Acute severe pancreatitis following induction with methylprednisolone in live donor kidney transplantation: A case report

Acute severe pancreatitis following induction with methylprednisolone in live donor kidney transplantation: A case report | Research Square window.SnipcartSettings = { analytics: { enabled: false } }; (function() { var accessVector = localStorage.getItem('access_vector') || ''; window.dataLayer = window.dataLayer || []; if (accessVector) { window.dataLayer.push({ user: { profile: { profileInfo: { snid: accessVector } } } }); } })(); (function(w,d,s,l,i){w[l]=w[l]||[];w[l].push({'gtm.start':new Date().getTime(),event:'gtm.js'});var f=d.getElementsByTagName(s)[0],j=d.createElement(s),dl=l!='dataLayer'?'&l='+l:'';j.async=true;j.src='https://www.googletagmanager.com/gtm.js?id='+i+dl;f.parentNode.insertBefore(j,f);})(window,document,'script','dataLayer','GTM-K279D39R'); Browse Preprints In Review Journals COVID-19 Preprints AJE Video Bytes Research Tools Research Promotion AJE Professional Editing AJE Rubriq About Preprint Platform In Review Editorial Policies Our Team Advisory Board Help Center Sign In Submit a Preprint Cite Share Download PDF Case Report Acute severe pancreatitis following induction with methylprednisolone in live donor kidney transplantation: A case report Vishnupriya Ravindran, Vinojan Satchithanantham, Thulashi Tharmalingam, and 2 more This is a preprint; it has not been peer reviewed by a journal. https://doi.org/ 10.21203/rs.3.rs-8071949/v1 This work is licensed under a CC BY 4.0 License Status: Posted Version 1 posted You are reading this latest preprint version Abstract Background Acute severe pancreatitis following kidney transplantation is a relatively rare complication. Its diagnosis and management are challenging due to the recent surgical state, altered postoperative physiology, and the effects of immunosuppressive therapy. Case Presentation: Here, we present a case of acute severe pancreatitis in the immediate postoperative period in a kidney transplant recipient. The disease process is complicated by multiorgan dysfunction syndrome (MODS), including acute respiratory distress syndrome (ARDS), hematemesis, and acute rejection. Despite these complications, prompt recognition and tailored supportive care with rational alteration of immunosuppressive treatment led to patient recovery and good graft function. Conclusion Acute severe pancreatitis in the early postoperative period following kidney transplantation is rare but potentially fatal. Early recognition, multidisciplinary management, and careful optimization of immunosuppressive therapy are crucial for improving outcomes and preserving graft function. Kidney transplantation severe pancreatitis immunosuppressive theraphy Figures Figure 1 Figure 5 Background Acute severe pancreatitis is a relatively rare but serious complication in the early postoperative period of kidney transplantation 1 , 2 . It presents diagnostic and therapeutic challenges due to the altered physiology of transplant patients and the use of high-dose immunosuppressive therapy 1 , 2 . Case Presentation A 54-year-old male with a history of diabetic nephropathy developed chronic kidney disease that progressed to end-stage renal disease (ESRD). He was maintained on hemodialysis for six months prior to undergoing living donor renal transplantation. The patient received a standard triple immunosuppressive regimen for renal transplantation. Induction therapy included 20 mg basiliximab on Day 0 and Day 4, tacrolimus 3.5mg bd, mycophenolate 500mg tds, and methyl prednisolone 500mg during the induction of anaesthesia. Immediate graft function was observed postoperatively, as evidenced by prompt normalization of serum creatinine levels and satisfactory urine output. On postoperative day 2, the patient developed reduced urine output and abdominal distension, without associated abdominal pain, refractory vomiting, or any clinically identifiable cause. The initial investigations were as follows: Investigations Results WBC 25.26×10 9 /L CRP 143.6 mg/dl Serum amylase 1696U/l AST 26 U/l ALT 20 U/l Serum creatinine 644 µmol/l Blood urea 16.3 mmol/l Serum Calcium 2.27 mmol/l USS Abdomen Gaseous distention of abdomen, Midline structures obscured, Bowel loops not distended Minimal free fluid in the hepatorenal pouch noted Gallbladder distended and no calculus observed NCCT Abdomen & Pelvis (Fig. 1 ) Fat stranding around the pancreas, bilateral perinephric spaces, and the