Clinical characteristics, risk predictors and outcomes of community-acquired acute kidney injury in children

Clinical characteristics, risk predictors and outcomes of community-acquired acute kidney injury in children | 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 Research Article Clinical characteristics, risk predictors and outcomes of community-acquired acute kidney injury in children Cagla Serpil Dogan, Nazife Huylu, Hasan Serdar Kıhtır, Erdem Çebişli, and 1 more This is a preprint; it has not been peer reviewed by a journal. https://doi.org/ 10.21203/rs.3.rs-8551808/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; Little data exist related to community-acquired acute kidney injury (CA-AKI) in children. We aimed to determine the etiology, clinical profile, risk factors, and outcomes of children hospitalized for CA-AKI. Methods; Patients, 1month to18 years, who had CA-AKI on or within 48 hours of hospital admission between January 2020 to June 2025 were included. KDIGO 2012 criteria were used for the diagnosis of AKI. The patients were divided into four groups according to their age; 1 month − 2 years, > 2–6, > 6–12, > 12–18 years. Demographic, clinical, and laboratory data were analyzed. Risk factors for severe CA-AKI (stage 2 and 3) were investigated. Results; 134 patients, male/female ratio; 1.23, with a median age of 10 years (2 months-17.9 years) were included. The most affected age group was > 12 to 18 years (39.6%). Intrinsic CA-AKI accounted for 72% of all cases, mostly glomerular and acute tubulointerstitial diseases. More than half of the patients (65.7%) developed severe AKI. Risk factors for severe CA-AKI were younger age (p = 0.04, OR;1.064, 95%CI:1.002–1.129), intrinsic AKI (p < 0.001, OR; 4.714, 95%CI:2.089–10.639), hyponatremia (p = 0.05, OR;2.114, 95%CI:0.978–4.570), thrombocytopenia (p = 0.003, OR;5.471, 95%CI:1.772–16.895), hyperphosphatemia (p = 0.02, OR;5.727, 95%CI:1.264–25.958) and hyperuricemia (p < 0.001, OR;5.217, 95%CI;2.321–11.730). At discharge, complete recovery was observed in 85%, and partial recovery in 14.8%. Three patients (2.4%) developed CKD. Mortality occurred in 6 (4.5%). Conclusions; Glomerular and tubulointerstitial diseases were the most common causes of CA-AKI, and short term kidney outcomes were favorable. Intrinsic etiology, serum electrolyte disturbances, thrombocytopenia and hyperuricemia were strong independent risk factors for severe CA-AKI. Community- acquired acute kidney injury child etiology risk factors outcome Introduction Acute kidney injury (AKI) is a complex and heterogeneous syndrome with different epidemiology, pathophysiology, and clinical trajectory, characterized by a sudden decline in kidney function. AKI is a common complication in both critically and non- critically ill children and is associated with increased morbidity, mortality, and the risk of progression to chronic kidney disease (CKD) [ 1 ]. AKI occurs in both community and hospital settings. Community-acquired AKI (CA-AKI) is defined as AKI developing outside the hospital. In pediatric population, its worldwide incidence broadly ranges from 0.26% to 56.4% across countries, depending on socioeconomic and environmental factors as well as the criteria used for determination of CA-AKI, (i.e., AKIN, pRIFLE, and more recently, the KDIGO criteria) [ 2 , 3 ]. Similarly, the etiologic spectrum and outcomes of pediatric CA-AKI widely differ in developing and developed world [ 3 – 6 ]. This form of AKI is more common than hospital-acquired AKI (HA-AKI) and has significant morbidity and mortality, especially in low-middle income countries [ 7 , 8 ]. However, in most cases, early identification and management of risk factors for CA-AKI may improve prognosis. In literature, although hospital-acquired AKI (HA-AKI), which develops after 48 hours of hospitalization, has been well-studied in pediatric population, less is known about CA-AKI [ 6 , 9 ]. In the current study, with an emphasis on the risk factors of severe kidney injury, we evaluated the etiology, clinical characteristics, risk predictors, and short-term outcomes of CA-AKI in children admitted to our center. Material and Methods Study Design, Patient Population and Data Collection Data from all patients admitted to an inpatient unit (wards or intensive care unit) of the Pediatrics Department at Antalya Training and Research Hospital, a tertiary healthcare center located in southern Türkiye, with a diagnosis of AKI between January 1, 2020 and June 30, 2025, were retrospectively reviewed. To obtain data, we first identified the patients who had an International Classification of Diseases (ICD)10 code for AKI. Then, we reviewed the medical records of patients who were given ICD codes for other medical conditions that may accompany AKI, such as acute nephritic syndrome, nephrotic syndrome, hemolytic uremic syndrome, and acute gastroenteritis. Exclusion criteria were; (i) aged 18 years, (ii) children presenting with acute exacerbation of pre-existing CKD, (iii) those who died within the first 24 hours of admission to pediatric intensive care unit (PICU), and (iv) those with incomplete medical records. The remaining patients who met the criteria for CA-AKI diagnosis were included in the study. All data including age, gender, comorbidities (such as nephro-urologic problems, neurological diseases, endocrine/metabolic disorders), the use of nephrotoxic medications and nephrotoxin exposure before admission, clinical and laboratory data, primary disease/condition leading to AKI, the type of CA-AKI (prerenal, renal/intrinsic, postrenal), the frequency of PICU admission, kidney replacement therapy, mechanical ventilation and inotropic drug requirement, length of stay (LOS) in PICU, and renal outcomes at the time of discharge were extracted from electronic patient records. If a patient was hospitalized multiple times during the study period, only the first one was considered. In the current study, due to the small number of patients in subphenotypes, such as sepsis-induced AKI, drug-induced AKI, or hypoperfusion -associated AKI, we used the traditional classification of AKI (i.e., prerenal, intrinsic, and postrenal types) [ 10 ]. However, in some cases, the pathophysiology of AKI was complex and multifactorial. In such cases, the primary cause of AKI was included in the category considered most relevant. For example, sepsis was categorized as intrinsic AKI instead of hypovolemia-related AKI (prerenal AKI) [ 11 , 12 ]. Similarly, in complex cases where multiple etiological factors could lead to CA-AKI, the medical condition considered most likely to cause kidney damage was identified as the primary cause of AKI. Definitions and Measurements Definition, diagnosis and staging of CA-AKI CA-AKI was defined as the presence of AKI on admission or AKI developing within 48 hours of hospital admission. A baseline serum creatinine (SCr) was considered the lowest level within the 90 days before admission (pre-admission SCr). In the absence of a known baseline SCr, the upper cutoff of age- and sex-based reference ranges was presumed as baseline Cr [ 2 , 13 ]. Diagnosis and staging of AKI was established according to Kidney Disease: Improving Global Outcomes (KDIGO) classification system (2012), and it was defined as either a ≥ 1.5-fold increase in SCr from baseline within the previous 7 days or a ≥ 0.3 mg/dl increase within 48 hours (Table 1) [ 14 ]. For each patient, a maximum AKI stage achieved during hospitalization or at the time of admission was noted, and stages 2 and 3 were considered severe AKI. Since hourly documentation of urine output (UOP) was not available, particularly in hospitalized children in the pediatric wards, UOP was not used to define AKI. On admission, serum uric acid (UA) (normal range; 3.5–7.2 mg/dl), calcium (Ca) (8.8–10.8 mg/dl), magnesium (Mg) (1.8–2.6 mg/dl), inorganic phosphorus (iP) (4–7 mg/dl), sodium (Na) (136–146 mmol/l), potassium (K) levels (3.5–5.1 mmol/l), hemoglobin (Hb) (12.5–16.1 g/dl), platelet count (Plt) (150-450x10 3 /mm 3 ) were recorded. Hyponatremia was categorized as mild (≤ 134 to ≥ 130 mEq/l), moderate (≤ 129 to ≥ 121 mEq/l), and severe (≤ 120 mEq/l). Hypernatremia was considered mild when Na + concentration was ≥ 146 to ≤ 149 mEq/l, moderate when ≥ 150 to ≤ 169 mEq/l, and severe when ≥ 