Search Results (4,172)

Background and Objectives: Sclerostin or dickkopf-1 (DKK1) inhibits the canonical Wnt/β-catenin signaling pathway, which regulates vascular calcification and may contribute to the development of arterial stiffness. The brachial–ankle pulse wave velocity (baPWV) measures peripheral arterial stiffness (PAS). This study aimed to investigate the correlation between sclerostin and DKK1 levels and PAS in patients with type 2 diabetes mellitus (T2DM). Materials and Methods: Biochemical data and sclerostin and DKK1 levels were analyzed in the fasting blood samples of 125 patients with T2DM. baPWV measurements using the VaSera VS-1000 automatic pulse wave analyzer classified patients with values > 18.0 m/s on either side into the PAS group. Results: Among patients with T2DM, 47 (37.6%) were classified as having PAS. These patients exhibited higher hypertension prevalence (p = 0.002); greater age (p < 0.001); elevated systolic (p < 0.001) and diastolic blood (p = 0.012) pressures; and increased fasting glucose (p = 0.001), glycated hemoglobin (p = 0.008), triglyceride (p = 0.001), blood urea nitrogen (p < 0.001), and creatinine (p = 0.001) levels, urine albumin-to-creatinine ratio (p = 0.039), and C-reactive protein (p = 0.024) and serum sclerostin (p < 0.001) levels, but decreased estimated glomerular filtration rate (p < 0.001). Multivariate logistic regression analysis identified serum sclerostin level (odds ratio, 1.127; 95% confidence interval, 1.058–1.200; p < 0.001) as an independent PAS predictor in patients with T2DM. Serum log-transformed sclerostin levels were positively correlated with left (p = 0.005) and right (p = 0.001) baPWV via Spearman’s rank-order correlation coefficient analysis. Conclusions: Serum sclerostin levels, but not DKK1 levels, are positively correlated with PAS in patients with T2DM. Full article

Hemotherapy in small ruminants is indicated for several acute and chronic conditions; however, its clinical use is often limited by the difficulty in identifying suitable donors, particularly regarding blood volume availability and hematologic compatibility. Xenotransfusion in small ruminants with bovine blood may represent a practical alternative in emergency situations involving severe anemia when homologous donors are unavailable. This study evaluated the clinical, hematologic, biochemical, and blood gas responses of sheep subjected to acute blood loss followed by bovine whole blood xenotransfusion. Six healthy adult castrated male sheep (mean body weight 44.3 ± 7.2 kg) underwent removal of 40% of their estimated total blood volume. Parameters were assessed before hemorrhage induction (T0) and at times T30, T6h, T12h, T24h, T48h, T72h, T96h, T5d, T6d, T7d, T8d and T16d after transfusion. Acute blood loss significantly reduced packed cell volume and erythrocyte count at T0 (p < 0.05). After xenotransfusion, packed cell volume increased at T30min, T6h, and T12h and remained stable until T72h (p < 0.05), with progressive erythrocyte recovery and sustained macrocytosis. Total leukocyte count remained unchanged, whereas platelets increased at T7D (p < 0.05). Total protein decreased at T0 and subsequently increased. Transient elevations in urea, creatinine, glucose, pO₂, and SO₂ were observed (p < 0.05), without acid–base imbalance. Clinical parameters progressively stabilized, and no severe transfusion reactions occurred. Bovine whole blood xenotransfusion may represent a promising therapeutic alternative for sheep subjected to acute blood loss under the experimental conditions evaluated in this study. The procedure was associated with improvements in clinical, hematological, and biochemical parameters, and no severe transfusion reactions were observed during the monitoring period. These findings support the potential clinical applicability of this approach as an emergency intervention in situations where homologous donors are not readily available. Full article