root of the mesentery. Minimal ascites and mild right-sided pleural effusion were noted. The transplanted kidney was in the right iliac fossa with two stents in situ and mild perinephric fluid collection. HRCT Chest Bilateral lower lobe consolidation with small pleural effusion UGIE Evidence of recent bleeding and multiple gastric erosions has been seen. The NCCT abdomen was suggestive of acute pancreatitis, and a timely serum amylase test was requested, which returned to elevated at 1696 U/L, thereby fulfilling the Atlanta criteria and confirming the diagnosis of acute pancreatitis. At the time of diagnosis, the 2nd dose of methylprednisolone was already given, and it was decided to complete the induction with the second dose of basiliximab 20 mg per the original induction regime. The course was further complicated by probable acute tubular necrosis necessitating regular hemodialysis for 10 days until the improvement of graft function. Furthermore, the patient developed hematemesis, and upper gastrointestinal endoscopy revealed multiple gastric erosions, which were managed with proton pump inhibitors. Unfortunately, his condition deteriorated further, and the high-resolution computed tomography (HRCT) chest revealed bilateral lower lobe consolidation with associated pleural effusion. Sputum cultures revealed Acinetobacter and Klebsiella species, confirming a diagnosis of hospital-acquired pneumonia (HAP) complicated with acute respiratory distress syndrome (ARDS). The patient required endotracheal intubation and mechanical ventilation for four days. He was treated with a combination of polymyxin, teicoplanin, and levofloxacin, alongside chest physiotherapy and postural drainage, to support respiratory function and promote secretion clearance. Owing to the severity of illness and complications, the patient had a prolonged intensive care unit (ICU) stay of 21 days. During the ICU stay, low-dose tacrolimus was continued with maintenance IV hydrocortisone of 50 mg 6 hours, and other immunosuppressants were withheld. He recovered gradually over the course of 21 days from acute severe pancreatitis and its complications. Immunosuppressive therapy was reintroduced to a modified steroid-free regime following discharge from the ICU. At 45 days post-transplant, the patient’s graft function recovered normally without further complications. Discussion and conclusion The first reported case of acute pancreatitis after renal transplantation dates back to 1964. 3 The incidence among renal transplant recipients ranges from 2% to 7%, with a high mortality rate of 50% to 100%. 1 Given the multifactorial aetiology of post-transplant pancreatitis, pinpointing a single cause is often difficult. Immunosuppressive agents, however, are a significant contributing factor. 1 , 4 , 5 Drug-induced pancreatitis represents up to 5% of all acute pancreatitis cases. There is a lack of definitive clinical or laboratory criteria for the diagnosis of drug-induced pancreatitis (DIP). Instead, the diagnosis is often based on a combination of clinical observations: resolution of symptoms and normalization of pancreatic enzymes after stopping the suspected drug, exclusion of more common causes, and recurrence of symptoms if the drug is reintroduced. 6 However, reintroducing the drug is rarely feasible in critically ill patients, even though it can help narrow the list of possible offending agents. Determining the true cause becomes especially challenging in patients on multiple medications, as excluding all other potential causes or drugs is difficult. 7 The Badalov classification system categorizes drug-induced acute pancreatitis into five classes: Ia, Ib, II, III, and IV. This classification is based on several factors, including the number of published case reports, whether rechallenge with the drug led to the recurrence of pancreatitis, and the latency period between drug exposure and symptom onset. In the Badalov classification system, steroids fall into the Ib category, and tacrolimus falls into the IV category. 7 , 8 Our patient had generalized abdominal distension from day 2 with features of paralytic ileus. He did not have any abdominal pain. Initially, we proceeded with a noncontrast CT scan of the abdomen, as there was a risk of contrast-induced nephropathy. This picked up some fat stranding around the pancreas. According to the revised Atlanta classification, we arrived at the diagnosis with radiological and biochemical components. Owing to the immunosuppressed state and altered physiology of transplant recipients, the clinical symptoms of acute pancreatitis may be subtle or atypical, as observed in this case. Therefore, early recognition through biochemical markers and imaging is essential 1 , 2 . Prompt diagnosis, appropriate supportive care, and careful adjustment of immunosuppressive therapy are key to improving patient and graft survival. 