170 mEq/l. Mild, moderate, severe, and very severe thrombocytopenia were defined as 100-150x10 3 /mm 3 , 50-99x10 3 /mm 3 , 20-49x10 3 /mm 3 , and < 20 x10 3 /mm 3 , respectively. For patients with hypoalbuminemia, a corrected calcium level was calculated. Dysphosphatemia was defined as a serum phosphorus concentration that is below or above age-specific normal phosphate ranges. In patients with diabetic ketoacidosis, serum sodium levels were adjusted according to glucose levels. The patients were divided into four groups according to their age; 1 month − 2 years, > 2–6, > 6–12, > 12–18. Demographic and clinical characteristics of the patients were examined according to age groups. Then, risk factors for severe CA-AKI were investigated. Kidney Recovery According to the SCr level at the time of discharge, complete recovery was defined as a post-AKI SCr within 25% of baseline in those with known baseline SCr levels and within the age and sex -adjusted reference range in patients with unknown baseline SCr. Partial recovery was defined as a fall in maximum AKI stage. CKD was considered the presence of reduced kidney function lasting > 3 months (CKD stage 2–5) [ 14 ]. The study protocol was approved by the ethics committee of our institution (Antalya Training and Research Hospital Ethics Committee, protocol number; 2025; 13/15). Written informed consent was not obtained due to the retrospective study design. Statistical analysis Descriptive data were presented as numbers and percentages for categorical variables; mean ± standard deviation for normally distributed continuous variables, and median (range) for non-normally distributed ones. The Chi-square test assessed categorical variables. The Kruskal–Wallis test was used for the comparison of continuous variables among multiple groups, and a p value < 0.05 was considered statistically significant. When the difference was significant, the Mann-Whitney U test was done between two groups. Univariate and multivariate logistic regression analyses were performed to determine risk factors for CA-AKI. For all statistical analyses, the SPSS version 21.0 package program for Windows (IBM, Armonk, NY) was used. Results Baseline characteristics A total of 134 patients, male/female ratio; 1.2, with a median age of 10.0 years (range; 2 months-17.9 years) were included. The most affected age group was > 12 to 18 years (39.6%) (p = 0.039). After discharge, 10 pediatric earthquake victims transferred to our center due to the earthquake that occurred in southeastern Türkiye in 2023 and 3 patients with prerenal CA-AKI due to acute gastroenteritis (AGE) were lost to follow-up. However, SCr values of these patients were within normal limits at discharge. Six patients died during the PICU stay. The remaining 115 patients were followed for a median of 10 months (range; 1month-5 years). Thirteen patients with stage 1 CA-AKI on admission progressed to stage 2 or 3 (severe CA-AKI), and overall, more than half of the children (n = 87, 65.7%) developed severe AKI. One quarter of patients had at least one medical comorbidity. In 78 (58.2%) patients who did not have a baseline SCr, the upper limit of reference ranges were used for the diagnosis of CA-AKI. Almost half of all patients (47.8%) were admitted to the PICU. The median LOS in PICU was 9 days (2–30 days). Of whom, 25% (n = 16) required mechanical ventilation, and 18.7% (n = 12) received inotropes. Overall, one quarter of patients underwent hemodialysis, mostly continuous renal replacement therapy (CRRT). Children aged 1 month-2 years, > 2–6 years and > 6–12 years received dialysis more frequently and were hospitalized for longer periods than those aged > 12–18 years. The baseline demographic and clinical characteristics of the whole cohort and subgroups according to their age are summarized in Table 2 . Etiology of CA-AKI The primary causes of CA-AKI are outlined in Table 3 . Intrinsic CA-AKI accounted for 72% of all cases (p = 0.001). Even after excluding earthquake victims, which is a unique case, intrinsic causes of CA-AKI were found more frequently in all age groups. In this subgroup, more than half of the patients had glomerular or tubulointerstitial disorders, followed by sepsis, AKI secondary to trauma/ traumatic brain injury, pyelonephritis and hypoxic/ischemic injury. Laboratory findings The frequency of anemia and thrombocytopenia were significantly higher in the severe CA-AKI group than in stage 1 CA-AKI (p = 0.01and p < 0.001, respectively). Dysnatremia (both hyponatremia and hypernatremia) was the most frequent electrolyte disorder in both groups, and significantly higher in the severe CA-AKI group (p = 0.005). Hyponatremia was the most common dysnatremia observed in 43% of children with severe CA-AKI, while 12% developed hypernatremia (p = 0.05 and p = 0.02, respectively). Hyperphosphatemia and hyperuricemia were found to be higher in the severe CA-AKI group compared to the stage 1 CA-AKI group (p = 0.05 and p < 0.001, respectively) (Table 4 ). Younger children were more likely to develop hyponatremia. The need for dialysis was higher in patients with hyponatremia compared to patients with normal serum sodium (p < 0.001) (Table 5 ). Risk factors for the development of severe CA-AKI Risk factors for severe CA-AKI were younger age (p = 0.04, OR; 1.064, 95% CI: 1.002–1.129), intrinsic AKI (p < 0.001, OR; 4.714, 95% CI: 2.089–10.639), hyponatremia (p = 0.05, OR; 2.114, 95%CI: 0.978–4.570), thrombocytopenia (p = 0.003, OR;5.471, 95%CI:1.772–16.895), hyperphosphatemia (p = 0.02, OR;5.727, 95%CI:1.264–25.958) and hyperuricemia (p < 0.001, OR;5.217, 95% CI; 2.321–11.730). A borderline p value was obtained for hypernatremia (p = 0.06, OR;7.579, 95%CI:0.911–63.067) (Table 6 ). Gender, presence of comorbidity, and anemia were not predictors of severe CA-AKI (p > 0.05). Kidney function recovery At hospital discharge, of the 128 surviving patients, 108 (84.3%) achieved complete remission and 17 (13.3%) were in partial remission. During the follow-up period, CKD developed in three patients (2.4%); two patients diagnosed with PUV and one with primary glomerulonephritis (Table 2 ). Mortality Mortality occurred in 6 (4.5%) patients during the PICU stay. Three patients with comorbidities (one patient diagnosed with West syndrome, one with propionic acidemia, and one with severe cerebral palsy) died due to severe sepsis, septic shock and CA-AKI. The other three previously healthy patients had severe multiple trauma from either a car accident or fall from height (Table 2 ). Risk factors for mortality were not investigated due to low mortality rate. Discussion In the current study, we described clinical characteristics and outcomes of hospitalized children with CA-AKI in a single-center and retrospective study. In the whole group, median age on admission was 10.0 years (range; 2 months–17.9 years), with the highest incidence between the ages of > 12–18. In line with other studies, CA-AKI was more common in boys (male/female ratio;1.2), but not statistically significant (3,6,8). The findings revealed that intrinsic CA-AKI accounted for the majority of cases (72%). In this subgroup, the prior use of nephrotoxic drugs, high consumption of energy drinks and/or creatine, and HUS were remarkable. In literature, the scarce data regarding the epidemiology of pediatric CA-AKI are avilable, and mostly derived from populations in low-middle income countries [ 9 ]. In tropical countries, diarrhea, vector-borne infections, traditional herbal medicines, and envenomation by snakes or insects account for pediatric CA-AKI in most cases [ 3 , 15 – 19 ]. In studies reported from other countries, the etiology of CA-AKI considerably varies, such as shock, sepsis, hypoxic ischemic encephalopathy, electrolyte and fluid disorders, primary renal diseases, due to the inclusion of different age groups, the use of different definitions of AKI (pRIFLE or KDIGO criteria), and environmental differences [ 6 , 8 , 20 – 24 ]. Although AKI is associated with increased morbidity and mortality, early detection and management of modifiable risk factors for severe AKI may improve prognosis. Therefore, in our study, we specifically focused on potential predictors of severe CA-AKI. Currently, very few studies have been investigated the relationship between serum electrolyte