Search Results (4,397)

Background: Systemic inflammation plays a central role in determining postoperative outcomes in patients undergoing isolated coronary artery bypass grafting with cardiopulmonary bypass. Traditional inflammatory indices such as the neutrophil-to-lymphocyte ratio and the platelet-to-lymphocyte ratio have prognostic value; however, their dynamic behavior during cardiopulmonary bypass remains insufficiently characterized. More comprehensive indices, including the systemic immune-inflammation index and the systemic inflammatory response index, may help characterize early intraoperative inflammatory activity; however, their prognostic relevance should be regarded as exploratory and requires prospective validation. Methods: This retrospective nested case–control study included 245 patients who underwent isolated coronary artery bypass grafting, and intraoperative inflammatory indices during cardiopulmonary bypass were evaluated. Because of the nested case–control design, mortality cases were intentionally overrepresented to improve statistical power; therefore, the observed mortality rate does not reflect the true institutional mortality rate. Inflammatory indices (NLR, PLR, SII, and SIRI) were calculated at induction, at the 5th, 45th, and 90th minutes during cardiopulmonary bypass, and in the early postoperative period. Associations between these indices and in-hospital mortality were evaluated using univariate and multivariable logistic regression analyses. Predictive performance was assessed using receiver operating characteristic (ROC) curve analysis and the area under the curve (AUC). Results: The final enriched analytical sample consisted of 51 mortality cases and 194 randomly sampled surviving controls. During cardiopulmonary bypass, inflammatory indices, particularly at the 5th minute, were significantly higher in patients who experienced mortality (p < 0.001 for all major indices). SII demonstrated the strongest predictive performance at the 5th minute (AUC = 0.790), followed by SIRI (AUC = 0.765), PLR (AUC = 0.687), and NLR (AUC = 0.681). In multivariable analysis, SII and SIRI measured at the 5th minute remained independent predictors of mortality. The addition of 5th-minute SII to the limited study-specific clinical model, which included age, ejection fraction, and preoperative creatinine, improved exploratory discrimination for in-hospital mortality (with AUC increasing from 0.698 to 0.797). Conclusions: Early intraoperative assessment of inflammatory indices during cardiopulmonary bypass may provide additional prognostic information in patients undergoing coronary artery bypass grafting. Composite indices, particularly SII and SIRI, showed stronger exploratory discrimination than traditional inflammatory markers in this enriched analytical sample. However, these findings should be considered hypothesis-generating and require prospective external validation before use in perioperative risk stratification or clinical decision-making can be recommended. Full article

Background: Autosomal dominant polycystic kidney disease (ADPKD) is a clinically heterogeneous disorder often leading to end-stage renal disease (ESRD). Prognostication of disease progression remains a major clinical challenge. This study aimed to identify plasma amino acid signatures associated with ADPKD progression and hypertension. Methods: We conducted targeted metabolomic analysis (LC-MS/MS) to quantify 38 plasma amino acids in 203 ADPKD patients, stratified by disease progression (rapid vs. slow) and hypertension status. Support Vector Machine (SVM) models were developed to predict outcomes using clinical data, amino acid profiles, and combined datasets. Results: Our findings revealed that specific amino acid signatures, including valine, glutamic acid, homocitrulline, and methylhistidines, were significantly elevated in both rapid progression and hypertensive groups. Isoleucine and citrulline were elevated only in rapid progressors. Phenylalanine, leucine, asparagine, and arginine were elevated in hypertensive patients. Machine learning analysis showed that integrating clinical and metabolic data modestly improved prediction for progression and hypertension. Proteinuria, glomerular filtration rate (GFR), and uric acid were the top clinical predictors; however, adding arginine, isoleucine, and 3-methylhistidine further enhanced prediction accuracy. Pathway analysis showed shared dysregulation in arginine biosynthesis and branched-chain amino acid (BCAA) metabolism. Specific amino acids were positively correlated with creatinine and uric acid and negatively correlated with GFR, and elevated levels of these metabolites were associated with increased mortality risk in survival analysis. Conclusions: Our results suggest that these plasma amino acid signatures, when combined with clinical markers, may serve as potential biomarkers for early risk stratification and precision prediction of ADPKD progression and hypertension. Full article