9 Even after the resolution of acute pancreatitis, the use of immunosuppressive agents remains a potential risk factor for recurrence. Minimizing corticosteroid exposure while maintaining adequate immunosuppression is crucial to prevent both pancreatitis and allograft rejection. 9 Patients presenting with abdominal symptoms after renal transplantation should be evaluated for acute pancreatitis, even in the absence of typical symptoms. Early diagnosis and prompt management can improve both patient outcomes and graft survival. Declarations Ethics approval and consent to participate: Ethical approval was not required for this case report as per institutional policy. The report was conducted in accordance with the ethical principles outlined in the Declaration of Helsinki. Consent for publication: Written informed consent was obtained from the patient for publication of this case report and any accompanying images. Availability of data and materials: Data sharing is not applicable to this article as no datasets were generated or analysed during the current study. Competing interests: Authors don’t have any competing interests. Funding: Not applicable to this study Authors contributions: Study design: VR, VS Data collection: VR, BT, SM, TT Manuscript writing: VR, VS Review and final approval: All authors References Tabakovic M, Salkic NN, Bosnjic J, Alibegovic E. Acute pancreatitis after kidney transplantation. Case Rep Transplantation. 2012;2012(1):768193. Taylor K, Sinha S, Cowie A, Babbs C, Reeve R, Kalra PA. Challenges in diagnosing acute pancreatitis in renal transplant patients. Clin Transplant. 2009;23(6). Starzl TE. Experience in renal transplantation. WB Saunders company; 1964. Slakey DP, Johnson CP, Cziperle DJ, Roza AM, Wittmann DH, Gray DW, Roake JA, Britton J, Morris PJ, Adams MB. Management of severe pancreatitis in renal transplant recipients. Ann Surg. 1997;225(2). Corrodi P, Knoblauch M, Binswanger U, Schölzel E, Largiader F. Pancreatitis after renal transplantation. Gut. 1975;16(4). Mallory A, Kern F Jr. Drug-induced pancreatitis: a critical review. Gastroenterology. 1980;78(4). Chadalavada P, Simons-Linares CR, Chahal P. Drug-induced acute pancreatitis: prevalence, causative agents, and outcomes. Pancreatology. 2020;20(7). Badalov N, Baradarian R, Iswara K, Li J, Steinberg W, Tenner S. Drug-induced acute pancreatitis: an evidence-based review. Clin Gastroenterol Hepatol. 2007;5(6). Renning JA, Warden GD, Stevens LE, Reemtsma K. Pancreatitis after renal transplantation. Am J Surg. 1972;123(3). Additional Declarations No competing interests reported. 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5","display":"","copyAsset":false,"role":"figure","size":51019,"visible":true,"origin":"","legend":"\u003cp\u003eNCCT Abdomen axial (a) and coronal (b) images show peripancreatic fat stranding.\u003c/p\u003e","description":"","filename":"groupimage1.jpeg","url":"https://assets-eu.researchsquare.com/files/rs-8071949/v1/d68e09407cde15d974d67912.jpeg"},{"id":97141018,"identity":"e8ad09cf-7311-4423-82a1-e2cdf70fe74d","added_by":"auto","created_at":"2025-12-01 10:06:08","extension":"pdf","order_by":0,"title":"","display":"","copyAsset":false,"role":"manuscript-pdf","size":497207,"visible":true,"origin":"","legend":"","description":"","filename":"manuscript.pdf","url":"https://assets-eu.researchsquare.com/files/rs-8071949/v1/944a0d89-9c96-481d-aa11-976d4314dcbd.pdf"}],"financialInterests":"No competing interests reported.","formattedTitle":"Acute severe pancreatitis following induction with methylprednisolone in live donor kidney transplantation: A case report","fulltext":[{"header":"Background","content":"\u003cp\u003eAcute severe pancreatitis is a relatively rare but serious complication in the early postoperative period of kidney transplantation\u003csup\u003e\u003cspan citationid=\"CR1\" class=\"CitationRef\"\u003e1\u003c/span\u003e,\u003cspan citationid=\"CR2\" class=\"CitationRef\"\u003e2\u003c/span\u003e\u003c/sup\u003e. It presents diagnostic and therapeutic challenges due to the altered physiology of transplant patients and the use of high-dose immunosuppressive therapy\u003csup\u003e\u003cspan citationid=\"CR1\" class=\"CitationRef\"\u003e1\u003c/span\u003e,\u003cspan citationid=\"CR2\" class=\"CitationRef\"\u003e2\u003c/span\u003e\u003c/sup\u003e.