Background: Determining the optimal duration of extracorporeal cardiopulmonary resuscitation (ECPR) remains challenging, as patient outcomes may vary significantly based on individual characteristics. We aimed to establish critical time thresholds for achieving favorable neurological outcomes with ECPR across different risk groups, potentially providing more tailored guidance for clinical decision-making. Methods: This single-center retrospective study screened 279 adult patients who received ECPR between 2013 and 2020. Through multivariate analysis of various clinical parameters, we developed a pragmatic bedside risk stratification framework to identify groups with different prognostic profiles. The primary outcome was neurological status at discharge, assessed by the Cerebral Performance Categories scale. Results: In multivariate analysis, age greater than 50 years with asystole (adjusted odds ratio [OR]: 4.89, 95% confidence interval [CI]: 1.41–17.00) or pulseless electrical activity (adjusted OR: 9.70, 95% CI: 2.80–33.60), aspartate transaminase (adjusted OR: 1.52, 95% CI: 1.15–1.99), creatinine (adjusted OR: 2.08, 95% CI: 1.30–3.34), initial lactate (adjusted OR: 1.88, 95% CI: 1.27–3.45), and low-flow time (adjusted OR: 3.50, 95% CI: 2.02–6.06) were associated with poor neurological outcomes. Based on these findings, we identified three distinct risk groups showing different acceptable low-flow time thresholds: low-risk (38 min), moderate-risk (27 min), and high-risk (20 min). Notably, no favorable neurological outcomes were observed beyond 70 min in the low-risk group and 90 min in moderate/high-risk groups. Risk group stratification effectively predicted neurological outcomes across different low-flow time intervals. Conclusions: Risk-stratified evaluation of low-flow time (cardiac arrest to ECMO pump-on) provides clinically relevant thresholds for different patient groups, suggesting that continuation of ECPR may be warranted in low-risk patients even with extended low-flow times. This approach may enable more personalized decision-making in ECPR implementation. Full article

Nateglinide (Nat) is an oral antidiabetic agent of the meglitinide class that has been reported to exert protective effects beyond glycemic control, particularly against oxidative stress and inflammation. Since oxidative stress and inflammation play a key role in the pathogenesis of acute kidney injury (AKI), especially following ischemia/reperfusion (I/R), this study aimed to evaluate the potential renoprotective effects of Nat in a rat model of I/R-induced AKI. Forty male Sprague Dawley rats were randomly divided into four groups (n = 10): Control, I/R, I/R + Nat (50 mg/kg), and I/R + Nat (100 mg/kg). Bilateral renal ischemia was induced by clamping renal arteries for 45 min, followed by 24 h of reperfusion. Nat was administered orally 1 h before ischemia. Renal levels of superoxide dismutase (SOD), catalase (CAT), glutathione (GSH), and thiobarbituric acid reactive substances (TBARSs) were assessed. Serum blood urea nitrogen (BUN), creatinine, tumor necrosis factor-α (TNF-α), and interleukin-1β (IL-1β) were also measured, and histopathological analyses were performed. Nat significantly increased renal antioxidant parameters and reduced TBARS levels. Moreover, Nat markedly decreased serum BUN, creatinine, TNF-α, and IL-1β levels compared with the I/R group (p < 0.05). Histopathology confirmed attenuated renal damage in Nat-treated groups (p < 0.0001). These results indicate that Nat confers significant renoprotection against renal I/R injury via suppression of oxidative stress and inflammation. Full article

Atrial fibrillation (AF) frequently coexists with chronic kidney disease (CKD), and their combination confers a disproportionate risk of both thromboembolic and bleeding events. Conventional anticoagulation strategies rely primarily on creatinine clearance-based dosing, which reflects pharmacokinetic safety but does not fully capture the biological processes underlying thrombohemorrhagic instability. This narrative review synthesizes recent mechanistic and translational evidence regarding the bidirectional cardio–renal axis in AF and CKD, focusing on systemic inflammation, endothelial dysfunction, platelet dysregulation, and altered coagulation. A structured literature search of PubMed/MEDLINE, Scopus, and Web of Science (2018–2026) was performed, complemented by manual review of key references and guidelines. The evidence indicates that inflammatory cytokine activation, oxidative stress, glycocalyx degradation, von Willebrand factor dysregulation, uremic platelet dysfunction, and enhanced thrombin generation converge to create a disrupted vascular interface in which stroke and bleeding arise from shared pathophysiological mechanisms. Renal trajectory and selected circulating biomarkers further highlight the dynamic and heterogeneous nature of risk in advanced CKD. These findings support reframing anticoagulation decision-making in AF with CKD from a static filtration-based model toward a biology-informed approach that integrates renal dynamics, endothelial and platelet phenotype, and clinical context to better align thromboembolic protection with hemorrhagic safety. Full article

