions with large populations and uneven access to healthcare, nephrolithiasis-related complications\u0026mdash;including severe infection and secondary malignancy\u0026mdash;continue to be encountered in routine clinical practice [\u003cspan citationid=\"CR3\" class=\"CitationRef\"\u003e3\u003c/span\u003e].\u003c/p\u003e \u003cp\u003eIn the era of open surgery, complex staghorn calculi associated with persistent infection and a destructive clinical course were described as \u0026ldquo;malignant lithiasis\u0026rdquo; (also termed \u0026ldquo;malignant nephrolithiasis\u0026rdquo; in historical reports) to convey clinical severity and poor outcomes rather than malignant histology [\u003cspan citationid=\"CR4\" class=\"CitationRef\"\u003e4\u003c/span\u003e]. Despite continuing advances in endourology, similar high-risk phenotypes persist, particularly in patients with longstanding stone disease complicated by chronic infection, delayed presentation, or inadequate follow-up, in whom recurrent or refractory infection, progressive stone growth, and renal functional decline may still occur. In this context, reconsidering this historical descriptor may help reinforce clinical vigilance and support risk stratification and timely escalation to definitive source control.\u003c/p\u003e \u003cp\u003eHowever, contemporary reports that systematically characterize this aggressive phenotype\u0026mdash;namely, longstanding nephrolithiasis with chronic infection complicated by extensive extrarenal extension with retroperitoneal abscess formation and/or occult malignancy\u0026mdash;remain limited.\u003c/p\u003e"},{"header":"Case presentation","content":"\u003ch2\u003e\u003cstrong\u003eCase 1\u003c/strong\u003e\u003c/h2\u003e\n\u003cp\u003eA 50-year-old woman was admitted on 27 July 2020 with recurrent right flank pain for 2 years, worsened over the preceding 3 months, with right lower-limb distension and pain and no recent fever. She had a 10-year history of right renal calculi without structured follow-up and denied tuberculosis exposure. At an outside hospital, contrast-enhanced CT excluded an overt renal malignant lesion but raised suspicion of genitourinary tuberculosis (GU-TB); empiric anti-tuberculous therapy for 2 months produced no improvement.\u003c/p\u003e\n\u003cp\u003eOn admission, temperature was 36.2 \u0026deg;C. Examination showed right costovertebral angle tenderness and a firm, tender mass extending from the right lower abdomen to the right inguinal region and medial thigh. Laboratory tests showed WBC 13.20 \u0026times; 10^9/L, hemoglobin 96 g/L, and serum creatinine 72 \u0026micro;mol/L. Urine culture and cytology were negative; interferon-\u0026gamma; release assay (IGRA) and serum anti-Mycobacterium tuberculosis IgG were negative.\u003c/p\u003e\n\u003cp\u003eNon-contrast CT (NCCT) demonstrated multiple right renal calculi with extensive perinephric inflammatory change and abscess formation, tracking inferiorly through the inguinal canal to the proximal thigh near the obturator region (Fig. 1). No adjacent organ involvement was reported, and GU-TB could not be excluded initially.\u0026nbsp;\u003c/p\u003e\n\u003cp\u003eAspiration from the inguinal abscess was negative for Mycobacterium tuberculosis by quantitative polymerase chain reaction (PCR) and smear microscopy, whereas culture grew \u003cem\u003eProteus mirabilis\u003c/em\u003e, excluding GU-TB. Incision and drainage (I\u0026amp;D) of the inguinal abscess was performed, followed by right percutaneous nephrostomy (PCN). One month later, the nephrostomy drained 5\u0026ndash;15 mL/day of turbid yellow pus and the inguinal drain produced 50\u0026ndash;80 mL/day of purulent fluid. Repeat CT showed only slight reduction of the iliac collection, with no significant change in the perinephric, psoas major, or iliopsoas lesions. Given inadequate response to drainage and antibiotics, percutaneous nephrolithotomy (PCNL) was performed to reduce stone burden and improve drainage for source control.\u003c/p\u003e\n\u003cp\u003eIntraoperatively, a large staghorn calculus occupied the renal pelvis and calyces with copious pus and necrotic tissue; the renal pelvic outlet could not be identified, and both antegrade and retrograde ureteral stent placement failed, suggesting complete obstruction. On postoperative day 1, she developed fever and hypotension consistent with urosepsis and septic shock, which improved with intensive supportive care. Infrared spectroscopic analysis confirmed a struvite (magnesium ammonium phosphate) stone. She was discharged with the nephrostomy tube in situ.\u003c/p\u003e\n\u003cp\u003eShe was readmitted on 19 April 2021. Contrast-enhanced CT on 20 April 2021 showed marked right renal atrophy with residual calculi and substantial regression of prior extrarenal extension (Fig. 2). Renal dynamic scintigraphy showed left GFR 88.65 mL/min and right GFR 6.36 mL/min, consistent with a non-functioning right kidney. After infection control, open right nephrectomy with retroperitoneal abscess debridement was performed on 25 April 2021. Histopathology showed chronic inflammation and necrosis; periodic acid\u0026ndash;Schiff (PAS) and acid-fast stains were negative. She was discharged 2 weeks postoperatively and remained clinically well at approximately 5-year follow-up, with normal serum creatinine.\u003c/p\u003e\n\u003ch2\u003e\u003cstrong\u003eCase 2\u003c/strong\u003e\u003c/h2\u003e\n\u003cp\u003eA 53-year-old man was admitted on 19 February 2024 with persistent left flank pain for 1 month and no recent fever. He had untreated left renal calculi diagnosed approximately 30 years earlier and denied tuberculosis exposure. Temperature was 36.3 \u0026deg;C, and examination showed left costovertebral angle tenderness. Laboratory tests showed WBC 7.66 \u0026times; 10^9/L, hemoglobin 119 g/L, platelets 439 \u0026times; 10^9/L, and serum creatinine 96 \u0026micro;mol/L. Urinalysis and urine culture were negative; repeated urine cytology was negative. IGRA and serum anti-Mycobacterium tuberculosis IgG were negative.