\u003c/p\u003e"},{"header":"Case Presentation","content":"\u003cp\u003eA 54-year-old male with a history of diabetic nephropathy developed chronic kidney disease that progressed to end-stage renal disease (ESRD). He was maintained on hemodialysis for six months prior to undergoing living donor renal transplantation. The patient received a standard triple immunosuppressive regimen for renal transplantation. Induction therapy included 20 mg basiliximab on Day 0 and Day 4, tacrolimus 3.5mg bd, mycophenolate 500mg tds, and methyl prednisolone 500mg during the induction of anaesthesia. Immediate graft function was observed postoperatively, as evidenced by prompt normalization of serum creatinine levels and satisfactory urine output.\u003c/p\u003e\u003cp\u003eOn postoperative day 2, the patient developed reduced urine output and abdominal distension, without associated abdominal pain, refractory vomiting, or any clinically identifiable cause. The initial investigations were as follows:\u003c/p\u003e\u003cp\u003e\u003cdiv class=\"gridtable\"\u003e\u003ctable float=\"No\" id=\"Taba\" border=\"1\"\u003e\u003ccolgroup cols=\"2\"\u003e\u003cdiv align=\"left\" class=\"colspec\" colname=\"c1\" colnum=\"1\"\u003e\u003c/div\u003e\u003cdiv align=\"left\" class=\"colspec\" colname=\"c2\" colnum=\"2\"\u003e\u003c/div\u003e\u003cthead\u003e\u003ctr\u003e\u003cth align=\"left\" colname=\"c1\"\u003e\u003cp\u003eInvestigations\u003c/p\u003e\u003c/th\u003e\u003cth align=\"left\" colname=\"c2\"\u003e\u003cp\u003eResults\u003c/p\u003e\u003c/th\u003e\u003c/tr\u003e\u003c/thead\u003e\u003ctbody\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003eWBC\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003e25.26\u0026times;10\u003csup\u003e9\u003c/sup\u003e/L\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003eCRP\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003e143.6 mg/dl\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003eSerum amylase\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003e1696U/l\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003eAST\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003e26 U/l\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003eALT\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003e20 U/l\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003eSerum creatinine\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003e644 \u0026micro;mol/l\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003eBlood urea\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003e16.3 mmol/l\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003eSerum Calcium\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003e2.27 mmol/l\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003eUSS Abdomen\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003eGaseous distention of abdomen, Midline structures obscured, Bowel loops not distended\u003c/p\u003e\u003cp\u003eMinimal free fluid in the hepatorenal pouch noted\u003c/p\u003e\u003cp\u003eGallbladder distended and no calculus observed\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003eNCCT Abdomen \u0026amp; Pelvis (Fig.\u0026nbsp;\u003cspan refid=\"Fig1\" class=\"InternalRef\"\u003e1\u003c/span\u003e)\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003eFat stranding around the pancreas, bilateral perinephric spaces, and the root of the mesentery.\u003c/p\u003e\u003cp\u003eMinimal ascites and mild right-sided pleural effusion were noted.\u003c/p\u003e\u003cp\u003eThe transplanted kidney was in the right iliac fossa with two stents in situ and mild perinephric fluid collection.\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003eHRCT Chest\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003eBilateral lower lobe consolidation with small pleural effusion\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003eUGIE\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003eEvidence of recent bleeding and multiple gastric erosions has been seen.\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003c/tbody\u003e\u003c/colgroup\u003e\u003c/table\u003e\u003c/div\u003e\u003c/p\u003e\u003cp\u003e\u003c/p\u003e\u003cp\u003eThe NCCT abdomen was suggestive of acute pancreatitis, and a timely serum amylase test was requested, which returned to elevated at 1696 U/L, thereby fulfilling the Atlanta criteria and confirming the diagnosis of acute pancreatitis.