Chronic kidney disease (CKD) involves uremic toxin-driven tubular injury and systemic vascular dysfunction, in which mitochondrial impairment and apoptotic cell loss contribute to progressive tissue deterioration. Accordingly, a targeted EV platform is required to enable efficient miRNA delivery to the toxin-stressed tubular–endothelial compartment. Based on our previous study showing that melatonin restores miR-4516 levels under CKD-related stress, we directly loaded miR-4516 into engineered extracellular vesicles (EVs) to evaluate its effects on mitochondrial function and cell survival. Here, we engineered EVs with a G3-C12/RGD surface modification and established a miR-4516 loading strategy to enhance delivery to kidney proximal tubule cells and vascular endothelial cells. miR-4516 loading increased EV-associated miR-4516 levels without major changes in particle size distribution, and EV identity was supported by CD9 and CD81 expression. Confocal microscopy and flow cytometry demonstrated increased cellular uptake of miR-4516-loaded G3-C12/RGD-EVs compared with control EVs in TH1 proximal tubule cells and HUVECs. Under indoxyl sulfate stress, engineered EV treatment restored intracellular miR-4516 and improved mitochondrial function, as indicated by recovery of respiratory Complex I and Complex IV activities and improved Seahorse bioenergetic parameters (OCR/ECAR, basal and maximal respiration, ATP-linked respiration, and spare respiratory capacity). Annexin V staining further indicated reduced toxin-induced apoptosis. In an adenine diet-induced CKD mouse model, intravenous administration of miR-4516-loaded G3-C12/RGD-EVs improved urinary albumin-to-creatinine ratio (UACR), blood urea nitrogen (BUN), and serum creatinine. These findings indicate that miR-4516-loaded, targeting-engineered EVs may mitigate uremic toxin-associated mitochondrial dysfunction and renal impairment in CKD. Full article

Background: The updated Schwartz and CKiDU25 bedside (SCr-based) formulae for the estimated glomerular filtration rate (eGFR) in children are defined by a constant term (with the latter formula dependent upon age and sex) multiplied by the ratio of patient’s height (m) to SCr (mg/dL). However, the Schwartz formula can severely underestimate the measured GFR (mGFR) at higher mGFR levels. Methods: For a single-center cohort of 92 pediatric kidney transplant recipients, we statistically determined if the log{eGFR} at 1 mo and 6 mo post-transplant might further depend upon patient demographics or height, indicating the inadequacy of these formulae for properly predicting the mGFR. We also determined how the log{SCr} at 1 mo and 6 mo post-transplant might depend upon patient demographics and height, helping to corroborate any arrived-at improved functional form for the eGFR. Results: Overall, our cohort received good-quality donor kidneys; however, both eGFR formulae calculated that the percentage of recipients with an eGFR < 60 mL/min/1.73 m² at 1 mo and 6 mo post-transplant was 26–28%. Furthermore, neither the updated Schwartz nor the CKiDU25 bedside formulae adequately controlled for the influence of patient height on SCr; in fact, the patient height squared was superior to its unidimensional value at accounting for the sharp increase in SCr that normally occurs as children grow from infancy to young adulthood (p < 0.000001 at mo1, p = 0.000003 at mo6 for the updated Schwartz bedside formula; p = 0.0009 at mo1, p = 0.005 at mo6 for the CKiDU25 bedside formula). The log{SCr} was also best fitted by a linear regression model that controlled for the log{patient height squared} (p < 0.000001 at both mo1 and mo6). Conclusions: A statistically more accurate eGFR formula should be based on using a power function (power > 1) for patient height rather than its unidimensional value. Full article

Background/Objectives: Cardiorenal syndrome type 2 (CRS-2) is characterized by progressive renal dysfunction caused by chronic heart failure (HF) and is associated with increased morbidity and mortality. However, the prognostic value of renal biomarkers in patients with CRS-2 hospitalized for decompensated HF remains unclear. Methods: This prospective observational cohort study included 200 consecutive patients hospitalized for decompensated HF in the Intensive Care Unit of the Clinic for Internal Medicine at the University Clinical Centre Tuzla between April and October 2025. CRS-2 was defined as chronic HF with chronic kidney disease persisting for ≥3 months before admission according to KDIGO criteria. Patients were followed for three months. The primary composite outcome was all-cause mortality or initiation of renal replacement therapy. Results: CRS-2 was identified in 130 patients (65.0%) and was associated with higher in-hospital mortality (32.3% vs. 11.4%, p = 0.002) and three-month mortality (44.6% vs. 21.4%, p = 0.002). Within the CRS-2 subgroup, patients who experienced the primary composite outcome had higher admission levels of cystatin C and urinary albumin-to-creatinine ratio (UACR) and lower estimated glomerular filtration rate (eGFR). ROC analysis demonstrated moderate discriminative ability of cystatin C (AUC 0.739) and UACR (AUC 0.733). In Cox regression analysis, cystatin C (HR 1.534, 95% CI 1.263–1.863, p < 0.001) and UACR (HR 1.003, 95% CI 1.001–1.006, p = 0.001) were significantly associated with the primary composite outcome. Conclusions: Renal dysfunction markers, particularly cystatin C and albuminuria, are associated with early adverse outcomes in CRS-2 patients hospitalized for decompensated HF. Routine assessment of these biomarkers may provide additional prognostic information and support risk assessment in this high-risk population. Full article