\u003c/p\u003e\n\u003cp\u003eNCCT demonstrated multiple left renal calculi with marked renal atrophy and a perinephric abscess involving the ipsilateral psoas major muscle, abutting the splenic flexure of the colon (Fig. 3). Concomitant non-obstructing right renal calculi were present. Contrast-enhanced CT showed no definite renal malignant lesion, and GU-TB remained in the differential diagnosis. Ultrasound-guided perinephric drainage yielded 5\u0026ndash;20 mL/day of purulent fluid. Quantitative PCR and smear microscopy for Mycobacterium tuberculosis were negative, whereas culture grew \u003cem\u003eBacteroides fragilis\u003c/em\u003e, excluding GU-TB. Targeted antimicrobial therapy was initiated with symptomatic improvement; drainage output gradually ceased and the catheter dislodged spontaneously without complication.\u003c/p\u003e\n\u003cp\u003eOn 17 June 2024, he was readmitted with anorexia and progressive anemia (hemoglobin 86 g/L), without fever or urinary symptoms. Renal dynamic scintigraphy showed right GFR 63.24 mL/min and left GFR 6.32 mL/min, consistent with a non-functioning left kidney. Repeat CT on 19 June 2024 showed no meaningful reduction in the perinephric or psoas collections. After multidisciplinary discussion, open left nephrectomy with retroperitoneal abscess debridement was performed on 25 June 2024; dense adhesions at the splenic flexure necessitated partial colectomy. Histopathology was consistent with a calculous renal abscess. He recovered uneventfully and was discharged 10 days postoperatively. One month later, he underwent holmium laser lithotripsy for right renal calculi. At approximately 18 months postoperatively, he remained clinically well without recurrent pain; serum creatinine was normal and there was no recurrence of right renal stones.\u003c/p\u003e\n\u003ch2\u003e\u003cstrong\u003eCase 3\u003c/strong\u003e\u003c/h2\u003e\n\u003cp\u003eA 59-year-old man was admitted on 11 October 2024 with intermittent right flank pain for 6 months, worsened over the preceding month, with purulent urine and abdominal distension, without recent fever. He had a \u0026gt;20-year history of nephrolithiasis with multiple prior stone-related procedures and residual right renal calculi; he denied tuberculosis. Temperature was 36.3 \u0026deg;C. Laboratory tests showed WBC 9.27 \u0026times; 10^9/L, hemoglobin 109 g/L, platelets 419 \u0026times; 10^9/L, and serum creatinine 169 \u0026micro;mol/L. Urinalysis showed RBC 86/\u0026micro;L and WBC 19,477/\u0026micro;L. Urine culture grew \u003cem\u003ePseudomonas aeruginosa\u003c/em\u003e, and repeated urine cytology was negative. Renal dynamic scintigraphy showed impaired bilateral renal function, predominantly affecting the right kidney (right GFR 10.92 mL/min; left GFR 29.42 mL/min).\u003c/p\u003e\n\u003cp\u003eNon-contrast and contrast-enhanced CT urography demonstrated multiple right renal calculi with severe hydronephrosis and pyonephrosis, with suspected involvement of the right psoas major muscle (Fig. 4A\u0026ndash;D). Percutaneous nephrostomy (PCN) was performed; because the renal pelvis was small with markedly dilated calyces, two nephrostomy tubes were placed (upper calyx and mid-to-lower calyces) to optimize drainage. Despite drainage and targeted antimicrobial therapy, symptoms worsened, and repeat imaging showed persistent infection with suspected pyonephrosis and progressive retroperitoneal spread (Fig. 4E\u0026ndash;G). Open right nephrectomy with psoas abscess resection/debridement was therefore performed to achieve definitive source control for uncontrolled infection.\u003c/p\u003e\n\u003cp\u003eUnexpectedly, histopathological examination of the nephrectomy specimen demonstrated a moderately to poorly differentiated squamous cell carcinoma (SCC) of the renal pelvis/upper urinary tract (Fig. 5). According to the final pathology report, the tumor invaded the renal sinus fat and perirenal adipose tissue with vascular tumor emboli, and metastatic carcinoma was present in 4 of 7 regional lymph nodes (pathological stage pT3N2Mx). Additional findings in the final pathology report not shown in Fig. 5 included focal sarcomatoid change, negativity for PAX8 and GATA3, and a high Ki-67 proliferation index (approximately 50%). He was discharged 2 weeks postoperatively but experienced rapid systemic progression and died 1 month later due to widespread metastases and multiorgan dysfunction.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eTable 1.\u003c/strong\u003e\u003cstrong\u003e\u0026nbsp;\u003c/strong\u003eClinical characteristics, interventions, and outcomes of three patients\u003c/p\u003e\n \u003ctable border=\"1\" cellspacing=\"0\" cellpadding=\"0\" width=\"567\"\u003e\n \u003ctbody\u003e\n \u003ctr\u003e\n \u003ctd style=\"width: 104px;\"\u003e\n \u003cp\u003e\u003cstrong\u003eKey elements\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 151px;\"\u003e\n \u003cp\u003e\u003cstrong\u003eCase 1\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 161px;\"\u003e\n \u003cp\u003e\u003cstrong\u003eCase 2\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 151px;\"\u003e\n \u003cp\u003e\u003cstrong\u003eCase 3\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd style=\"width: 104px;\"\u003e\n \u003cp\u003e\u003cstrong\u003eAge / Sex\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 151px;\"\u003e\n \u003cp\u003e50 / Female\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 161px;\"\u003e\n \u003cp\u003e53 / Male\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 151px;\"\u003e\n \u003cp\u003e59 / Male\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd style=\"width: 104px;\"\u003e\n \u003cp\u003e\u003cstrong\u003eHistory\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 151px;\"\u003e\n \u003cp\u003e10-year renal calculi; no structured follow-up\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 161px;\"\u003e\n \u003cp\u003e~30-year left renal calculi; untreated\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 151px;\"\u003e\n \u003cp\u003e\u0026gt;20-year; multiple prior procedures\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd style=\"width: 104px;\"\u003e\n \u003cp\u003e\u003cstrong\u003eExtrarenal extension (CT)\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 151px;\"\u003e\n \u003cp\u003eAbscess tracking to inguinal canal and proximal thigh\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 161px;\"\u003e\n \u003cp\u003ePerinephric abscess involving ipsilateral psoas major; abutting splenic flexure\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 151px;\"\u003e\n \u003cp\u003eSuspected pyonephrosis and progressive retroperitoneal spread\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd style=\"width: 104px;\"\u003e\n \u003cp\u003e\u003cstrong\u003eMicrobiology\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 151px;\"\u003e\n \u003cp\u003eAbscess:\u003cem\u003e\u0026nbsp;P. mirabilis\u003c/em\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 161px;\"\u003e\n \u003cp\u003eAbscess:\u003cem\u003e\u0026nbsp;B. fragilis\u003c/em\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 151px;\"\u003e\n \u003cp\u003eUrine: \u003cem\u003eP. aeruginosa\u003c/em\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd style=\"width: 104px;\"\u003e\n \u003cp\u003e\u003cstrong\u003eKey interventions\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 151px;\"\u003e\n \u003cp\u003eI\u0026amp;D; PCN; PCNL \u0026rarr; Open nephrectomy + debridement\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 161px;\"\u003e\n \u003cp\u003eDrainage \u0026rarr; Open nephrectomy + debridement (partial colectomy)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 151px;\"\u003e\n \u003cp\u003ePCN \u0026rarr; Open nephrectomy + psoas abscess debridement\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd style=\"width: 104px;\"\u003e\n \u003cp\u003e\u003cstrong\u003eSplit function (GFR, mL/min)\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 151px;\"\u003e\n \u003cp\u003eRight: 6.36;\u0026nbsp;\u003c/p\u003e\n \u003cp\u003eLeft: 88.65\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 161px;\"\u003e\n \u003cp\u003eRight: 63.24;\u0026nbsp;\u003c/p\u003e\n \u003cp\u003eLeft: 6.32\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 151px;\"\u003e\n \u003cp\u003eRight: 10.92;\u003c/p\u003e\n \u003cp\u003e\u0026nbsp;Left: 29.42\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd style=\"width: 104px;\"\u003e\n \u003cp\u003e\u003cstrong\u003ePathology\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 151px;\"\u003e\n \u003cp\u003eChronic inflammation/necrosis\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 161px;\"\u003e\n \u003cp\u003eCalculous renal abscess\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 151px;\"\u003e\n \u003cp\u003eSquamous cell carcinoma (SCC)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd style=\"width: 104px;\"\u003e\n \u003cp\u003e\u003cstrong\u003eOutcome\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 151px;\"\u003e\n \u003cp\u003eRecovered; ~5-year follow-up\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 161px;\"\u003e\n \u003cp\u003eRecovered; ~18 months\u003c/p\u003e\n \u003cp\u003efollow-up\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 151px;\"\u003e\n \u003cp\u003eDied 1 month postoperatively\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003c/tbody\u003e\n \u003c/table\u003e\n\u003c/div\u003e\n\u003cp\u003e\u003cstrong\u003eAbbreviations:\u003c/strong\u003e CT, computed tomography; GFR, glomerular filtration rate; I\u0026amp;D, incision and drainage; PCN, percutaneous nephrostomy; PCNL, percutaneous nephrolithotomy; SCC, squamous cell carcinoma.\u003c/p\u003e"},{"header":"Discussion","content":"\u003cp\u003eAcross our three patients, longstanding nephrolithiasis with chronic infection followed a destructive trajectory: persistent stones complicated by infection; recurrent or smoldering infection; radiographically evident extrarenal extension; and progressive loss of renal function ultimately necessitating nephrectomy. In one case, systematic histopathological evaluation of the nephrectomy specimen revealed occult squamous cell carcinoma. These cases foreground three practical red flags that should trigger timely escalation of evaluation and management: (1) recurrent or refractory infection; (2) imaging evidence of extrarenal extension; and (3) progressive decline in split renal function. In this context, we reconsider \u0026ldquo;malignant lithiasis\u0026rdquo; as a historical descriptor of a high-risk clinical course rather than a diagnostic label implying malignant histology.\u003c/p\u003e\n\u003cp\u003eUrolithiasis is increasingly recognized as a chronic condition with a notable global health burden that requires long-term prevention and follow-up [1\u0026ndash;2]. Despite advances in minimally invasive techniques, recurrence remains common, and severe infectious complications and renal destruction still occur in a subset of patients. In this report, we use \u0026ldquo;nephrolithiasis with chronic infection\u0026rdquo; to describe longstanding stones complicated by persistent or recurrent infection, regardless of stone composition; infection-related (struvite) stones are a common, but not exclusive, substrate for this phenotype. Clinically, this phenotype can be operationally suspected when a prolonged stone history coexists with the red flags above\u0026mdash;recurrent or refractory infection, imaging evidence of extrarenal inflammatory extension (e.g., perinephric or iliopsoas involvement), and/or progressive loss of ipsilateral renal function\u0026mdash;prompting timely progression from temporizing measures to definitive source control.