\u003c/p\u003e\u003cp\u003eAt the time of diagnosis, the 2nd dose of methylprednisolone was already given, and it was decided to complete the induction with the second dose of basiliximab 20 mg per the original induction regime.\u003c/p\u003e\u003cp\u003eThe course was further complicated by probable acute tubular necrosis necessitating regular hemodialysis for 10 days until the improvement of graft function. Furthermore, the patient developed hematemesis, and upper gastrointestinal endoscopy revealed multiple gastric erosions, which were managed with proton pump inhibitors. Unfortunately, his condition deteriorated further, and the high-resolution computed tomography (HRCT) chest revealed bilateral lower lobe consolidation with associated pleural effusion. Sputum cultures revealed \u003cem\u003eAcinetobacter\u003c/em\u003e and \u003cem\u003eKlebsiella\u003c/em\u003e species, confirming a diagnosis of hospital-acquired pneumonia (HAP) complicated with acute respiratory distress syndrome (ARDS).\u003c/p\u003e\u003cp\u003eThe patient required endotracheal intubation and mechanical ventilation for four days. He was treated with a combination of polymyxin, teicoplanin, and levofloxacin, alongside chest physiotherapy and postural drainage, to support respiratory function and promote secretion clearance. Owing to the severity of illness and complications, the patient had a prolonged intensive care unit (ICU) stay of 21 days. During the ICU stay, low-dose tacrolimus was continued with maintenance IV hydrocortisone of 50 mg 6 hours, and other immunosuppressants were withheld.\u003c/p\u003e\u003cp\u003eHe recovered gradually over the course of 21 days from acute severe pancreatitis and its complications. Immunosuppressive therapy was reintroduced to a modified steroid-free regime following discharge from the ICU. At 45 days post-transplant, the patient\u0026rsquo;s graft function recovered normally without further complications.\u003c/p\u003e"},{"header":"Discussion and conclusion","content":"\u003cdiv id=\"Sec3\" class=\"Section2\"\u003e\u003cp\u003eThe first reported case of acute pancreatitis after renal transplantation dates back to 1964.\u003csup\u003e\u003cspan citationid=\"CR3\" class=\"CitationRef\"\u003e3\u003c/span\u003e\u003c/sup\u003e The incidence among renal transplant recipients ranges from 2% to 7%, with a high mortality rate of 50% to 100%.\u003csup\u003e1\u003c/sup\u003e Given the multifactorial aetiology of post-transplant pancreatitis, pinpointing a single cause is often difficult. Immunosuppressive agents, however, are a significant contributing factor.\u003csup\u003e\u003cspan citationid=\"CR1\" class=\"CitationRef\"\u003e1\u003c/span\u003e,\u003cspan citationid=\"CR4\" class=\"CitationRef\"\u003e4\u003c/span\u003e,\u003cspan citationid=\"CR5\" class=\"CitationRef\"\u003e5\u003c/span\u003e\u003c/sup\u003e\u003c/p\u003e\u003cp\u003eDrug-induced pancreatitis represents up to 5% of all acute pancreatitis cases. There is a lack of definitive clinical or laboratory criteria for the diagnosis of drug-induced pancreatitis (DIP). Instead, the diagnosis is often based on a combination of clinical observations: resolution of symptoms and normalization of pancreatic enzymes after stopping the suspected drug, exclusion of more common causes, and recurrence of symptoms if the drug is reintroduced.\u003csup\u003e\u003cspan citationid=\"CR6\" class=\"CitationRef\"\u003e6\u003c/span\u003e\u003c/sup\u003e However, reintroducing the drug is rarely feasible in critically ill patients, even though it can help narrow the list of possible offending agents. Determining the true cause becomes especially challenging in patients on multiple medications, as excluding all other potential causes or drugs is difficult.\u003csup\u003e\u003cspan citationid=\"CR7\" class=\"CitationRef\"\u003e7\u003c/span\u003e\u003c/sup\u003e\u003c/p\u003e\u003cp\u003eThe Badalov classification system categorizes drug-induced acute pancreatitis into five classes: Ia, Ib, II, III, and IV. This classification is based on several factors, including the number of published case reports, whether rechallenge with the drug led to the recurrence of pancreatitis, and the latency period between drug exposure and symptom onset. In the Badalov classification system, steroids fall into the Ib category, and tacrolimus falls into the IV category.