Background and Objectives: Sepsis-associated acute kidney injury (SA-AKI) is driven by exaggerated inflammation and oxidative stress, with the HMGB1–RAGE axis playing a pivotal role in amplifying tissue damage. This study aimed to investigate the renoprotective effects of papaverine in a feces-induced peritonitis (FIP) model of sepsis and to explore its impact on HMGB1–RAGE-mediated inflammatory and oxidative pathways. Materials and Methods: Sepsis was induced in male Wistar rats by intraperitoneal injection of fecal slurry (1 g/kg). Animals were treated with papaverine (20 or 40 mg/kg, i.p.) one hour after FIP induction and evaluated at 24 h. Renal function (BUN, creatinine, lactate), inflammatory markers (HMGB1, TNF-α, CRP), oxidative stress (MDA), circulating sRAGE levels, renal NF-κB levels, and histopathological injury scores were assessed. Results: The FIP model resulted in an early mortality rate of 20% and produced marked renal histopathological alterations. Biochemically, FIP increased plasma HMGB1, TNF-α, CRP, MDA, BUN, creatinine, and lactate levels while decreasing sRAGE. Papaverine treatment dose-dependently reduced inflammatory and oxidative markers, restored sRAGE levels, improved renal function parameters, and attenuated histopathological injury. In addition, renal NF-κB levels were significantly elevated in the FIP group compared to controls and were dose-dependently reduced following papaverine treatment. Conclusions: FIP-induced sepsis activates an HMGB1-driven inflammatory–oxidative cascade contributing to SA-AKI. Papaverine confers dose-dependent renoprotection by suppressing HMGB1–RAGE signaling, attenuating NF-κB activation, reducing oxidative stress, and preserving renal structure and function. Targeting the HMGB1–sRAGE axis may represent a promising therapeutic strategy in sepsis-associated renal injury. Full article

Background/Objectives: Cardiac and renal dysfunction frequently coexist and interact bidirectionally, constituting cardiorenal syndrome (CRS). In aging societies, this overlap is increasingly conceptualized within cardiovascular–kidney–metabolic (CKM) syndrome, in which metabolic risk factors, chronic kidney disease (CKD), and cardiovascular disease cluster and worsen prognosis. Patients with cardiorenal multimorbidity exhibit reduced exercise tolerance, physical activity, and skeletal muscle function, leading to frailty, disability, recurrent hospitalization, and reduced tolerance of disease-modifying therapies. Although exercise-based rehabilitation is central to cardiovascular care and increasingly recognized in nephrology, its role in combined cardiac and renal dysfunction remains insufficiently integrated. Methods: This narrative review synthesizes cardiology and nephrology evidence using a functional framework. We address (i) the epidemiology and clinical significance of cardiorenal overlap across CRS/CKM, (ii) functional phenotypes defined by inactivity, low exercise capacity, sarcopenia/frailty, and disability, (iii) rehabilitation effects on physical function and renal trajectories, including renal endpoint validity (creatinine vs. cystatin C), and (iv) prognostic implications and evidence gaps. Results: Evidence from heart failure trials demonstrates that exercise-based cardiac rehabilitation improves health-related quality of life and reduces hospital admissions. In CKD, systematic reviews support exercise benefits for physical function and cardiometabolic risk. Conclusions: Although evidence remains limited, data support rehabilitation as a biologically plausible, function-centered therapeutic strategy. Full article