abnormalities and severity of CA-AKI in children, and these studies are limited to CA-AKI subgroups such as earthquake-related AKI (25,26). Döven et al. [ 25 ] evaluated 649 pediatric victims of the 2023 southeastern Türkiye earthquake. In that study, hyponatremia was the most common electrolyte disorder on admission, and patients with AKI had lower serum sodium levels compared to non-AKI patients. More recently, Ozdemir et al. [ 26 ] evaluated dysnatremia in 312 children affected by the same earthquake. Of whom, 36% were hyponatremic and 17% were hypernatremic. The frequency of AKI and dialysis treatment was significantly higher in the hyponatremic group compared to those with normal sodium levels. Other studies involving adult patients also highlighted the frequency and significance of the sodium deviations in earthquake-related AKI [ 27 , 28 ]. Zhang et al. [ 27 ] showed that hyponatremic patients were significantly younger than those with normonatraemia, and had a significantly lower urine output in the first 24 h of admission. In addition, dialysis was performed more often in patients with hyponatraemia compared to those with normal Na level. Similarly, the relationship between dysnatremia and the risk of HA-AKI have been demonstrated in few adult studies. In two papers involving adults, the authors noted a strong and independent association between dysnatremi (hyponatremia or hypernatremia) and the risk of AKI development [ 29 , 30 ]. Furthermore, Lombardi et al. [ 29 ] considered that high Na fluctuations before the development of AKI may be an independent early indicator for the development of kidney damage during hospital stay. As for our study, in line with literature, abnormal serum sodium levels at presentation was the most common electrolyte disorder. Hyponatremia was more prevalent than hypernatremia, and significantly higher in the severe CA-AKI group than in stage 1 CA-AKI (p = 0.05) (Table 4 ). Younger patients were more likely to develop hyponatremia. The need for dialysis was higher in patients with hyponatremia compared to patients with normal serum sodium (p < 0.001) (Table 5 ). In the current study, we also identified thrombocytopenia as a strong risk factor for the development of severe CA-AKI. Almost all patients with thrombocytopenia were diagnosed with HUS or sepsis-associated AKI. To our knowledge, there is no study examining the relationship between thrombocytopenia and CA-AKI in pediatric patients, however, a limited number of studies in adults have shown the prognostic value of low platelet count on admission in the development of AKI. Chao et al. [ 31 ] noted that the presence of initial thrombocytopenia among elderly patients who visited emergency department (ED) for any medical condition predicted nearly 2-fold higher risk of subsequent AKI during their ED stay. In another study examining the association of thrombocytopenia and AKI developing in the first 48 h of admission in HIV-positive adult patients presenting with sepsis, thrombocytopenia was identified as an independent risk factor for AKI (32). Suh et al. [ 33 ] investigated risk factors of septic AKI in adult patients who visited the emergency department, and revealed a significant association between thrombocytopenia and sepsis-associated AKI on admission. Furthermore, a recent study showed that aspirin theraphy was associated with reduced kidney injury incidence in septic patients, suggesting a potential role for platelet-associated injury in AKI [ 34 ]. In literature, the association between hyperuricemia and acute kidney damage has been long established. In addition to acute urate nephropathy, studies have demonstrated that uric acid may cause AKI due to its vasoactive and proinflammatory effects in glomeruli and the tubulointerstitium [ 35 – 37 ]. Similarly, in the present study, hyperuricemia was significantly higher in patients who developed severe CA-AKI compared to stage 1 (p < 0.001), and associated with a five-fold increased risk of AKI (OR 5.217, 95% CI 2.321–11.730). Recently, studies in pediatric and adult patients have focused on the impact of hyperphosphatemia on AKI in critically ill patient subgroups. Biró et al. [ 38 ] revealed that daily increases in serum phosphate levels can be early and reliable indicator of AKI in children with tumor lysis syndrome (TLS). In that study, the cut-off value of daily change in serum phosphate concentration before the onset of AKI was 0.32 mmol/L for severe TLS-AKI. In another study, Fang et al. [ 39 ] enrolled data of septic adult patients from two different databases, and evaluated the relationship between serum phosphorus with the development of AKI within 48 h of sepsis diagnosis. In both groups, the authors reported that each 1 mg/dL increase in phosphate levels was associated with a 1.51 to 1.64-fold (OR 2.51–2.64, p < 0.001) and 0.29 to 0.38-fold (OR 1.29–1.38, p < 0.001) increase in the risk of AKI. Other studies also determined that hyperphosphatemia on admission was an independent risk factor for the development of AKI during hospital stay [ 40 – 42 ]. In our study, the total number of patients with hyperphosphatemia was 22. Of whom, 20 were in the severe AKI group and elevated phosphate levels increased almost sixfold the risk of severe CA-AKI. However, given the small number of patients with hyperphosphatemia, our results and causal role of serum phosphate in AKI should be interpreted with caution. In summary, the role of conventional biyomarkers, such as electrolyte abnormalities, hyperuricemia and thrombocytopenia, in the onset and progression of AKI have increasingly drawn attention in recent years. However, whether these factors are a result of AKI rather than a potential cause requires further studies. Although CA-AKI is associated with a high rate of the short- and long- term adverse outcomes, in our study, more than three-quarters of the children had fully recovered kidney function at discharge, and mortality rate remained low. In addition, progression to CKD occured in only a small percentage of patients. However, it should be considered that the absence of patients with systemic and multiple organ dysfunction such as SLE and malignancies in our study may have affected our results. Strengths and limitations First of all, the present study is one of the few studies in literatue specifically evaluating pediatric CA-AKI and is the first comprehensive analysis investigating the risk predictors of CA-AKI. However, this study has some limitations. First, our results is a single-center experience with a relatively small number of patients and may not reflect national data. Second, we may have missed the patients who actually experienced AKI, but were not tagged as AKI due to miscoded ICD-10 diagnoses in the medical records. Furthermore, we were not able to use urine output for AKI identification because these data were not available in the whole cohort, which may have led to an underestimation of CA-AKI diagnosis. Conclusion In this study, the most common causes of CA-AKI were glomerular and tubulointerstitial diseases, and the short-term kidney prognosis was favorable. Furthermore, our study identified reliable and easily accessible predictors of severe kidney injury. 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Pediatr Nephrol 38:3117–3127 Fang Y, Zhang Y, Zhang X (2024) Serum phosphate levels and the development of sepsis associated acute kidney injury: evidence from two independent databases. Front Med (Lausanne) 11:1367064 Moon H, Chin HJ, Na KY, Joo KW, Kim YS, Kim S, Han SS (2019) Hyperphosphatemia and risks of acute kidney injury, end-stage renal disease, and mortality in hospitalized patients. BMC Nephrol 20:362 Thongprayoon C, Cheungpasitporn W, Mao MA, Sakhuja A, Erickson SB (2018) Admission hyperphosphatemia increases the risk of acute kidney injury in hospitalized patients. J Nephrol 31:241–247 Wen T, Mao Z, Liu C, Wang X, Tian S, Zhou F (2023) Association between admission serum phosphate and risk of acute kidney injury in critically ill patients with rhabdomyolysis: A retrospective study based on MIMIC-Ⅲ. Injury 54:189–197 Tables Tables 1 to 6 are available in the Supplementary Files section. Supplementary Files Table1.docx Table2.doc Table3.doc Table4.doc Table5.doc Table6.docx Cite Share Download PDF Status: Posted Version 1 posted 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. Our growing team is made up of researchers and industry professionals working together to solve the most critical problems facing scientific publishing. 