\u003c/p\u003e\n\u003cp\u003eHistorically, in the era of open surgery, complex staghorn calculi associated with chronic infection were described as \u0026ldquo;malignant lithiasis\u0026rdquo; to convey clinical severity and poor prognosis rather than malignant histology [4]. Mart\u0026iacute;nez-Pi\u0026ntilde;eiro et al. emphasized the close association between staghorn calculi and infection, including a high likelihood of recurrence and progressive stone growth in the presence of persistent bacteriuria\u0026mdash;features that can drive repeated infectious episodes and progressive renal damage when management is delayed or incomplete [4]. Subsequent work and contemporary reviews continue to underscore this infection\u0026ndash;recurrence\u0026ndash;progression paradigm and the risk of renal functional decline when definitive management is delayed or incomplete, supporting the ongoing clinical relevance of this historical descriptor even in the modern era [5]. In a related context, Pagano et al. used \u0026ldquo;malignant lithiasis\u0026rdquo; to describe cases with severely compromised renal function and heterogeneous postoperative renal functional trajectories, reinforcing that this label captured a function-threatening course rather than malignant histology [6]. Cystine stones, characterized by frequent recurrence and rapid progression, have also been discussed under this descriptor as a marker of a high-risk course rather than malignant histology [7]. More broadly, infection-related stones constitute a high-risk subtype, often characterized by rapid growth, persistent bacterial colonization, frequent recurrence, and an increased risk of functional decline or nephrectomy if definitive management is delayed [8\u0026ndash;10]. Inadequate treatment may progress to recurrent pyelonephritis, urosepsis, and even death [11,12]. Infection/struvite stones have also been associated with increased postoperative sepsis after endourological stone surgery; these findings align with evidence linking positive stone culture to higher postoperative sepsis rates, supporting the concept that stone-associated bacterial reservoirs can amplify infectious risk [13,14]. Together, these data reinforce the value of recognizing high-risk phenotypes consistent with the historical concept of \u0026ldquo;malignant lithiasis\u0026rdquo; as a descriptor of destructive stone disease with potential irreversible renal functional loss.\u003c/p\u003e\n\u003cp\u003eAlthough nephrolithiasis is often perceived as benign, the mortality risk\u0026mdash;while overall low\u0026mdash;is real in severe or complicated disease. A systematic review spanning the past two decades summarized reported deaths related to kidney stone disease, identified sepsis as the leading cause, and noted that high stone burden and comorbidities were common among fatal cases [15]. These findings reinforce meticulous preoperative optimization and timely definitive management when stone disease is complicated by infection and systemic illness, consistent with guideline-based principles for surgical management of urinary stones [16].\u003c/p\u003e\n\u003cp\u003eSevere renal infection can be complicated by extensive perinephric/pararenal involvement on CT, and escalation to definitive management may be required [17,18]. In longstanding nephrolithiasis, extrarenal extension can mark one of the most severe trajectories of infection [17,18]. Perinephric infection may extend contiguously beyond the perirenal space into the iliopsoas compartment, resulting in iliopsoas abscesses associated with notable morbidity; mortality has been reported in severe or advanced cases [19,20,23]. Cross-sectional imaging\u0026mdash;particularly CT\u0026mdash;defines disease extent and guides drainage and surgical planning [18,21]. Because iliopsoas abscesses are frequently secondary to adjacent or distant foci, careful evaluation of potential sources, including genitourinary infection, remains important [23]. Management emphasizes timely source control with appropriate antimicrobial therapy, often combined with image-guided drainage when feasible [18,22,24]. After stabilization, minimally invasive drainage and other source control strategies may be used to control infection and, in selected patients, facilitate subsequent definitive stone management [25]. When the affected kidney is irreversibly damaged, definitive source control may require surgical intervention, and nephrectomy should be considered in selected cases [10,18].\u003c/p\u003e\n\u003cp\u003eA further concern is the association between longstanding nephrolithiasis and upper urinary tract malignancy, particularly renal pelvic squamous cell carcinoma (SCC) [26\u0026ndash;28]. Chronic irritation and infection are recognized drivers of squamous metaplasia and malignant transformation [28], yet preoperative diagnosis remains challenging because stones and inflammation can render clinical and radiological findings nonspecific [27,30]. Upper urinary tract malignancies have been incidentally detected during or after percutaneous nephrolithotomy (PCNL), underscoring that cancer may coexist with stone disease and be missed on preoperative assessment [29,30]. Epidemiological data also suggest an increased risk of upper urinary tract urothelial carcinoma (UTUC)\u0026mdash;and, in some cohorts, renal cell carcinoma\u0026mdash;in patients with nephrolithiasis [3,26,31]. Tumors with squamous differentiation tend to be high-risk [27], while xanthogranulomatous pyelonephritis or genitourinary tuberculosis can mimic malignancy and further complicate the differential diagnosis [32,36]. Accordingly, European Association of Urology (EAU) guidance supports diagnostic ureteroscopy (preferably without biopsy) when imaging and/or voided urine cytology are insufficient for diagnosis and/or risk stratification [33]. When suspicious upper urinary tract mucosal abnormalities are encountered, targeted biopsy has been advocated to facilitate timely diagnosis in selected high-risk patients [34]. Occult malignancy has also been reported in nephrectomy specimens from stone-related non-functioning kidneys, supporting systematic histopathological assessment in this setting [35].