Objectives: Aspidopterys obcordata has been traditionally used by the Dai people in Xishuangbanna, China, for the prevention and treatment of renal calculi. This study aimed to investigate the inhibitory effect of A. tomentosa extracts on calcium oxalate stone formation. Methods: The extracts of A. tomentosa (EA) were obtained via 95% ethanol reflux extraction, followed by multi-polar solvent extraction and elution. The HK-2 cell injury model induced by calcium oxalate and the renal calculus mouse model established by intraperitoneal injection of glyoxylic acid were established to assess drug efficacy. EA intervention was performed to evaluate its effects on calcium oxalate crystal deposition, renal tubular injury, cell apoptosis, and serum creatinine (Scr) and blood urea nitrogen (BUN) levels. Furthermore, the potential mechanism underlying, particularly the regulation of PERK/ATF4/CHOP signaling pathway and endoplasmic reticulum stress-mediated apoptosis, was investigated. Results: EA treatment significantly reduced renal calcium oxalate crystal deposition, alleviated renal tubular injury, inhibited cell apoptosis, and decreased Scr and BUN levels. Mechanistically, the protective effects of EA were mediated by the downregulation of the PERK/ATF4/CHOP signaling pathway and the suppression of endoplasmic reticulum stress-mediated apoptosis. Conclusions: These findings provide experimental evidence supporting that A. tomentosa can be developed as a promising agent for the prevention of nephrolithiasis. Full article

Cisplatin-induced acute kidney injury (AKI) remains a dose-limiting complication in cancer chemotherapy with restricted preventive measures. Carthamus tinctorius L. (safflower) is known to exhibit effective antioxidant and anti-inflammatory properties; however its potential in renoprotective mechanisms remains poorly understood. The present study utilized a cisplatin-induced AKI mouse model to evaluate the renoprotective potential of CT (Carthamus tinctorius) extract. Integrated multi-omics along with in silico and in vivo approaches were used to elucidate the underlying mechanisms of action. The results initially demonstrated a rich phytochemical profile of CT extract characterized by abundant polysaccharides and flavonoids, with Hydroxysafflor Yellow A as a dominant bioactive constituent. In a cisplatin-induced acute kidney injury (AKI) mouse model, CT extract noticeably ameliorated the abnormalities of renal injury, as suggested by improved histopathology, reduced serum creatinine and BUN levels, and regulation of redox homeostasis. Metabolically, CT extract partially reversed AKI-associated disturbances by affecting 21 key metabolites, likely associated with histidine and alanine-aspartate-glutamate biosynthesis, and modulating amino acid and energy metabolism pathways. Concurrently, CT extract improved gut microbial homeostasis, increasing microbial diversity, normalizing the Firmicutes/Bacteroidota ratio, suppressing pathogens, and enriching beneficial Ligilactobacillus. Network pharmacology and molecular docking identified AKT1, RELA, MAPK, and TP53 as central targets of core compounds (rutin and kaempferol derivatives), apparently targeting the PI3K-AKT and RELA (NF-kappaB) hubs. These results suggested that the renoprotective effects of CT extract are associated with transcriptional upregulation of the PI3K/Akt/Nrf2 pathway-related genes, increased expression of antioxidant genes (Ho-1, Sod1), and reduced expression of pro-inflammatory mediators (RelA, Cdk2) in the cisplatin-induced AKI mouse model. Full article

Chronic kidney disease, acute kidney injury and cardiorenal syndrome are major determinants of cardiovascular morbidity and mortality, yet conventional renal assessment based on serum creatinine, estimated glomerular filtration rate and urine output often fails to detect early structural injury or pathway-specific cardiorenal risk. This narrative review synthesized recent evidence on emerging renal and cardiorenal biomarkers with potential value for cardiovascular risk stratification beyond creatinine. Literature published between 2015 and April 2026 was reviewed, focusing on biomarkers of tubular injury, functional renal impairment, fibrosis/remodeling and mineral metabolism. NGAL and KIM-1 may detect tubular stress and proximal tubular injury before overt functional decline and have shown relevance in heart failure, acute coronary syndromes and post-cardiac surgery settings. Cystatin C and pro-enkephalin refine functional renal assessment and may improve prognostic classification when creatinine is confounded by frailty, muscle mass or acute hemodynamic changes. Soluble ST2 and galectin-3 reflect inflammation, fibrosis and cardiorenal remodeling, while FGF-23 links kidney dysfunction to cardiovascular risk through phosphate imbalance, vascular calcification and myocardial hypertrophy. Multi-biomarker panels may help identify dominant cardiorenal phenotypes and personalize monitoring intensity. However, routine implementation requires standardized assays, validated thresholds, cost-effectiveness data and prospective evidence that biomarker-guided management improves clinical outcomes. Full article