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13:02:35","extension":"pdf","order_by":0,"title":"","display":"","copyAsset":false,"role":"manuscript-pdf","size":538351,"visible":true,"origin":"","legend":"","description":"","filename":"manuscript.pdf","url":"https://assets-eu.researchsquare.com/files/rs-8551808/v1/9686fe7e-b704-4a7f-9b17-1556be6555dd.pdf"},{"id":100240330,"identity":"f19d476c-c241-4631-88f3-74d5f72d2291","added_by":"auto","created_at":"2026-01-14 13:18:30","extension":"docx","order_by":2,"title":"","display":"","copyAsset":false,"role":"supplement","size":26901,"visible":true,"origin":"","legend":"","description":"","filename":"Table1.docx","url":"https://assets-eu.researchsquare.com/files/rs-8551808/v1/a6bdb06603ab55d35ef548b8.docx"},{"id":100370544,"identity":"b5ee3012-b25f-4604-a218-be15f8745861","added_by":"auto","created_at":"2026-01-16 08:06:24","extension":"doc","order_by":4,"title":"","display":"","copyAsset":false,"role":"supplement","size":60416,"visible":true,"origin":"","legend":"","description":"","filename":"Table2.doc","url":"https://assets-eu.researchsquare.com/files/rs-8551808/v1/7c24dd8848e199118d1c2c18.doc"},{"id":100370527,"identity":"09ff31b1-324f-411d-b1b4-fa45c4684288","added_by":"auto","created_at":"2026-01-16 08:06:19","extension":"doc","order_by":6,"title":"","display":"","copyAsset":false,"role":"supplement","size":55296,"visible":true,"origin":"","legend":"","description":"","filename":"Table3.doc","url":"https://assets-eu.researchsquare.com/files/rs-8551808/v1/5cb26fb455e0301ab8adeda6.doc"},{"id":100240302,"identity":"3db5d4d9-6bc7-4668-b34b-99fb0f6489d5","added_by":"auto","created_at":"2026-01-14 13:18:28","extension":"doc","order_by":8,"title":"","display":"","copyAsset":false,"role":"supplement","size":48640,"visible":true,"origin":"","legend":"","description":"","filename":"Table4.doc","url":"https://assets-eu.researchsquare.com/files/rs-8551808/v1/a3b2e63eb4e86331dd2efba4.doc"},{"id":100370228,"identity":"25b57a98-74bf-442d-81b4-2650a6987e07","added_by":"auto","created_at":"2026-01-16 08:00:37","extension":"doc","order_by":10,"title":"","display":"","copyAsset":false,"role":"supplement","size":37376,"visible":true,"origin":"","legend":"","description":"","filename":"Table5.doc","url":"https://assets-eu.researchsquare.com/files/rs-8551808/v1/3a3c7a521be6882f88639a4d.doc"},{"id":100240321,"identity":"c9227ad9-a1bc-456b-a5b9-35757233f2f9","added_by":"auto","created_at":"2026-01-14 13:18:30","extension":"docx","order_by":12,"title":"","display":"","copyAsset":false,"role":"supplement","size":22759,"visible":true,"origin":"","legend":"","description":"","filename":"Table6.docx","url":"https://assets-eu.researchsquare.com/files/rs-8551808/v1/002a15d4a4ef9e198e35cdf4.docx"}],"financialInterests":"","formattedTitle":"\u003cp\u003eClinical characteristics, risk predictors and outcomes of community-acquired acute kidney injury in children\u003c/p\u003e","fulltext":[{"header":"Introduction","content":"\u003cp\u003eAcute kidney injury (AKI) is a complex and heterogeneous syndrome with different epidemiology, pathophysiology, and clinical trajectory, characterized by a sudden decline in kidney function. AKI is a common complication in both critically and non- critically ill children and is associated with increased morbidity, mortality, and the risk of progression to chronic kidney disease (CKD) [\u003cspan citationid=\"CR1\" class=\"CitationRef\"\u003e1\u003c/span\u003e].\u003c/p\u003e \u003cp\u003eAKI occurs in both community and hospital settings. Community-acquired AKI (CA-AKI) is defined as AKI developing outside the hospital. In pediatric population, its worldwide incidence broadly ranges from 0.26% to 56.4% across countries, depending on socioeconomic and environmental factors as well as the criteria used for determination of CA-AKI, (i.e., AKIN, pRIFLE, and more recently, the KDIGO criteria) [\u003cspan citationid=\"CR2\" class=\"CitationRef\"\u003e2\u003c/span\u003e, \u003cspan citationid=\"CR3\" class=\"CitationRef\"\u003e3\u003c/span\u003e]. Similarly, the etiologic spectrum and outcomes of pediatric CA-AKI widely differ in developing and developed world [\u003cspan additionalcitationids=\"CR4 CR5\" citationid=\"CR3\" class=\"CitationRef\"\u003e3\u003c/span\u003e\u0026ndash;\u003cspan citationid=\"CR6\" class=\"CitationRef\"\u003e6\u003c/span\u003e]. This form of AKI is more common than hospital-acquired AKI (HA-AKI) and has significant morbidity and mortality, especially in low-middle income countries [\u003cspan citationid=\"CR7\" class=\"CitationRef\"\u003e7\u003c/span\u003e, \u003cspan citationid=\"CR8\" class=\"CitationRef\"\u003e8\u003c/span\u003e]. However, in most cases, early identification and management of risk factors for CA-AKI may improve prognosis.\u003c/p\u003e \u003cp\u003eIn literature, although hospital-acquired AKI (HA-AKI), which develops after 48 hours of hospitalization, has been well-studied in pediatric population, less is known about CA-AKI [\u003cspan citationid=\"CR6\" class=\"CitationRef\"\u003e6\u003c/span\u003e, \u003cspan citationid=\"CR9\" class=\"CitationRef\"\u003e9\u003c/span\u003e]. In the current study, with an emphasis on the risk factors of severe kidney injury, we evaluated the etiology, clinical characteristics, risk predictors, and short-term outcomes of CA-AKI in children admitted to our center.\u003c/p\u003e"},{"header":"Material and Methods","content":"\u003cdiv id=\"Sec3\" class=\"Section2\"\u003e \u003ch2\u003eStudy Design, Patient Population and Data Collection\u003c/h2\u003e \u003cp\u003eData from all patients admitted to an inpatient unit (wards or intensive care unit) of the Pediatrics Department at Antalya Training and Research Hospital, a tertiary healthcare center located in southern T\u0026uuml;rkiye, with a diagnosis of AKI between January 1, 2020 and June 30, 2025, were retrospectively reviewed. To obtain data, we first identified the patients who had an International Classification of Diseases (ICD)10 code for AKI. Then, we reviewed the medical records of patients who were given ICD codes for other medical conditions that may accompany AKI, such as acute nephritic syndrome, nephrotic syndrome, hemolytic uremic syndrome, and acute gastroenteritis. Exclusion criteria were; (i) aged\u0026thinsp;\u0026lt;\u0026thinsp;1 month to \u0026gt;\u0026thinsp;18 years, (ii) children presenting with acute exacerbation of pre-existing CKD, (iii) those who died within the first 24 hours of admission to pediatric intensive care unit (PICU), and (iv) those with incomplete medical records. The remaining patients who met the criteria for CA-AKI diagnosis were included in the study.\u003c/p\u003e \u003cp\u003eAll data including age, gender, comorbidities (such as nephro-urologic problems, neurological diseases, endocrine/metabolic disorders), the use of nephrotoxic medications and nephrotoxin exposure before admission, clinical and laboratory data, primary disease/condition leading to AKI, the type of CA-AKI (prerenal, renal/intrinsic, postrenal), the frequency of PICU admission, kidney replacement therapy, mechanical ventilation and inotropic drug requirement, length of stay (LOS) in PICU, and renal outcomes at the time of discharge were extracted from electronic patient records. If a patient was hospitalized multiple times during the study period, only the first one was considered.\u003c/p\u003e \u003cp\u003eIn the current study, due to the small number of patients in subphenotypes, such as sepsis-induced AKI, drug-induced AKI, or hypoperfusion -associated AKI, we used the traditional classification of AKI (i.e., prerenal, intrinsic, and postrenal types) [\u003cspan citationid=\"CR10\" class=\"CitationRef\"\u003e10\u003c/span\u003e]. However, in some cases, the pathophysiology of AKI was complex and multifactorial. In such cases, the primary cause of AKI was included in the category considered most relevant. For example, sepsis was categorized as intrinsic AKI instead of hypovolemia-related AKI (prerenal AKI) [\u003cspan citationid=\"CR11\" class=\"CitationRef\"\u003e11\u003c/span\u003e, \u003cspan citationid=\"CR12\" class=\"CitationRef\"\u003e12\u003c/span\u003e]. Similarly, in complex cases where multiple etiological factors could lead to CA-AKI, the medical condition considered most likely to cause kidney damage was identified as the primary cause of AKI.