\u003c/p\u003e\n\u003cp\u003eThese challenges may be amplified in socioeconomically disadvantaged settings, where barriers to timely care and fragmented follow-up are more prevalent. Evidence suggests that neighborhood socioeconomic disadvantage is associated with worse urinary risk factors for recurrent urolithiasis and reduced access to medical management, while adherence to guideline-based prevention and follow-up remains suboptimal in diverse low-resource populations [37,38].\u003c/p\u003e\n\u003cp\u003eTaken together, the clinical trajectory observed in our cases and the supporting literature support a pragmatic, escalation-oriented approach anchored on the three red flags above and operationalized as practical management considerations (summarized in the Practical points section below).\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003ePractical points.\u003c/strong\u003e\u003c/p\u003e\n\u003col start=\"1\" type=\"1\"\u003e\n \u003cli\u003e\u003cstrong\u003eRisk recognition:\u003c/strong\u003e Treat longstanding nephrolithiasis with chronic or refractory infection, extrarenal extension (e.g., perinephric abscess), or progressive renal functional decline as a high-risk clinical entity [10,39]. Socioeconomic disadvantage may further increase the likelihood of irreversible complications [37,38]. Early recognition should prompt timely intervention to optimize outcomes [10,16].\u003c/li\u003e\n \u003cli\u003e\u003cstrong\u003eInitial source control and exclusion of mimics:\u003c/strong\u003e After genitourinary tuberculosis has been reasonably excluded [36], prioritize early urinary drainage (retrograde ureteral stenting or percutaneous nephrostomy) and stabilization; defer definitive stone manipulation until sepsis is controlled and infection has been appropriately treated [10].\u003c/li\u003e\n \u003cli\u003e\u003cstrong\u003eDefinitive management and functional triage:\u003c/strong\u003e Aim for complete stone clearance where feasible [9]. If clearance is incomplete, counsel patients and ensure structured follow-up, as residual fragments\u0026mdash;especially in infection/struvite stone disease\u0026mdash;may perpetuate bacteriuria, recurrent infection, and stone regrowth [9,11,40]. Quantify split renal function early (e.g., nuclear renography) and reassess after infection control to guide kidney-preserving versus extirpative surgery [10,40]. Consider timely nephrectomy for stone-related non-functioning kidneys to achieve definitive source control and to exclude occult malignancy, which can be challenging to detect preoperatively [35,40\u0026ndash;42].\u003c/li\u003e\n \u003cli\u003e\u003cstrong\u003eOperative planning:\u003c/strong\u003e In advanced infection with extrarenal extension, anticipate dense adhesions, distorted hilar anatomy, and potential adjacent-organ involvement, which may increase procedural complexity and complications [32,42]. Meticulous imaging review, proactive planning, and multidisciplinary collaboration may improve safety [16,40].\u003c/li\u003e\n \u003cli\u003e\u003cstrong\u003eMalignancy vigilance:\u003c/strong\u003e Maintain a high index of suspicion for occult malignancy and perform systematic histopathological evaluation of nephrectomy specimens, particularly in stone-related non-functioning kidneys [26,31,35].\u003c/li\u003e\n\u003c/ol\u003e\n\u003cp\u003e\u003cstrong\u003eLimitations and future directions.\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eThis small case series is subject to selection and referral biases and cannot quantify risk or establish causality between chronic infection, extrarenal extension, renal functional loss, and management decisions. Clinical heterogeneity (patient factors, microbiology, prior interventions, and timing of definitive surgery) may have influenced outcomes. \u0026ldquo;Nephrolithiasis with chronic infection\u0026rdquo; is used as a pragmatic clinical construct rather than a validated classification. Multicenter cohorts are needed to refine imaging- and function-based criteria, identify predictors of irreversible damage and extrarenal spread, and evaluate whether earlier escalation to definitive source control improves outcomes.\u003c/p\u003e"},{"header":"Conclusions","content":"\u003cp\u003eLongstanding nephrolithiasis with chronic infection may follow an aggressive, destructive course, leading to extensive retroperitoneal infection, renal functional loss, and, occasionally, occult malignancy [35,40]. Despite improved stone clearance with endoscopic and other minimally invasive approaches, recurrence remains substantial and delayed care continues to contribute to irreversible complications [1,2,10,40]. Reconsidering \u0026ldquo;malignant lithiasis\u0026rdquo; as a historical descriptor of a destructive clinical trajectory\u0026mdash;rather than a diagnostic label\u0026mdash;may help clinicians recognize high-risk presentations earlier, including recurrent or refractory infection, imaging evidence of extrarenal extension, and progressive decline in split renal function, and prompt clinical vigilance, structured follow-up, and timely escalation to definitive source control [4,6,16,40]. Accordingly, in refractory or complex stone disease, timely progression to definitive treatment (including nephrectomy for non-functioning kidneys) and routine histopathology of nephrectomy specimens should be considered to support individualized decision-making and minimize missed malignancy [16,35].