\u003csup\u003e\u003cspan citationid=\"CR7\" class=\"CitationRef\"\u003e7\u003c/span\u003e,\u003cspan citationid=\"CR8\" class=\"CitationRef\"\u003e8\u003c/span\u003e\u003c/sup\u003e\u003c/p\u003e\u003cp\u003eOur patient had generalized abdominal distension from day 2 with features of paralytic ileus. He did not have any abdominal pain. Initially, we proceeded with a noncontrast CT scan of the abdomen, as there was a risk of contrast-induced nephropathy. This picked up some fat stranding around the pancreas. According to the revised Atlanta classification, we arrived at the diagnosis with radiological and biochemical components.\u003c/p\u003e\u003cp\u003eOwing to the immunosuppressed state and altered physiology of transplant recipients, the clinical symptoms of acute pancreatitis may be subtle or atypical, as observed in this case. Therefore, early recognition through biochemical markers and imaging is essential\u003csup\u003e\u003cspan citationid=\"CR1\" class=\"CitationRef\"\u003e1\u003c/span\u003e,\u003cspan citationid=\"CR2\" class=\"CitationRef\"\u003e2\u003c/span\u003e\u003c/sup\u003e. Prompt diagnosis, appropriate supportive care, and careful adjustment of immunosuppressive therapy are key to improving patient and graft survival.\u003csup\u003e\u003cspan citationid=\"CR9\" class=\"CitationRef\"\u003e9\u003c/span\u003e\u003c/sup\u003e\u003c/p\u003e\u003cp\u003eEven after the resolution of acute pancreatitis, the use of immunosuppressive agents remains a potential risk factor for recurrence. Minimizing corticosteroid exposure while maintaining adequate immunosuppression is crucial to prevent both pancreatitis and allograft rejection.\u003csup\u003e\u003cspan citationid=\"CR9\" class=\"CitationRef\"\u003e9\u003c/span\u003e\u003c/sup\u003e\u003c/p\u003e\u003cp\u003ePatients presenting with abdominal symptoms after renal transplantation should be evaluated for acute pancreatitis, even in the absence of typical symptoms. Early diagnosis and prompt management can improve both patient outcomes and graft survival.\u003c/p\u003e\u003c/div\u003e"},{"header":"Declarations","content":"\u003cp\u003e\u003cstrong\u003eEthics approval and consent to participate:\u0026nbsp;\u003c/strong\u003eEthical approval was not required for this case report as per institutional policy. The report was conducted in accordance with the ethical principles outlined in the Declaration of Helsinki.\u0026nbsp;\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eConsent for publication:\u003c/strong\u003e Written informed consent was obtained from the patient for publication of this case report and any accompanying images.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eAvailability of data and materials:\u003c/strong\u003e Data sharing is not applicable to this article as no datasets were generated or analysed during the current study.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eCompeting interests:\u003c/strong\u003e Authors don’t have any competing interests.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eFunding:\u003c/strong\u003e Not applicable to this study\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eAuthors contributions:\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eStudy design: VR, VS\u003c/p\u003e\n\u003cp\u003eData collection: VR, BT, SM, TT\u003c/p\u003e\n\u003cp\u003eManuscript writing: VR, VS\u003c/p\u003e\n\u003cp\u003eReview and final approval: All authors\u003c/p\u003e"},{"header":"References","content":"\u003col\u003e\u003cli\u003e\u003cspan\u003eTabakovic M, Salkic NN, Bosnjic J, Alibegovic E. Acute pancreatitis after kidney transplantation. Case Rep Transplantation. 2012;2012(1):768193.\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003eTaylor K, Sinha S, Cowie A, Babbs C, Reeve R, Kalra PA. Challenges in diagnosing acute pancreatitis in renal transplant patients. Clin Transplant. 2009;23(6).\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003eStarzl TE. Experience in renal transplantation. WB Saunders company; 1964.\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003eSlakey DP, Johnson CP, Cziperle DJ, Roza AM, Wittmann DH, Gray DW, Roake JA, Britton J, Morris PJ, Adams MB. Management of severe pancreatitis in renal transplant recipients. Ann Surg. 1997;225(2).\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003eCorrodi P, Knoblauch M, Binswanger U, Sch\u0026ouml;lzel E, Largiader F. Pancreatitis after renal transplantation. Gut. 1975;16(4).