\u003c/p\u003e \u003c/div\u003e\n\u003ch3\u003eDefinitions and Measurements\u003c/h3\u003e\n\u003cdiv id=\"Sec5\" class=\"Section2\"\u003e \u003ch2\u003eDefinition, diagnosis and staging of CA-AKI\u003c/h2\u003e \u003cp\u003eCA-AKI was defined as the presence of AKI on admission or AKI developing within 48 hours of hospital admission. A baseline serum creatinine (SCr) was considered the lowest level within the 90 days before admission (pre-admission SCr). In the absence of a known baseline SCr, the upper cutoff of age- and sex-based reference ranges was presumed as baseline Cr [\u003cspan citationid=\"CR2\" class=\"CitationRef\"\u003e2\u003c/span\u003e, \u003cspan citationid=\"CR13\" class=\"CitationRef\"\u003e13\u003c/span\u003e]. Diagnosis and staging of AKI was established according to Kidney Disease: Improving Global Outcomes (KDIGO) classification system (2012), and it was defined as either a\u0026thinsp;\u0026ge;\u0026thinsp;1.5-fold increase in SCr from baseline within the previous 7 days or a\u0026thinsp;\u0026ge;\u0026thinsp;0.3 mg/dl increase within 48 hours (Table\u0026nbsp;1) [\u003cspan citationid=\"CR14\" class=\"CitationRef\"\u003e14\u003c/span\u003e]. For each patient, a maximum AKI stage achieved during hospitalization or at the time of admission was noted, and stages 2 and 3 were considered severe AKI. Since hourly documentation of urine output (UOP) was not available, particularly in hospitalized children in the pediatric wards, UOP was not used to define AKI.\u003c/p\u003e \u003cp\u003eOn admission, serum uric acid (UA) (normal range; 3.5\u0026ndash;7.2 mg/dl), calcium (Ca) (8.8\u0026ndash;10.8 mg/dl), magnesium (Mg) (1.8\u0026ndash;2.6 mg/dl), inorganic phosphorus (iP) (4\u0026ndash;7 mg/dl), sodium (Na) (136\u0026ndash;146 mmol/l), potassium (K) levels (3.5\u0026ndash;5.1 mmol/l), hemoglobin (Hb) (12.5\u0026ndash;16.1 g/dl), platelet count (Plt) (150-450x10\u003csup\u003e3\u003c/sup\u003e/mm\u003csup\u003e3\u003c/sup\u003e) were recorded. Hyponatremia was categorized as mild (\u0026le;\u0026thinsp;134 to \u0026ge;\u0026thinsp;130 mEq/l), moderate (\u0026le;\u0026thinsp;129 to \u0026ge;\u0026thinsp;121 mEq/l), and severe (\u0026le;\u0026thinsp;120 mEq/l). Hypernatremia was considered mild when Na\u003csup\u003e+\u003c/sup\u003e concentration was \u0026ge;\u0026thinsp;146 to \u0026le;\u0026thinsp;149 mEq/l, moderate when \u0026ge;\u0026thinsp;150 to \u0026le;\u0026thinsp;169 mEq/l, and severe when \u0026ge;\u0026thinsp;170 mEq/l. Mild, moderate, severe, and very severe thrombocytopenia were defined as 100-150x10\u003csup\u003e3\u003c/sup\u003e/mm\u003csup\u003e3\u003c/sup\u003e, 50-99x10\u003csup\u003e3\u003c/sup\u003e/mm\u003csup\u003e3\u003c/sup\u003e, 20-49x10\u003csup\u003e3\u003c/sup\u003e/mm\u003csup\u003e3\u003c/sup\u003e, and \u0026lt;\u0026thinsp;20 x10\u003csup\u003e3\u003c/sup\u003e/mm\u003csup\u003e3\u003c/sup\u003e, respectively. For patients with hypoalbuminemia, a corrected calcium level was calculated. Dysphosphatemia was defined as a serum phosphorus concentration that is below or above age-specific normal phosphate ranges. In patients with diabetic ketoacidosis, serum sodium levels were adjusted according to glucose levels.\u003c/p\u003e \u003cp\u003eThe patients were divided into four groups according to their age; 1 month \u0026minus;\u0026thinsp;2 years, \u0026gt;\u0026thinsp;2\u0026ndash;6, \u0026gt;\u0026thinsp;6\u0026ndash;12, \u0026gt;\u0026thinsp;12\u0026ndash;18. Demographic and clinical characteristics of the patients were examined according to age groups. Then, risk factors for severe CA-AKI were investigated.\u003c/p\u003e \u003c/div\u003e\n\u003ch3\u003eKidney Recovery\u003c/h3\u003e\n\u003cp\u003eAccording to the SCr level at the time of discharge, complete recovery was defined as a post-AKI SCr within 25% of baseline in those with known baseline SCr levels and within the age and sex -adjusted reference range in patients with unknown baseline SCr. Partial recovery was defined as a fall in maximum AKI stage. CKD was considered the presence of reduced kidney function lasting\u0026thinsp;\u0026gt;\u0026thinsp;3 months (CKD stage 2\u0026ndash;5) [\u003cspan citationid=\"CR14\" class=\"CitationRef\"\u003e14\u003c/span\u003e].\u003c/p\u003e \u003cp\u003e The study protocol was approved by the ethics committee of our institution (Antalya Training and Research Hospital Ethics Committee, protocol number; 2025; 13/15). Written informed consent was not obtained due to the retrospective study design.\u003c/p\u003e \u003cdiv id=\"Sec7\" class=\"Section2\"\u003e \u003ch2\u003eStatistical analysis\u003c/h2\u003e \u003cp\u003eDescriptive data were presented as numbers and percentages for categorical variables; mean\u0026thinsp;\u0026plusmn;\u0026thinsp;standard deviation for normally distributed continuous variables, and median (range) for non-normally distributed ones. The Chi-square test assessed categorical variables. The Kruskal\u0026ndash;Wallis test was used for the comparison of continuous variables among multiple groups, and a p value\u0026thinsp;\u0026lt;\u0026thinsp;0.05 was considered statistically significant. When the difference was significant, the Mann-Whitney U test was done between two groups. Univariate and multivariate logistic regression analyses were performed to determine risk factors for CA-AKI. For all statistical analyses, the SPSS version 21.0 package program for Windows (IBM, Armonk, NY) was used.\u003c/p\u003e \u003c/div\u003e"},{"header":"Results","content":"\u003cdiv id=\"Sec9\" class=\"Section2\"\u003e\n \u003ch2\u003eBaseline characteristics\u003c/h2\u003e\n \u003cp\u003eA total of 134 patients, male/female ratio; 1.2, with a median age of 10.0 years (range; 2 months-17.9 years) were included. The most affected age group was \u0026gt;\u0026thinsp;12 to 18 years (39.6%) (p\u0026thinsp;=\u0026thinsp;0.039). After discharge, 10 pediatric earthquake victims transferred to our center due to the earthquake that occurred in southeastern T\u0026uuml;rkiye in 2023 and 3 patients with prerenal CA-AKI due to acute gastroenteritis (AGE) were lost to follow-up. However, SCr values of these patients were within normal limits at discharge. Six patients died during the PICU stay. The remaining 115 patients were followed for a median of 10 months (range; 1month-5 years). Thirteen patients with stage 1 CA-AKI on admission progressed to stage 2 or 3 (severe CA-AKI), and overall, more than half of the children (n\u0026thinsp;=\u0026thinsp;87, 65.7%) developed severe AKI.\u003c/p\u003e\n \u003cp\u003eOne quarter of patients had at least one medical comorbidity. In 78 (58.2%) patients who did not have a baseline SCr, the upper limit of reference ranges were used for the diagnosis of CA-AKI. Almost half of all patients (47.8%) were admitted to the PICU. The median LOS in PICU was 9 days (2\u0026ndash;30 days). Of whom, 25% (n\u0026thinsp;=\u0026thinsp;16) required mechanical ventilation, and 18.7% (n\u0026thinsp;=\u0026thinsp;12) received inotropes. Overall, one quarter of patients underwent hemodialysis, mostly continuous renal replacement therapy (CRRT). Children aged 1 month-2 years, \u0026gt;\u0026thinsp;2\u0026ndash;6 years and \u0026gt;\u0026thinsp;6\u0026ndash;12 years received dialysis more frequently and were hospitalized for longer periods than those aged\u0026thinsp;\u0026gt;\u0026thinsp;12\u0026ndash;18 years.\u003c/p\u003e\n \u003cp\u003eThe baseline demographic and clinical characteristics of the whole cohort and subgroups according to their age are summarized in Table \u003cspan class=\"InternalRef\"\u003e2\u003c/span\u003e.\u003c/p\u003e\n\u003c/div\u003e\n\u003ch3\u003eEtiology of CA-AKI\u003c/h3\u003e\n\u003cp\u003eThe primary causes of CA-AKI are outlined in Table \u003cspan class=\"InternalRef\"\u003e3\u003c/span\u003e. Intrinsic CA-AKI accounted for 72% of all cases (p\u0026thinsp;=\u0026thinsp;0.001). Even after excluding earthquake victims, which is a unique case, intrinsic causes of CA-AKI were found more frequently in all age groups. In this subgroup, more than half of the patients had glomerular or tubulointerstitial disorders, followed by sepsis, AKI secondary to trauma/ traumatic brain injury, pyelonephritis and hypoxic/ischemic injury.