\u003c/p\u003e"},{"header":"Abbreviations","content":"\u003cp\u003eCT: Computed tomography; EAU: European Association of Urology; GFR: Glomerular filtration rate; GU-TB: Genitourinary tuberculosis; I\u0026amp;D: Incision and drainage; PCN: Percutaneous nephrostomy; PCNL: Percutaneous nephrolithotomy; SCC: Squamous cell carcinoma; UTUC: Upper urinary tract urothelial carcinoma.\u003c/p\u003e"},{"header":"Declarations","content":"\u003cp\u003e\u003cstrong\u003eAcknowledgements\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eThe authors sincerely thank the patients in Cases 1 and 2, and the family of the patient in Case 3, for providing consent for publication of this case series.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eAuthors\u0026rsquo; contributions\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eDL drafted the manuscript and reviewed the literature. MM and XY acquired the clinical data and contributed to drafting the manuscript. ZB interpreted the imaging findings and reviewed the literature. HX interpreted the pathological findings. CL revised the manuscript for important intellectual content. All authors read and approved the final manuscript.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eFunding\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eThis study received no specific grant from any funding agency in the public, commercial, or not-for-profit sectors.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eAvailability of data and materials\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eNo datasets were generated or analysed during the current study.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eEthics approval and consent to participate\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eThis case series was approved by the Ethics Committee of Haikou Municipal People\u0026rsquo;s Hospital.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eConsent for publication\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eWritten informed consent was obtained from the patients in Cases 1 and 2 for publication of this case series and any accompanying images. For Case 3, written informed consent for publication (including any accompanying images) was obtained from the patient\u0026rsquo;s legal next of kin because the patient is deceased.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eCompeting interests\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eThe authors declare that they have no competing interests.\u003c/p\u003e"},{"header":"References","content":"\u003col\u003e\n\u003cli\u003eVera-Ponce VJ, Sanchez-Tamay NM, Ballena-Caicedo J, et al. Global prevalence of urolithiasis: a meta-analysis accounting for methodological heterogeneity. Front Urol. 2025; 5:1705953. doi:10.3389/fruro.2025.1705953.\u003c/li\u003e\n\u003cli\u003eZeng G, Zhu W, Robertson WG, et al. International Alliance of Urolithiasis (IAU) guidelines on the metabolic evaluation and medical management of urolithiasis. Urolithiasis. 2023;51(1):4. doi:10.1007/s00240-022-01387-2.\u003c/li\u003e\n\u003cli\u003eCheungpasitporn W, Thongprayoon C, O\u0026apos;Corragain OA, et al. The risk of kidney cancer in patients with kidney stones: a systematic review and meta-analysis. QJM. 2015;108(3):205\u0026ndash;212. doi:10.1093/qjmed/hcu195.\u003c/li\u003e\n\u003cli\u003eMart\u0026iacute;nez-Pi\u0026ntilde;eiro JA, de Iriarte EG, Armero AH. The problem of recurrences and infection after surgical removal of staghorn calculi. Eur Urol. 1982;8(2):94\u0026ndash;101. doi:10.1159/000473488.\u003c/li\u003e\n\u003cli\u003eDiri A, Diri B. Management of staghorn renal stones. Ren Fail. 2018;40(1):357\u0026ndash;362. doi:10.1080/0886022X.2018.1459306.\u003c/li\u003e\n\u003cli\u003ePagano F, Tasca A, Oliva G. The evolution of renal function after surgical treatment of malignant lithiasis with severely compromised renal function. Eur Urol. 1982;8(1):1\u0026ndash;4. doi:10.1159/000473466.\u003c/li\u003e\n\u003cli\u003eEgghart G, Marquardt HD, Kastert HB, et al. Percutaneous nephrostomy and irrigation lithochemolysis: a new concept for the treatment of cystine stones. Int Urol Nephrol. 1983;15(2):131\u0026ndash;136. doi:10.1007/BF02085442.\u003c/li\u003e\n\u003cli\u003eWang LP, Wong HY, Griffith DP. Treatment options in struvite stones. Urol Clin North Am. 1997;24(1):149\u0026ndash;162. doi:10.1016/S0094-0143(05)70360-8.\u003c/li\u003e\n\u003cli\u003eMarien T, Miller NL. Treatment of the infected stone. Urol Clin North Am. 2015;42(4):459\u0026ndash;472. doi:10.1016/j.ucl.2015.05.009.\u003c/li\u003e\n\u003cli\u003eSkolarikos A, Geraghty R, Somani B, et al. European Association of Urology guidelines on the diagnosis and treatment of urolithiasis. Eur Urol. 2025;88(1):64\u0026ndash;75. doi:10.1016/j.eururo.2025.03.011.\u003c/li\u003e\n\u003cli\u003eEspinosa-Ortiz EJ, Eisner BH, Lange D, Gerlach R. Current insights into the mechanisms and management of infection stones. Nat Rev Urol. 2019;16(1):35\u0026ndash;53. doi:10.1038/s41585-018-0120-z.\u003c/li\u003e\n\u003cli\u003eFlannigan R, Choy WH, Chew B, et al. Renal struvite stones: pathogenesis, microbiology, and management strategies. Nat Rev Urol. 2014;11(6):333\u0026ndash;341. doi:10.1038/nrurol.2014.99.\u003c/li\u003e\n\u003cli\u003eGao X, Lu C, Xie F, et al. Risk factors for sepsis in patients with struvite stones following percutaneous nephrolithotomy. World J Urol. 2020;38(1):219\u0026ndash;229. doi:10.1007/s00345-019-02748-0.\u003c/li\u003e\n\u003cli\u003eEswara JR, Shariftabrizi A, Sacco D. Positive stone culture is associated with a higher rate of sepsis after endourological procedures. Urolithiasis. 2013;41(5):411\u0026ndash;414. doi:10.1007/s00240-013-0581-8.\u003c/li\u003e\n\u003cli\u003eWhitehurst L, Jones P, Somani BK. Mortality from kidney stone disease (KSD) as reported in the literature over the last two decades: a systematic review. World J Urol. 2019;37(5):759\u0026ndash;776. doi:10.1007/s00345-018-2424-2.