Background/Objectives: Acute pulmonary embolism (PE) is a major cause of cardiovascular mortality, with prognosis influenced by hemodynamic status, comorbidities, and biomarker profiles. Although several laboratory markers have demonstrated prognostic relevance in PE, it remains unclear whether their predictive performance differs in patients with active malignancy. This study aimed to identify laboratory predictors of in-hospital mortality in acute PE and evaluate the modifying effect of malignancy on biomarker-based prognostic stratification. Methods: This retrospective multicenter cohort study included 2803 consecutive patients with confirmed acute PE enrolled in the Regional Pulmonary Embolism Registry (REPER) between January 2015 and April 2026. Univariate and multivariable logistic regression analyses were performed to identify predictors of in-hospital mortality in the overall cohort and subgroups stratified by malignancy status. Interaction analyses were used to formally assess effect modification by malignancy. Results: Active malignancy was present in 14.02% of patients, and overall in-hospital mortality was 11.10%. Multivariable analysis identified malignancy, CRP, glucose, creatinine clearance (CrCl), platelet count, and ESC risk category as independent predictors of in-hospital mortality. In-hospital mortality was significantly higher in patients with malignancy compared with those without (16.54% vs. 10.21%, p < 0.001). In the malignant subgroup, CRP and glucose remained independent predictors, whereas in non-malignant patients, CRP, glucose, CrCl, and ESC risk category were independently associated with outcome. Significant interactions between malignancy status and CrCl, age, glucose, and total leukocyte count suggest that the prognostic contribution of these variables may differ according to cancer status. Conclusions: Active malignancy is an independent predictor of in-hospital mortality in acute PE and appears to be associated with a more severe presentation. Our findings suggest that malignancy may also modify the prognostic performance of certain biomarkers. These observations suggest that conventional risk stratification tools may require cautious, malignancy-aware interpretation and that prospective studies validating malignancy-adapted prognostic frameworks are warranted. Full article

Background: Sodium–glucose cotransporter 2 (SGLT2) inhibitors have demonstrated significant renoprotective effects in patients with chronic kidney disease. However, kidney transplant recipients have been excluded from major randomized trials, and evidence in non-diabetic transplant patients remains limited. This study aimed to investigate the potential effects of SGLT2 inhibitors in non-diabetic kidney transplant recipients. Methods: Kidney transplant recipients were screened retrospectively and divided into two groups based on SGLT2 inhibitor use. A total of 18 non-diabetic patients receiving SGLT2 inhibitors (Group 1) were compared with 30 matched controls (Group 2). Patients were followed at baseline, 3, 6, and 12 months. Proteinuria, serum creatinine, eGFR, uric acid, and tacrolimus levels were analyzed. Results: Baseline demographic and biochemical characteristics were similar between groups. In Group 1, proteinuria decreased by 20% at 6 months and 26% at 12 months compared with baseline. The reduction in proteinuria from baseline to 6 months was significantly greater in Group 1 than in controls (p = 0.037). No significant changes were observed in serum creatinine, eGFR, tacrolimus levels, or infection-related adverse events between groups. Conclusions: SGLT2 inhibitors may confer an early antiproteinuric benefit in non-diabetic kidney transplant recipients without apparent adverse effects on renal function or safety. Larger prospective studies are needed to confirm long-term effects. Full article