\u003c/p\u003e\n\u003cdiv id=\"Sec11\" class=\"Section2\"\u003e\n \u003ch2\u003eLaboratory findings\u003c/h2\u003e\n \u003cp\u003eThe frequency of anemia and thrombocytopenia were significantly higher in the severe CA-AKI group than in stage 1 CA-AKI (p\u0026thinsp;=\u0026thinsp;0.01and p\u0026thinsp;\u0026lt;\u0026thinsp;0.001, respectively). Dysnatremia (both hyponatremia and hypernatremia) was the most frequent electrolyte disorder in both groups, and significantly higher in the severe CA-AKI group (p\u0026thinsp;=\u0026thinsp;0.005). Hyponatremia was the most common dysnatremia observed in 43% of children with severe CA-AKI, while 12% developed hypernatremia (p\u0026thinsp;=\u0026thinsp;0.05 and p\u0026thinsp;=\u0026thinsp;0.02, respectively). Hyperphosphatemia and hyperuricemia were found to be higher in the severe CA-AKI group compared to the stage 1 CA-AKI group (p\u0026thinsp;=\u0026thinsp;0.05 and p\u0026thinsp;\u0026lt;\u0026thinsp;0.001, respectively) (Table \u003cspan class=\"InternalRef\"\u003e4\u003c/span\u003e). Younger children were more likely to develop hyponatremia. The need for dialysis was higher in patients with hyponatremia compared to patients with normal serum sodium (p\u0026thinsp;\u0026lt;\u0026thinsp;0.001) (Table \u003cspan class=\"InternalRef\"\u003e5\u003c/span\u003e).\u003c/p\u003e\n\u003c/div\u003e\n\u003cdiv id=\"Sec12\" class=\"Section2\"\u003e\n \u003ch2\u003eRisk factors for the development of severe CA-AKI\u003c/h2\u003e\n \u003cp\u003eRisk factors for severe CA-AKI were younger age (p\u0026thinsp;=\u0026thinsp;0.04, OR; 1.064, 95% CI: 1.002\u0026ndash;1.129), intrinsic AKI (p\u0026thinsp;\u0026lt;\u0026thinsp;0.001, OR; 4.714, 95% CI: 2.089\u0026ndash;10.639), hyponatremia (p\u0026thinsp;=\u0026thinsp;0.05, OR; 2.114, 95%CI: 0.978\u0026ndash;4.570), thrombocytopenia (p\u0026thinsp;=\u0026thinsp;0.003, OR;5.471, 95%CI:1.772\u0026ndash;16.895), hyperphosphatemia (p\u0026thinsp;=\u0026thinsp;0.02, OR;5.727, 95%CI:1.264\u0026ndash;25.958) and hyperuricemia (p\u0026thinsp;\u0026lt;\u0026thinsp;0.001, OR;5.217, 95% CI; 2.321\u0026ndash;11.730). A borderline p value was obtained for hypernatremia (p\u0026thinsp;=\u0026thinsp;0.06, OR;7.579, 95%CI:0.911\u0026ndash;63.067) (Table \u003cspan class=\"InternalRef\"\u003e6\u003c/span\u003e). Gender, presence of comorbidity, and anemia were not predictors of severe CA-AKI (p\u0026thinsp;\u0026gt;\u0026thinsp;0.05).\u003c/p\u003e\n\u003c/div\u003e\n\u003cdiv id=\"Sec13\" class=\"Section2\"\u003e\n \u003ch2\u003eKidney function recovery\u003c/h2\u003e\n \u003cp\u003eAt hospital discharge, of the 128 surviving patients, 108 (84.3%) achieved complete remission and 17 (13.3%) were in partial remission. During the follow-up period, CKD developed in three patients (2.4%); two patients diagnosed with PUV and one with primary glomerulonephritis (Table \u003cspan class=\"InternalRef\"\u003e2\u003c/span\u003e).\u003c/p\u003e\n\u003c/div\u003e\n\u003cdiv id=\"Sec14\" class=\"Section2\"\u003e\n \u003ch2\u003eMortality\u003c/h2\u003e\n \u003cp\u003eMortality occurred in 6 (4.5%) patients during the PICU stay. Three patients with comorbidities (one patient diagnosed with West syndrome, one with propionic acidemia, and one with severe cerebral palsy) died due to severe sepsis, septic shock and CA-AKI. The other three previously healthy patients had severe multiple trauma from either a car accident or fall from height (Table \u003cspan class=\"InternalRef\"\u003e2\u003c/span\u003e). Risk factors for mortality were not investigated due to low mortality rate.\u003c/p\u003e\n\u003c/div\u003e"},{"header":"Discussion","content":"\u003cp\u003eIn the current study, we described clinical characteristics and outcomes of hospitalized children with CA-AKI in a single-center and retrospective study. In the whole group, median age on admission was 10.0 years (range; 2 months\u0026ndash;17.9 years), with the highest incidence between the ages of \u0026gt;\u0026thinsp;12\u0026ndash;18. In line with other studies, CA-AKI was more common in boys (male/female ratio;1.2), but not statistically significant (3,6,8). The findings revealed that intrinsic CA-AKI accounted for the majority of cases (72%). In this subgroup, the prior use of nephrotoxic drugs, high consumption of energy drinks and/or creatine, and HUS were remarkable.\u003c/p\u003e \u003cp\u003eIn literature, the scarce data regarding the epidemiology of pediatric CA-AKI are avilable, and mostly derived from populations in low-middle income countries [\u003cspan citationid=\"CR9\" class=\"CitationRef\"\u003e9\u003c/span\u003e]. In tropical countries, diarrhea, vector-borne infections, traditional herbal medicines, and envenomation by snakes or insects account for pediatric CA-AKI in most cases [\u003cspan citationid=\"CR3\" class=\"CitationRef\"\u003e3\u003c/span\u003e, \u003cspan additionalcitationids=\"CR16 CR17 CR18\" citationid=\"CR15\" class=\"CitationRef\"\u003e15\u003c/span\u003e\u0026ndash;\u003cspan citationid=\"CR19\" class=\"CitationRef\"\u003e19\u003c/span\u003e]. In studies reported from other countries, the etiology of CA-AKI considerably varies, such as shock, sepsis, hypoxic ischemic encephalopathy, electrolyte and fluid disorders, primary renal diseases, due to the inclusion of different age groups, the use of different definitions of AKI (pRIFLE or KDIGO criteria), and environmental differences [\u003cspan citationid=\"CR6\" class=\"CitationRef\"\u003e6\u003c/span\u003e, \u003cspan citationid=\"CR8\" class=\"CitationRef\"\u003e8\u003c/span\u003e, \u003cspan additionalcitationids=\"CR21 CR22 CR23\" citationid=\"CR20\" class=\"CitationRef\"\u003e20\u003c/span\u003e\u0026ndash;\u003cspan citationid=\"CR24\" class=\"CitationRef\"\u003e24\u003c/span\u003e].\u003c/p\u003e \u003cp\u003eAlthough AKI is associated with increased morbidity and mortality, early detection and management of modifiable risk factors for severe AKI may improve prognosis. Therefore, in our study, we specifically focused on potential predictors of severe CA-AKI.\u003c/p\u003e \u003cp\u003eCurrently, very few studies have been investigated the relationship between serum electrolyte abnormalities and severity of CA-AKI in children, and these studies are limited to CA-AKI subgroups such as earthquake-related AKI (25,26). D\u0026ouml;ven et al. [\u003cspan citationid=\"CR25\" class=\"CitationRef\"\u003e25\u003c/span\u003e] evaluated 649 pediatric victims of the 2023 southeastern T\u0026uuml;rkiye earthquake. In that study, hyponatremia was the most common electrolyte disorder on admission, and patients with AKI had lower serum sodium levels compared to non-AKI patients. More recently, Ozdemir et al. [\u003cspan citationid=\"CR26\" class=\"CitationRef\"\u003e26\u003c/span\u003e] evaluated dysnatremia in 312 children affected by the same earthquake. Of whom, 36% were hyponatremic and 17% were hypernatremic. The frequency of AKI and dialysis treatment was significantly higher in the hyponatremic group compared to those with normal sodium levels. Other studies involving adult patients also highlighted the frequency and significance of the sodium deviations in earthquake-related AKI [\u003cspan citationid=\"CR27\" class=\"CitationRef\"\u003e27\u003c/span\u003e, \u003cspan citationid=\"CR28\" class=\"CitationRef\"\u003e28\u003c/span\u003e]. Zhang et al. [\u003cspan citationid=\"CR27\" class=\"CitationRef\"\u003e27\u003c/span\u003e] showed that hyponatremic patients were significantly younger than those with normonatraemia, and had a significantly lower urine output in the first 24 h of admission. In addition, dialysis was performed more often in patients with hyponatraemia compared to those with normal Na level.\u003c/p\u003e \u003cp\u003eSimilarly, the relationship between dysnatremia and the risk of HA-AKI have been demonstrated in few adult studies. In two papers involving adults, the authors noted a strong and independent association between dysnatremi (hyponatremia or hypernatremia) and the risk of AKI development [\u003cspan citationid=\"CR29\" class=\"CitationRef\"\u003e29\u003c/span\u003e, \u003cspan citationid=\"CR30\" class=\"CitationRef\"\u003e30\u003c/span\u003e]. Furthermore, Lombardi et al. [\u003cspan citationid=\"CR29\" class=\"CitationRef\"\u003e29\u003c/span\u003e] considered that high Na fluctuations before the development of AKI may be an independent early indicator for the development of kidney damage during hospital stay.