\u003c/li\u003e\n\u003cli\u003eAssimos D, Krambeck A, Miller NL, et al. Surgical management of stones: American Urological Association/Endourological Society guideline, Part II. J Urol. 2016;196:1161\u0026ndash;1169. doi:10.1016/j.juro.2016.05.091.\u003c/li\u003e\n\u003cli\u003eHuang JJ, Tseng CC. Emphysematous pyelonephritis: clinicoradiological classification. Arch Intern Med. 2000;160(6):797\u0026ndash;805. doi:10.1001/archinte.160.6.797.\u003c/li\u003e\n\u003cli\u003eRubilotta E, Balzarro M, Lacola V, Sarti A, Porcaro AB, Artibani W. Current clinical management of renal and perinephric abscesses: a literature review. Urologia. 2014;81(3):144\u0026ndash;147. doi:10.5301/urologia.5000044.\u003c/li\u003e\n\u003cli\u003eRicci MA, Rose FB, Meyer KK. Pyogenic psoas abscess: worldwide variations in etiology. World J Surg. 1986 Oct;10(5):834-843. doi:10.1007/BF01655254.\u003c/li\u003e\n\u003cli\u003eMallick IH, Thoufeeq MH, Rajendran TP. Iliopsoas abscesses. Postgrad Med J. 2004;80(946):459\u0026ndash;462. doi:10.1136/pgmj.2003.017665.\u003c/li\u003e\n\u003cli\u003eShields D, Robinson P, Crowley TP. Iliopsoas abscess--a review and update on the literature. Int J Surg. 2012;10(9):466-9. doi:10.1016/j.ijsu.2012.08.016.\u003c/li\u003e\n\u003cli\u003eShu T, Green JM, Orihuela E. Renal and perirenal abscesses in patients with otherwise anatomically normal urinary tracts. J Urol. 2004 Jul;172(1):148-50. doi:10.1097/01.ju.0000132140.48587.b8.\u003c/li\u003e\n\u003cli\u003eSantaella RO, Fishman EK, Lipsett PA. Primary vs secondary iliopsoas abscess: presentation, microbiology, and treatment. Arch Surg. 1995;130(12):1309\u0026ndash;1313. doi:10.1001/archsurg.1995.01430120063009.\u003c/li\u003e\n\u003cli\u003eBrook I. Microbiology and management of abdominal abscesses. Dig Dis Sci. 2008;53(10):2585\u0026ndash;2591. doi:10.1007/s10620-007-0194-6.\u003c/li\u003e\n\u003cli\u003eLi E, Hong J, Zhou M, et al. Percutaneous nephroscopy combined with ultrasound-guided negative-pressure suction for the treatment of perinephric abscess: a case series. BMC Urol. 2022;22(1):140. doi:10.1186/s12894-022-01091-8.\u003c/li\u003e\n\u003cli\u003eChow WH, Lindblad P, Gridley G, et al. Risk of urinary tract cancers following kidney or ureter stones. J Natl Cancer Inst. 1997;89(19):1453\u0026ndash;1457. doi:10.1093/jnci/89.19.1453.\u003c/li\u003e\n\u003cli\u003eHolm\u0026auml;ng S, Lele SM, Johansson SL. Squamous cell carcinoma of the renal pelvis and ureter: incidence, symptoms, treatment and outcome. J Urol. 2007;178(1):51\u0026ndash;56. doi:10.1016/j.juro.2007.03.033.\u003c/li\u003e\n\u003cli\u003eBhaijee F. Squamous cell carcinoma of the renal pelvis. Ann Diagn Pathol. 2012;16(2):124\u0026ndash;127. doi:10.1016/j.anndiagpath.2011.08.009.\u003c/li\u003e\n\u003cli\u003eAn L, Xiong L, Xu Q, et al. Incidental diagnosis of renal pelvic tumor in patients who underwent percutaneous nephrolithotomy: a report of 6 cases and review of the literature. Urology. 2023;171:64\u0026ndash;70. doi:10.1016/j.urology.2022.09.005.\u003c/li\u003e\n\u003cli\u003eKatz R, Gofrit ON, Golijanin D, et al. Urothelial cancer of the renal pelvis in percutaneous nephrolithotomy patients. Urol Int. 2005;75(1):17\u0026ndash;20. doi:10.1159/000085921.\u003c/li\u003e\n\u003cli\u003evan de Pol JAA, van den Brandt PA, Schouten LJ. Kidney stones and the risk of renal cell carcinoma and upper urinary tract urothelial carcinoma: the Netherlands Cohort Study. Br J Cancer. 2019;120(3):368\u0026ndash;374. doi:10.1038/s41416-018-0356-7.\u003c/li\u003e\n\u003cli\u003eGravestock P, Moore L, Harding C, et al. Xanthogranulomatous pyelonephritis: a review and meta-analysis with a focus on management. 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Radiographics. 2021;41(4):1123\u0026ndash;1143. doi:10.1148/rg.2021200154.\u003c/li\u003e\n\u003cli\u003eHo L, Chehroudi C, Jevnikar B, et al. Neighborhood socioeconomic disadvantage is associated with worse urinary risk factors and access to medical management for urolithiasis. J Endourol. 2025;39(3):314\u0026ndash;321. doi:10.1089/end.2024.0384.\u003c/li\u003e\n\u003cli\u003eHunt ER, Bergeron T, Edelblute B, et al. Physician and patient adherence to kidney stone prevention guidelines in a diverse, low-resource, urban population. Urology. 2025;201:1\u0026ndash;7. doi:10.1016/j.urology.2025.02.040.\u003c/li\u003e\n\u003cli\u003eLiu XQ, Wang CC, Liu YB, Liu K. Renal and perinephric abscesses in West China Hospital: 10-year retrospective-descriptive study. World J Nephrol. 2016;5(1):108\u0026ndash;114. doi:10.5527/wjn.v5.i1.108.\u003c/li\u003e\n\u003cli\u003eSharbaugh A, Morgan Nikonow T, Kunkel G, et al. Contemporary best practice in the management of staghorn calculi. Ther Adv Urol. 2019;11:1756287219847099. doi:10.1177/1756287219847099.\u003c/li\u003e\n\u003cli\u003eZengin K, Tanik S, Sener NC, et al. Incidence of renal carcinoma in non-functioning kidney due to renal pelvic stone disease. Mol Clin Oncol. 2015;3(4):941\u0026ndash;943. doi:10.3892/mco.2015.550.\u003c/li\u003e\n\u003cli\u003eDanilovic A, Ferreira TAC, Maia GVA, et al. Predictors of surgical complications of nephrectomy for urolithiasis. Int Braz J Urol. 2019;45(1):100\u0026ndash;107. doi:10.1590/S1677-5538.IBJU.2018.0246.