Background: Nutritional status is an important determinant of outcomes after kidney transplantation, yet the prognostic significance of longitudinal changes in nutritional indices remains insufficiently investigated. We evaluated whether first-year changes in the Prognostic Nutritional Index (PNI) and Controlling Nutritional Status (CONUT) score were associated with long-term adverse outcomes in kidney transplant recipients (KTRs). Methods: This retrospective cohort study included 352 adult KTRs with a median follow-up of 11.4 years. PNI and CONUT were calculated before transplantation and at the first post-transplant year. Patients were categorized according to changes in nutritional status as improved/stable or worsened. The primary outcome was a composite of end-stage renal disease (ESRD) or death with a functioning graft. Two separate multivariable logistic regression models were constructed to evaluate the associations of changes in first-year PNI and CONUT with the composite outcome after adjustment for clinically relevant demographic and transplant-specific variables, including first-year rejection episodes, estimated glomerular filtration rate (eGFR), and urine protein-to-creatinine ratio (PCR). Additional analyses were performed separately for graft loss and death with a functioning graft. Results: Baseline PNI and CONUT scores were comparable between patients with and without adverse outcomes. Patients who reached the composite outcome had significantly lower first-year eGFR (p = 0.001), whereas first-year rejection episodes and urine PCR were similar between the groups. After multivariable adjustment, worsening first-year PNI (OR: 2.02, 95% CI: 1.08–3.77, p = 0.028) and worsening first-year CONUT (OR: 2.01, 95% CI: 1.11–3.65, p = 0.022) remained independently associated with the composite outcome. Higher first-year eGFR was independently associated with a lower risk of adverse outcomes. Separate analyses of graft loss and death with a functioning graft supported the primary findings, with stronger associations observed for graft-related outcomes. Conclusions: Early deterioration in nutritional status, reflected by worsening changes in PNI and CONUT during the first post-transplant year, was independently associated with adverse long-term outcomes in KTRs. Serial assessment of these simple and inexpensive nutritional indices may improve long-term risk stratification and help identify patients who could benefit from closer clinical follow-up and individualized nutritional assessment. Full article

Clostridioides difficile infection (CDI) is a leading healthcare-associated infection worldwide, causing significant morbidity, mortality, healthcare burden, and costs. Clinical manifestations range from mild, self-limiting diarrhea to severe, life-threatening complications such as toxic megacolon and septic shock. Early identification of patients at high risk of severe disease is essential to guide clinical decision-making and optimize therapy. This narrative review summarizes recent epidemiological data, current trends, and known risk factors as clinical context for severity prediction and then examines the utility and limitations of biomarkers that may predict CDI severity, including inflammatory, hematological, fecal, renal, and immune-response biomarkers. While some markers are already used in guideline-based assessment or routine clinical practice (e.g., C-reactive protein, white blood cell count, serum creatinine), they have limited specificity. Other markers emerging from CDI research, including procalcitonin, interleukins, and presepsin, may provide complementary prognostic information. The key challenge is not simply to identify additional biomarkers but to determine which biomarkers are clinically useful, at which stage of CDI progression, and in which patients they add value beyond conventional severity criteria. Validated predictive models integrating combinations of these biomarkers with clinical and microbiological data are needed to support early risk stratification and therapeutic decision-making at the time of diagnosis. Full article

Background: Parathyroid hormone (PTH) is mainly regulated by calcium, vitamin D, and renal function, but metabolic factors may also influence its levels. The uric acid/creatinine (UA/Cr) ratio reflects uric acid metabolism and renal handling. This study evaluated its association with elevated PTH in adults without known parathyroid disease. Methods: This retrospective cross-sectional study included 244 adults undergoing routine biochemical evaluation. The uric acid-to-creatinine ratio (UA/Cr) was calculated. Participants were categorized according to PTH levels (≤65 pg/mL vs. >65 pg/mL). Logistic regression analyses were performed to identify factors associated with elevated PTH levels. Results: A total of 244 individuals (mean age 40.6 ± 11.7 years; 70.9% female) were included in the analysis. Participants with elevated PTH levels had significantly higher UA/Cr ratios compared with those with normal PTH levels (8.93 ± 1.82 vs. 7.47 ± 1.79, p = 0.031). In univariate logistic regression analysis, UA/Cr was associated with elevated PTH (OR 1.15, 95% CI 1.01–1.32, p = 0.043). In multivariable logistic regression analysis adjusting for vitamin D, magnesium, phosphorus, corrected calcium, age, sex, body mass index, and the estimated glomerular filtration rate, the UA/Cr ratio remained significantly associated with elevated PTH levels (OR 1.41, 95% CI 1.036–1.66, p = 0.024). Conclusions: The UA/Cr ratio was associated with elevated PTH levels in adults without known parathyroid disease, independently of vitamin D status, mineral metabolism parameters, and renal function. These findings suggest that the UA/Cr ratio may help characterize a broader metabolic context associated with elevated PTH levels, rather than serving as a diagnostic marker. Further prospective studies are needed to clarify the clinical relevance and direction of this association. Full article