\u003c/p\u003e \u003cp\u003eAs for our study, in line with literature, abnormal serum sodium levels at presentation was the most common electrolyte disorder. Hyponatremia was more prevalent than hypernatremia, and significantly higher in the severe CA-AKI group than in stage 1 CA-AKI (p\u0026thinsp;=\u0026thinsp;0.05) (Table\u0026nbsp;\u003cspan refid=\"Tab3\" class=\"InternalRef\"\u003e4\u003c/span\u003e). Younger patients were more likely to develop hyponatremia. The need for dialysis was higher in patients with hyponatremia compared to patients with normal serum sodium (p\u0026thinsp;\u0026lt;\u0026thinsp;0.001) (Table\u0026nbsp;\u003cspan refid=\"Tab4\" class=\"InternalRef\"\u003e5\u003c/span\u003e).\u003c/p\u003e \u003cp\u003eIn the current study, we also identified thrombocytopenia as a strong risk factor for the development of severe CA-AKI. Almost all patients with thrombocytopenia were diagnosed with HUS or sepsis-associated AKI. To our knowledge, there is no study examining the relationship between thrombocytopenia and CA-AKI in pediatric patients, however, a limited number of studies in adults have shown the prognostic value of low platelet count on admission in the development of AKI. Chao et al. [\u003cspan citationid=\"CR31\" class=\"CitationRef\"\u003e31\u003c/span\u003e] noted that the presence of initial thrombocytopenia among elderly patients who visited emergency department (ED) for any medical condition predicted nearly 2-fold higher risk of subsequent AKI during their ED stay. In another study examining the association of thrombocytopenia and AKI developing in the first 48 h of admission in HIV-positive adult patients presenting with sepsis, thrombocytopenia was identified as an independent risk factor for AKI (32). Suh et al. [\u003cspan citationid=\"CR33\" class=\"CitationRef\"\u003e33\u003c/span\u003e] investigated risk factors of septic AKI in adult patients who visited the emergency department, and revealed a significant association between thrombocytopenia and sepsis-associated AKI on admission. Furthermore, a recent study showed that aspirin theraphy was associated with reduced kidney injury incidence in septic patients, suggesting a potential role for platelet-associated injury in AKI [\u003cspan citationid=\"CR34\" class=\"CitationRef\"\u003e34\u003c/span\u003e].\u003c/p\u003e \u003cp\u003eIn literature, the association between hyperuricemia and acute kidney damage has been long established. In addition to acute urate nephropathy, studies have demonstrated that uric acid may cause AKI due to its vasoactive and proinflammatory effects in glomeruli and the tubulointerstitium [\u003cspan additionalcitationids=\"CR36\" citationid=\"CR35\" class=\"CitationRef\"\u003e35\u003c/span\u003e\u0026ndash;\u003cspan citationid=\"CR37\" class=\"CitationRef\"\u003e37\u003c/span\u003e]. Similarly, in the present study, hyperuricemia was significantly higher in patients who developed severe CA-AKI compared to stage 1 (p\u0026thinsp;\u0026lt;\u0026thinsp;0.001), and associated with a five-fold increased risk of AKI (OR 5.217, 95% CI 2.321\u0026ndash;11.730).\u003c/p\u003e \u003cp\u003eRecently, studies in pediatric and adult patients have focused on the impact of hyperphosphatemia on AKI in critically ill patient subgroups. Bir\u0026oacute; et al. [\u003cspan citationid=\"CR38\" class=\"CitationRef\"\u003e38\u003c/span\u003e] revealed that daily increases in serum phosphate levels can be early and reliable indicator of AKI in children with tumor lysis syndrome (TLS). In that study, the cut-off value of daily change in serum phosphate concentration before the onset of AKI was 0.32 mmol/L for severe TLS-AKI. In another study, Fang et al. [\u003cspan citationid=\"CR39\" class=\"CitationRef\"\u003e39\u003c/span\u003e] enrolled data of septic adult patients from two different databases, and evaluated the relationship between serum phosphorus with the development of AKI within 48 h of sepsis diagnosis. In both groups, the authors reported that each 1 mg/dL increase in phosphate levels was associated with a 1.51 to 1.64-fold (OR 2.51\u0026ndash;2.64, p\u0026thinsp;\u0026lt;\u0026thinsp;0.001) and 0.29 to 0.38-fold (OR 1.29\u0026ndash;1.38, p\u0026thinsp;\u0026lt;\u0026thinsp;0.001) increase in the risk of AKI. Other studies also determined that hyperphosphatemia on admission was an independent risk factor for the development of AKI during hospital stay [\u003cspan additionalcitationids=\"CR41\" citationid=\"CR40\" class=\"CitationRef\"\u003e40\u003c/span\u003e\u0026ndash;\u003cspan citationid=\"CR42\" class=\"CitationRef\"\u003e42\u003c/span\u003e]. In our study, the total number of patients with hyperphosphatemia was 22. Of whom, 20 were in the severe AKI group and elevated phosphate levels increased almost sixfold the risk of severe CA-AKI. However, given the small number of patients with hyperphosphatemia, our results and causal role of serum phosphate in AKI should be interpreted with caution.\u003c/p\u003e \u003cp\u003eIn summary, the role of conventional biyomarkers, such as electrolyte abnormalities, hyperuricemia and thrombocytopenia, in the onset and progression of AKI have increasingly drawn attention in recent years. However, whether these factors are a result of AKI rather than a potential cause requires further studies.\u003c/p\u003e \u003cp\u003eAlthough CA-AKI is associated with a high rate of the short- and long- term adverse outcomes, in our study, more than three-quarters of the children had fully recovered kidney function at discharge, and mortality rate remained low. In addition, progression to CKD occured in only a small percentage of patients. However, it should be considered that the absence of patients with systemic and multiple organ dysfunction such as SLE and malignancies in our study may have affected our results.\u003c/p\u003e \u003cdiv id=\"Sec16\" class=\"Section2\"\u003e \u003ch2\u003eStrengths and limitations\u003c/h2\u003e \u003cp\u003eFirst of all, the present study is one of the few studies in literatue specifically evaluating pediatric CA-AKI and is the first comprehensive analysis investigating the risk predictors of CA-AKI. However, this study has some limitations. First, our results is a single-center experience with a relatively small number of patients and may not reflect national data. Second, we may have missed the patients who actually experienced AKI, but were not tagged as AKI due to miscoded ICD-10 diagnoses in the medical records. Furthermore, we were not able to use urine output for AKI identification because these data were not available in the whole cohort, which may have led to an underestimation of CA-AKI diagnosis.\u003c/p\u003e \u003c/div\u003e"},{"header":"Conclusion","content":"\u003cp\u003eIn this study, the most common causes of CA-AKI were glomerular and tubulointerstitial diseases, and the short-term kidney prognosis was favorable. Furthermore, our study identified reliable and easily accessible predictors of severe kidney injury. Monitoring serum levels of these biomarkers may provide early detection and management in children at high risk of CA-AKI, however, large-scale cohort studies are needed to confirm our findings.\u003c/p\u003e "},{"header":"Declarations","content":"\u003cp\u003e\u003cstrong\u003eData availability statement\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eAll data are available on request from the corresponding author.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eConflict of interest; \u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eThe authors declare no competing interests.