\u003c/li\u003e\n\u003c/ol\u003e"}],"fulltextSource":"","fullText":"","funders":[],"hasAdminPriorityOnWorkflow":false,"hasManuscriptDocX":true,"hasOptedInToPreprint":true,"hasPassedJournalQc":"","hasAnyPriority":false,"hideJournal":false,"highlight":"","institution":"","isAcceptedByJournal":false,"isAuthorSuppliedPdf":false,"isDeskRejected":"","isHiddenFromSearch":false,"isInQc":false,"isInWorkflow":false,"isPdf":false,"isPdfUpToDate":true,"isWithdrawnOrRetracted":false,"journal":{"display":true,"email":"[email protected]","identity":"bmc-urology","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":false,"externalIdentity":"buro","sideBox":"Learn more about [BMC Urology](http://bmcurol.biomedcentral.com/)","snPcode":"","submissionUrl":"https://www.editorialmanager.com/buro/default.aspx","title":"BMC Urology","twitterHandle":"BMC_series","acdcEnabled":true,"dfaEnabled":false,"editorialSystem":"em","reportingPortfolio":"BMC Series","inReviewEnabled":true,"inReviewRevisionsEnabled":true},"keywords":"malignant lithiasis, nephrolithiasis, nephrolithiasis with chronic infection, perinephric abscess, iliopsoas abscess, extrarenal extension, renal squamous cell carcinoma, nephrectomy","lastPublishedDoi":"10.21203/rs.3.rs-8688678/v1","lastPublishedDoiUrl":"https://doi.org/10.21203/rs.3.rs-8688678/v1","license":{"name":"CC BY 4.0","url":"https://creativecommons.org/licenses/by/4.0/"},"manuscriptAbstract":"\u003ch2\u003eBackground\u003c/h2\u003e \u003cp\u003eSevere complications of longstanding nephrolithiasis with chronic infection remain clinically relevant despite continuing advances in endourological techniques. This phenotype may extend beyond the collecting system, resulting in extensive retroperitoneal infection with extrarenal extension, irreversible renal functional loss, and, in rare instances, occult malignancy. Reconsidering the historical descriptor \u0026ldquo;malignant lithiasis\u0026rdquo; may help frame this aggressive clinical trajectory, particularly in patients with delayed presentation or limited access to timely care.\u003c/p\u003e\u003ch2\u003eCase presentation:\u003c/h2\u003e \u003cp\u003eWe report three cases of longstanding nephrolithiasis with chronic infection with iliopsoas involvement. Case 1 was a 50-year-old woman with perinephric and iliopsoas abscesses, with inferior tracking along the iliopsoas compartment into the obturator region. Case 2 was a 53-year-old man with perinephric and iliopsoas abscesses and inflammatory involvement extending to the colon. Case 3 was a 59-year-old man with a large renal abscess who underwent nephrectomy to achieve definitive source control for uncontrolled infection, revealing an incidental diagnosis of renal pelvic squamous cell carcinoma. Across cases, infection was recurrent or refractory, temporizing measures (e.g., percutaneous drainage and/or nephrostomy) did not achieve sustained definitive source control, and two patients developed non-functioning kidneys requiring nephrectomy after infection control.\u003c/p\u003e\u003ch2\u003eConclusions\u003c/h2\u003e \u003cp\u003eThese cases illustrate an aggressive phenotype of longstanding nephrolithiasis with chronic infection, consistent with \u0026ldquo;malignant lithiasis\u0026rdquo; as a marker of clinical severity rather than malignant histology. Recognizing red flags\u0026mdash;recurrent or refractory infection, imaging evidence of extrarenal extension (e.g., iliopsoas and perinephric involvement), and progressive functional decline\u0026mdash;may support timely escalation to definitive source control. Routine histopathology of nephrectomy specimens is critical to minimize missed malignancy in stone-related non-functioning kidneys.\u003c/p\u003e","manuscriptTitle":"Iliopsoas involvement complicating longstanding nephrolithiasis with chronic infection: a three-patient case series reconsidering “malignant lithiasis”","msid":"","msnumber":"","nonDraftVersions":[{"code":1,"date":"2026-02-27 11:24:21","doi":"10.21203/rs.3.rs-8688678/v1","editorialEvents":[{"type":"communityComments","content":0},{"type":"reviewerAgreed","content":"284945236270452507268637272679726516677","date":"2026-03-05T19:00:57+00:00","index":"hide","fulltext":""},{"type":"editorInvitedReview","content":"","date":"2026-03-01T16:45:29+00:00","index":"hide","fulltext":""},{"type":"reviewerAgreed","content":"39696790052409868888112224574964428445","date":"2026-02-26T21:14:03+00:00","index":"hide","fulltext":""},{"type":"reviewerAgreed","content":"192510217257043023174736480503042098082","date":"2026-02-26T21:00:10+00:00","index":"hide","fulltext":""},{"type":"reviewerAgreed","content":"168187460452016416653210415802345186134","date":"2026-02-24T12:41:23+00:00","index":"hide","fulltext":""},{"type":"reviewersInvited","content":"","date":"2026-02-24T08:52:59+00:00","index":"","fulltext":""},{"type":"editorInvited","content":"","date":"2026-01-30T19:35:11+00:00","index":"","fulltext":""},{"type":"editorAssigned","content":"","date":"2026-01-28T06:27:54+00:00","index":"","fulltext":""},{"type":"checksComplete","content":"","date":"2026-01-28T06:22:06+00:00","index":"","fulltext":""},{"type":"submitted","content":"BMC Urology","date":"2026-01-24T18:25:51+00:00","index":"","fulltext":""}],"status":"published","journal":{"display":true,"email":"[email protected]","identity":"bmc-urology","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":false,"externalIdentity":"buro","sideBox":"Learn more about [BMC Urology](http://bmcurol.biomedcentral.com/)","snPcode":"","submissionUrl":"https://www.editorialmanager.com/buro/default.aspx","title":"BMC Urology","twitterHandle":"BMC_series","acdcEnabled":true,"dfaEnabled":false,"editorialSystem":"em","reportingPortfolio":"BMC Series","inReviewEnabled":true,"inReviewRevisionsEnabled":true}}],"origin":"","ownerIdentity":"e4663ebf-2641-4b3e-8842-552f6d4f6486","owner":[],"postedDate":"February 27th, 2026","published":true,"recentEditorialEvents":[],"rejectedJournal":[],"revision":"","amendment":"","status":"under-review","subjectAreas":[],"tags":[],"updatedAt":"2026-02-27T11:24:24+00:00","versionOfRecord":[],"versionCreatedAt":"2026-02-27 11:24:21","video":"","vorDoi":"","vorDoiUrl":"","workflowStages":[]},"version":"v1","identity":"rs-8688678","journalConfig":"researchsquare"},"__N_SSP":true},"page":"/article/[identity]/[[...version]]","query":{"redirect":"/article/rs-8688678","identity":"rs-8688678","version":["v1"]},"buildId":"XKTyCvWXoU3ODBz1xrDgd","isFallback":false,"isExperimentalCompile":false,"dynamicIds":[84888],"gssp":true,"scriptLoader":[]}

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