Background/Objectives. Neurofilament light chain (NfL) is a biomarker of axonal injury with prognostic value in acute ischemic stroke and a promising surrogate outcome marker. This study evaluated whether serum NfL concentrations in ischemic stroke were modified by varying degrees of renal function. Methods. In this prospective, single-center observational study, patients aged 18–80 y admitted to the IRCCS Mondino Foundation—Stroke Unit between May 2022 and August 2024 were enrolled. Inclusion criteria were: radiologically confirmed ischemic stroke within 24 h of onset, NIHSS ≥ 1 at admission, pre-stroke mRS < 2, no other neurological comorbidities, and eGFR > 30 mL/min/1.73 m². Serum creatinine was measured on admission, and eGFR was calculated using the CKD-EPI equation. Serum NfL was measured by Ella™ immunoassay at T0 (≤24 h), T1 (5 ± 3 d), and T2 (7 ± 3 d). Factors associated with serum NfL concentrations were assessed using linear mixed-effects models, and prognostic associations were evaluated by multivariate logistic regression. Results. Ninety-seven patients were included (median age 68.3 y; 39.2% female). Higher NfL levels were independently associated with lower eGFR (−2.4% per mL/min/1.73 m² increase; 95% CI −3.2% to −1.6%; p < 0.001), and higher NIHSS at admission (+3.5% per point; 95% CI 0.7% to 6.4%; p = 0.014). Time from stroke onset was also associated with NfL (p < 0.001). Among patients with 3-month follow-up and T2 measurement (n = 62), the main effects of log10-transformed NfL at T2 and eGFR were not independently associated with unfavorable outcomes. However, a significant log10 NfL × eGFR interaction was observed (OR 0.22; 95% CI 0.07–0.73; p = 0.014), indicating that the prognostic association of NfL varied according to renal function. Conclusions. Renal function affects serum NfL after ischemic stroke and appears to modify its prognostic association with 3-month outcomes. Full article

This study evaluated the effects of dietary non-fiber carbohydrate to neutral detergent fiber ratio (NFC/NDF) and allicin supplementation on serum electrolytes, urinary biochemical indicators, nitrogen (N) and phosphorus excretion, and fecal microbiota in beef bulls. Forty 12-month-old beef bulls were assigned to a 2 × 2 factorial design based on dietary NFC/NDF (0.75 and 1.02) and allicin supplementation (0 and 0.04% on a DM basis), resulting in four treatment groups with 10 replicates per group. Increasing dietary NFC/NDF decreased serum pH and increased the anion gap (p < 0.05). An interaction between NFC/NDF and allicin supplementation was observed for the serum concentrations of non-ionized calcium and total calcium (p < 0.05), with the highest concentrations detected in cattle fed high-NFC/NDF diets supplemented with allicin. Serum uric acid was elevated by high NFC/NDF (p < 0.05). High dietary NFC/NDF also increased urine pH (p < 0.05). Significant interactions between dietary NFC/NDF and allicin supplementation were observed for allantoin, creatinine, and urease activity (p < 0.05). High NFC/NDF increased N excretion, total N excretion, and N excretion rate (p < 0.01). Additionally, allicin supplementation reduced fecal N excretion and N excretion rate and increased the apparent total-tract digestibility of N (p < 0.05). Fecal microbiota Alpha diversity analysis showed that high NFC/NDF decreased the Chao1, observed features, and Shannon (p < 0.05). At the phylum level, high NFC/NDF increased Pseudomonadota but decreased Cyanobacteriota, and a significant interaction between NFC/NDF and allicin was observed for Spirochaetota (p < 0.05). At the genus level, high NFC/NDF reduced unclassified_UCG-010 but increased Succinivibrio, unclassified_Muribaculaceae, and Methanobrevibacter (p < 0.05). Allicin increased Rikenellaceae_RC9_gut_group abundance (p < 0.05). In conclusion, dietary NFC/NDF and allicin supplementation modulate acid–base balance, N utilization, and fecal microbial composition in beef bulls, providing a scientific basis for improving feed efficiency. Full article