\u003c/p\u003e"},{"header":"References","content":"\u003col\u003e\u003cli\u003e\u003cspan\u003eStrau\u0026szlig; C, Booke H, Forni L, Zarbock A (2024) Biomarkers of acute kidney injury: From discovery to the future of clinical practice. J Clin Anesth 95:111458\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eO'Neil ER, Devaraj S, Mayorquin L, Starke HE, Buffone GJ, Loftis LL, Arikan AA, Cruz AT (2020) Defining pediatric community-acquired acute kidney injury: an observational study. Pediatr Res 87:564\u0026ndash;568\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eDuzova A, Bakkaloglu A, Kalyoncu M, Poyrazoglu H, Delibas A, Ozkaya O et al (2010) Etiology and outcome of acute kidney injury in children. Pediatr Nephrol 25:1453\u0026ndash;1461\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eEvans RDR, Docherty M, Seeley A, Craik A, Mpugna M, Mann S, Dube Q, Dreyer G, Hemmila U (2018) Incidence, Etiology, and Outcomes of Community-Acquired Acute Kidney Injury in Pediatric Admissions in Malawi. 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Intern Emerg Med 16:617\u0026ndash;624\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eLee SW, Baek SH, Ahn SY, Na KY, Chae DW, Chin HJ, Kim S (2016) The effects of pre-existing hyponatremia and subsequent-developing acute kidney injury on in-hospital mortality: a retrospective cohort study. PLoS ONE 11:e0162990\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eChao CT, Tsai HB, Chiang CK, Huang JW COGENT (COhort of GEriatric Nephrology in NTUH) study group (2017) Thrombocytopenia on the first day of emergency department visit predicts higher risk of acute kidney injury among elderly patients. Scand J Trauma Resusc Emerg Med ;25:114\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eKimweri D, Ategeka J, Ceasor F, Muyindike W, Nuwagira E, Muhindo R (2021) Incidence and risk predictors of acute kidney injury among HIV-positive patients presenting with sepsis in a low resource setting. BMC Nephrol 22:238\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eSuh SH, Kim CS, Choi JS, Bae EH, Ma SK, Kim SW (2013) Acute Kidney Injury in Patients with Sepsis and Septic Shock: Risk Factors and Clinical Outcomes. Yonsei Med J 54:965\u0026ndash;972\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eLuo Y, Li H, Li J, Li D, Zhen Qiu S 1, Fu Q, Xia Z (2025) Aspirin use is associated with attenuated risk of severe acute kidney injury in septic patients: a dual-center retrospective analysis from MIMIC-IV and eICU cohorts. Ren Fail 47:2568650\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eEjaz AA, Mu W, Kang DH, Roncal C, Sautin YY, Henderson G et al (2007) Could Uric Acid Have a Role in Acute Renal Failure? Clin J Am Soc Nephrol 2:16\u0026ndash;21\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eJohnson RJ, Bakris GL, Borghi C, Chonchol MB, Feldman D, Miguel A, Lanaspa MA (2018) Hyperuricemia, Acute and Chronic Kidney Disease, Hypertension, and Cardiovascular Disease: Report of a Scientific Workshop Organized by the National Kidney Foundation. Am J Kidney Dis 71:851\u0026ndash;865\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eEjaz AA, Johnson RJ, Shimada M, Mohandas R, Alquadan KF, Beaver TM, Lapsia V, Dass B (2019) The Role of Uric Acid in Acute Kidney Injury. Nephron 142:275\u0026ndash;283\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eBir\u0026oacute; E, Erd\u0026eacute;lyi D, Varga P, Sink\u0026oacute; M, Bartyik K, Kov\u0026aacute;cs G, Ott\u0026oacute;ffy G, Vincze F, Szegedi I, Kiss C, Szab\u0026oacute; T (2023) Daily serum phosphate increase as early and reliable indicator of kidney injury in children with leukemia and lymphoma developing tumor lysis syndrome. Pediatr Nephrol 38:3117\u0026ndash;3127\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eFang Y, Zhang Y, Zhang X (2024) Serum phosphate levels and the development of sepsis associated acute kidney injury: evidence from two independent databases. Front Med (Lausanne) 11:1367064\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eMoon H, Chin HJ, Na KY, Joo KW, Kim YS, Kim S, Han SS (2019) Hyperphosphatemia and risks of acute kidney injury, end-stage renal disease, and mortality in hospitalized patients. BMC Nephrol 20:362\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eThongprayoon C, Cheungpasitporn W, Mao MA, Sakhuja A, Erickson SB (2018) Admission hyperphosphatemia increases the risk of acute kidney injury in hospitalized patients. J Nephrol 31:241\u0026ndash;247\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eWen T, Mao Z, Liu C, Wang X, Tian S, Zhou F (2023) Association between admission serum phosphate and risk of acute kidney injury in critically ill patients with rhabdomyolysis: A retrospective study based on MIMIC-Ⅲ. Injury 54:189\u0026ndash;197\u003c/span\u003e\u003c/li\u003e\u003c/ol\u003e"},{"header":"Tables","content":"\u003cp\u003eTables 1 to 6 are available in the Supplementary Files section.\u003c/p\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":"Community- acquired acute kidney injury, child, etiology, risk factors, outcome","lastPublishedDoi":"10.21203/rs.3.rs-8551808/v1","lastPublishedDoiUrl":"https://doi.org/10.21203/rs.3.rs-8551808/v1","license":{"name":"CC BY 4.0","url":"https://creativecommons.org/licenses/by/4.0/"},"manuscriptAbstract":"\u003ch2\u003eBackground;\u003c/h2\u003e \u003cp\u003eLittle data exist related to community-acquired acute kidney injury (CA-AKI) in children. We aimed to determine the etiology, clinical profile, risk factors, and outcomes of children hospitalized for CA-AKI.\u003c/p\u003e\u003ch2\u003eMethods;\u003c/h2\u003e \u003cp\u003ePatients, 1month to18 years, who had CA-AKI on or within 48 hours of hospital admission between January 2020 to June 2025 were included. KDIGO 2012 criteria were used for the diagnosis of AKI. The patients were divided into four groups according to their age; 1 month \u0026minus;\u0026thinsp;2 years, \u0026gt;\u0026thinsp;2\u0026ndash;6, \u0026gt;\u0026thinsp;6\u0026ndash;12, \u0026gt;\u0026thinsp;12\u0026ndash;18 years. Demographic, clinical, and laboratory data were analyzed. Risk factors for severe CA-AKI (stage 2 and 3) were investigated.\u003c/p\u003e\u003ch2\u003eResults;\u003c/h2\u003e \u003cp\u003e134 patients, male/female ratio; 1.23, with a median age of 10 years (2 months-17.9 years) were included. The most affected age group was \u0026gt;\u0026thinsp;12 to 18 years (39.6%). Intrinsic CA-AKI accounted for 72% of all cases, mostly glomerular and acute tubulointerstitial diseases. More than half of the patients (65.7%) developed severe AKI. Risk factors for severe CA-AKI were younger age (p\u0026thinsp;=\u0026thinsp;0.04, OR;1.064, 95%CI:1.002\u0026ndash;1.129), intrinsic AKI (p\u0026thinsp;\u0026lt;\u0026thinsp;0.001, OR; 4.714, 95%CI:2.089\u0026ndash;10.639), hyponatremia (p\u0026thinsp;=\u0026thinsp;0.05, OR;2.114, 95%CI:0.978\u0026ndash;4.570), thrombocytopenia (p\u0026thinsp;=\u0026thinsp;0.003, OR;5.471, 95%CI:1.772\u0026ndash;16.895), hyperphosphatemia (p\u0026thinsp;=\u0026thinsp;0.02, OR;5.727, 95%CI:1.264\u0026ndash;25.958) and hyperuricemia (p\u0026thinsp;\u0026lt;\u0026thinsp;0.001, OR;5.217, 95%CI;2.321\u0026ndash;11.730). At discharge, complete recovery was observed in 85%, and partial recovery in 14.8%. Three patients (2.4%) developed CKD. Mortality occurred in 6 (4.5%).\u003c/p\u003e\u003ch2\u003eConclusions;\u003c/h2\u003e \u003cp\u003eGlomerular and tubulointerstitial diseases were the most common causes of CA-AKI, and short term kidney outcomes were favorable. Intrinsic etiology, serum electrolyte disturbances, thrombocytopenia and hyperuricemia were strong independent risk factors for severe CA-AKI.\u003c/p\u003e","manuscriptTitle":"Clinical characteristics, risk predictors and outcomes of community-acquired acute kidney injury in children","msid":"","msnumber":"","nonDraftVersions":[{"code":1,"date":"2026-01-14 13:18:22","doi":"10.21203/rs.3.rs-8551808/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":"8280458b-b14c-447a-bbc9-5d2641c63f31","owner":[],"postedDate":"January 14th, 2026","published":true,"recentEditorialEvents":[],"rejectedJournal":[],"revision":"","amendment":"","status":"posted","subjectAreas":[],"tags":[],"updatedAt":"2026-02-11T18:14:54+00:00","versionOfRecord":[],"versionCreatedAt":"2026-01-14 13:18:22","video":"","vorDoi":"","vorDoiUrl":"","workflowStages":[]},"version":"v1","identity":"rs-8551808","journalConfig":"researchsquare"},"__N_SSP":true},"page":"/article/[identity]/[[...version]]","query":{"redirect":"/article/rs-8551808","identity":"rs-8551808","version":["v1"]},"buildId":"XKTyCvWXoU3ODBz1xrDgd","isFallback":false,"isExperimentalCompile":false,"dynamicIds":[84888],"gssp":true,"scriptLoader":[]}