\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003eMallory A, Kern F Jr. Drug-induced pancreatitis: a critical review. Gastroenterology. 1980;78(4).\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003eChadalavada P, Simons-Linares CR, Chahal P. Drug-induced acute pancreatitis: prevalence, causative agents, and outcomes. Pancreatology. 2020;20(7).\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003eBadalov N, Baradarian R, Iswara K, Li J, Steinberg W, Tenner S. Drug-induced acute pancreatitis: an evidence-based review. Clin Gastroenterol Hepatol. 2007;5(6).\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003eRenning JA, Warden GD, Stevens LE, Reemtsma K. Pancreatitis after renal transplantation. Am J Surg. 1972;123(3).\u003c/span\u003e\u003c/li\u003e\u003c/ol\u003e"}],"fulltextSource":"","fullText":"","funders":[],"hasAdminPriorityOnWorkflow":false,"hasManuscriptDocX":true,"hasOptedInToPreprint":true,"hasPassedJournalQc":"","hasAnyPriority":false,"hideJournal":true,"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":"researchsquare","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":true,"externalIdentity":"","sideBox":"","snPcode":"","submissionUrl":"/submission","title":"Research Square","twitterHandle":"researchsquare","acdcEnabled":true,"dfaEnabled":false,"editorialSystem":"","reportingPortfolio":"","inReviewEnabled":false,"inReviewRevisionsEnabled":true},"keywords":"Kidney transplantation, severe pancreatitis, immunosuppressive theraphy","lastPublishedDoi":"10.21203/rs.3.rs-8071949/v1","lastPublishedDoiUrl":"https://doi.org/10.21203/rs.3.rs-8071949/v1","license":{"name":"CC BY 4.0","url":"https://creativecommons.org/licenses/by/4.0/"},"manuscriptAbstract":"\u003ch2\u003eBackground\u003c/h2\u003e\u003cp\u003eAcute severe pancreatitis following kidney transplantation is a relatively rare complication. Its diagnosis and management are challenging due to the recent surgical state, altered postoperative physiology, and the effects of immunosuppressive therapy.\u003c/p\u003e\u003ch2\u003eCase Presentation:\u003c/h2\u003e\u003cp\u003eHere, we present a case of acute severe pancreatitis in the immediate postoperative period in a kidney transplant recipient. The disease process is complicated by multiorgan dysfunction syndrome (MODS), including acute respiratory distress syndrome (ARDS), hematemesis, and acute rejection. Despite these complications, prompt recognition and tailored supportive care with rational alteration of immunosuppressive treatment led to patient recovery and good graft function.\u003c/p\u003e\u003ch2\u003eConclusion\u003c/h2\u003e\u003cp\u003eAcute severe pancreatitis in the early postoperative period following kidney transplantation is rare but potentially fatal. Early recognition, multidisciplinary management, and careful optimization of immunosuppressive therapy are crucial for improving outcomes and preserving graft function.\u003c/p\u003e","manuscriptTitle":"Acute severe pancreatitis following induction with methylprednisolone in live donor kidney transplantation: A case report","msid":"","msnumber":"","nonDraftVersions":[{"code":1,"date":"2025-12-01 07:40:34","doi":"10.21203/rs.3.rs-8071949/v1","editorialEvents":[{"type":"communityComments","content":0}],"status":"published","journal":{"display":true,"email":"[email protected]","identity":"researchsquare","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":true,"externalIdentity":"","sideBox":"","snPcode":"","submissionUrl":"/submission","title":"Research Square","twitterHandle":"researchsquare","acdcEnabled":true,"dfaEnabled":false,"editorialSystem":"","reportingPortfolio":"","inReviewEnabled":false,"inReviewRevisionsEnabled":true}}],"origin":"","ownerIdentity":"153add45-3b82-4b7d-a434-65de13b1a6cf","owner":[],"postedDate":"December 1st, 2025","published":true,"recentEditorialEvents":[],"rejectedJournal":[],"revision":"","amendment":"","status":"posted","subjectAreas":[],"tags":[],"updatedAt":"2025-12-01T09:23:45+00:00","versionOfRecord":[],"versionCreatedAt":"2025-12-01 07:40:34","video":"","vorDoi":"","vorDoiUrl":"","workflowStages":[]},"version":"v1","identity":"rs-8071949","journalConfig":"researchsquare"},"__N_SSP":true},"page":"/article/[identity]/[[...version]]","query":{"redirect":"/article/rs-8071949","identity":"rs-8071949","version":["v1"]},"buildId":"8U1c8b4HqxoKbykW_rLl7","isFallback":false,"isExperimentalCompile":false,"dynamicIds":[84888],"gssp":true,"scriptLoader":[]}