Background/Objectives: Intraoperative oliguria has long been considered a marker of impaired renal perfusion, but its prognostic value for postoperative acute kidney injury (AKI) remains controversial, particularly within Enhanced Recovery After Surgery (ERAS) protocols. We investigated the association between intraoperative oliguria and postoperative AKI in patients undergoing major hepatobiliary and pancreatic surgery within an ERAS protocol. Methods: Patients who underwent major hepatobiliary and pancreatic surgery within an institutional ERAS protocol were retrospectively analyzed. Intraoperative oliguria was defined as urine output < 0.3 mL kg⁻¹ h⁻¹. Postoperative AKI was defined according to the KDIGO serum creatinine criterion within 7 days after surgery. The association was assessed using multivariable logistic regression and sensitivity analyses were performed using an alternative oliguria threshold of <0.5 mL kg⁻¹ h⁻¹ and incorporating additional surgical covariates. Results: Among 816 patients, intraoperative oliguria occurred in 51 (6.3%), and postoperative AKI developed in 60 (7.4%). AKI incidence did not differ between the oliguria and non-oliguria groups (11.8% vs. 7.1%, p = 0.332), and median intraoperative urine output was comparable between the AKI and non-AKI groups (0.7 [0.5–1.1] vs. 0.8 [0.6–1.4] mL kg⁻¹ h⁻¹, p = 0.069). In multivariable analysis, intraoperative oliguria was not independently associated with AKI (OR 1.68, 95% CI 0.60–4.01; p = 0.276). Oral carbohydrate loading, thoracic epidural analgesia, and total intraoperative fluid volume were not associated with AKI. Results were consistent across both sensitivity analyses. Conclusions: In patients undergoing hepatobiliary and pancreatic surgery within the ERAS protocol, intraoperative oliguria was not associated with postoperative AKI, although modest association cannot be excluded given the limited number of AKI and oliguria events. These findings suggest that intraoperative urine output alone may not be a reliable indication for additional fluid administration, and larger prospective studies are needed to confirm this. Full article

Alterations of gut microbiota are common in chronic kidney disease (CKD) and contribute to increased uremic toxins including indoxyl sulfate (IS), p-cresyl sulfate (pCS) and trimethylamine N-oxide (TMAO), which are linked to cerebrovascular disease risk. This study examined the kidney–gut–brain axis in CKD mice and in dialysis patients. Male and female mice with adenine-induced CKD were fed a high-amino-acid (HAA) diet to increase precursors of gut-derived uremic toxins. A subgroup of mice received antibiotics in drinking water to suppress gut microbiota and evaluate its role in toxin generation. Behavior tests, gut microbiome composition and brain histology for cerebral microhemorrhages were analyzed. CKD mice had higher serum levels of creatinine, cystatin C and gut-derived toxins, a 2.5-fold increase in brain microhemorrhages, and decreased locomotor activity. The HAA diet significantly increased serum TMAO but not IS and pCS, and all three toxins were reduced by antibiotic therapy. Sex differences were observed; in male animals, higher TMAO was associated with increased brain microhemorrhages, whereas in female mice, pCS was associated with brain microhemorrhage burden. The suppression of toxins with antibiotics improved working memory in male animals. Gut microbiota analysis revealed the expansion of Lactobacillus and Ileibacterium in CKD mice. The HAA diet and antibiotics altered gut microbiota composition without changing alpha diversity. The human study utilized biobanked serum samples and a retrospective review of brain imaging scans in a hemodialysis patient cohort; TMAO levels were associated with increased lobar microbleeds. Our study supports a role for bacterial-derived uremic toxins in the kidney–gut–brain axis and cerebral microhemorrhage formation in CKD. Full article

African pygmy hedgehogs (APHs) are increasingly kept as companion animals, yet evidence-based nutritional recommendations for this species remain limited. Commercial cat or kitten diets are still commonly used by owners and veterinarians in practice, despite being formulated exclusively for domestic cats rather than for hedgehogs with omnivorous–insectivorous feeding habits. This cross-sectional study evaluated the association between dietary regimen and serum biochemical parameters associated with renal function in APHs. Blood samples were collected from 19 client-owned APHs aged 12–68 months: 10 hedgehogs fed a commercial kitten diet and 9 fed a commercial APH-specific diet. Serum concentrations of blood urea nitrogen, creatinine, phosphorus, and calcium were measured, and the nutritional composition of the two diets was compared using manufacturer declarations and targeted laboratory analyses. Hedgehogs fed the commercial kitten diet had significantly higher serum blood urea nitrogen (p = 0.0133), creatinine (p = 0.0279), and phosphorus (p = 0.0279) concentrations than those fed the APH-specific diet, whereas serum calcium concentrations did not differ significantly (p = 0.3846). These differences occurred despite similar dietary phosphorus content, while the commercial kitten diet had higher declared fat and lower fiber content. The findings suggest that dietary regimen may be associated with alterations in renal biochemical profiles in APHs and support the use of species-appropriate diets in clinical practice. Full article