Background/Objectives: Exertional rhabdomyolysis (ER) is a possibly fatal condition resulting from extreme or novel exercise that causes substantial muscle breakdown. ER has been observed during preseason football; however, prospective research has yet to characterize normal versus ER responses using a repeated measures design. This study characterized ER biomarker responses related to muscle damage, and renal and hepatic stress, after two NCAA Division I preseason football scrimmages. Methods: Following a prospective, repeated measures design, blood and urine samples from 17 players were collected immediately (IPS) and 24 h post-scrimmage (24hPS). A subset (n = 13) provided samples after 48 h of rest as a non-exertion (NE) comparator group. A Comprehensive Metabolic Panel was run on serum samples, and urine samples were analyzed for myoglobin and creatinine. Values were compared with reference ranges, mixed models evaluated time effects, and linear regressions examined associations between CPK and renal and hepatic biomarkers. Results: No participants were diagnosed with ER. A time effect was observed for CPK (p < 0.01), with CPK greater IPS (991.6 ± 560.8 IU/L) compared to NE (267.7 ± 205.3 IU/L), and remaining elevated above reference ranges at 24hPS (739.2 ± 442.6 IU/L). Similar time effects were observed with LDH, AST, and ALT (p < 0.01). Serum creatinine increased above reference values and NE concentrations (p < 0.01). CPK correlated (p < 0.01 for all) with LDH (r = 0.69), serum myoglobin (r = 0.57), creatinine (r = 0.42), AST (r = 0.77), and ALT (r = 0.38). Conclusions: Biomarkers of muscle damage, renal stress, and liver function were higher IPS, with only partial recovery by 24hPS. These findings provide preliminary reference patterns for biomarker fluctuations and support individualized, serial monitoring to identify abnormal responses and promote early detection of ER. Full article

Background/Objectives: Although the Calvert formula has been widely used to guide carboplatin dosing, it may yield inaccurate dose predictions in certain patient populations. We aimed to evaluate the adequacy of the conventional Calvert formula and to propose structural modifications to enhance dosing accuracy in breast cancer patients with preserved renal function (CrCL ≥ 55 mL/min). Methods: A systematic review and meta-analysis were conducted to integrate published pharmacokinetic models in patients with breast cancer. Two retrospective datasets (n = 154) were combined into a single analysis dataset and used to calculate carboplatin doses based on the conventional formulas using creatinine clearance (CrCL) or estimated glomerular filtration rate (eGFR), as well as a modified formula incorporating an additional constant (α). Performance was assessed by the proportion of subjects achieving target area under the curve (AUC) attainment (4–6 mg·min/mL), underexposure (<4 mg·min/mL), and overexposure (≥7 mg·min/mL). All AUC metrics were derived from model-based predictions rather than measured carboplatin concentrations, and no clinical toxicities or efficacy outcomes were used for validation. Results: Meta-analysis yielded fixed-effect parameter estimates (CL: 131.8 mL/min, V₁: 15.39 L, K₁₂: 0.002 min⁻¹, and K₂₁: 0.003 min⁻¹) with a random effect model. The conventional CrCL-based formula yielded 66.0% target attainment, 22.1% underexposure, and 4.5% overexposure. Switching to eGFR improved attainment to 88.3%, reduced underexposure to 5.8%, and lowered overexposure to 0.65%. A modified formula with α = 1 further decreased underexposure (4.5%) while target attainment and overexposure remained unchanged. Conclusions: Replacing CrCL with Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI)-derived eGFR in the Calvert formula markedly improved dosing accuracy, while modest structural modification offered additional benefit. The incremental benefit of α = 1 should be considered hypothesis-generating and requires prospective validation with measured carboplatin concentrations and clinical outcomes before applying it in practice. These findings support adopting eGFR-based dosing in breast cancer and suggest the need for future clinical validation. Full article

Background: This study aimed to evaluate the prognostic performance of four albumin-anchored ratios—blood urea nitrogen/albumin ratio (BAR), C-reactive protein/albumin ratio (CAR), lactate/albumin ratio (LAR), and albumin/creatinine ratio (ACR)—in predicting short-term mortality among intensive care unit (ICU) patients with pre-existing chronic comorbidities. Additionally, we assessed their incremental prognostic value beyond established severity scores such as APACHE II and SOFA. Materials and Methods: This retrospective cohort study included 520 chronically ill adult ICU patients admitted between July 2022 and July 2025. Patients with missing laboratory data, ICU stay <24 h, or postoperative monitoring only were excluded. BAR, CAR, LAR, and ACR were calculated from admission laboratory values. The primary outcome was 28-day mortality. Receiver operating characteristic (ROC) analyses, multivariate logistic regression, and model improvement metrics (C-statistics, NRI, IDI) were used to assess predictive performance. Results: Non-survivors had significantly higher BAR (15.0 vs. 8.2), CAR (39.2 vs. 19.1), and LAR (0.86 vs. 0.44) values and lower ACR (2.0 vs. 3.4) (all p < 0.001). In multivariate analysis, all four ratios independently predicted 28-day mortality (p < 0.001 for each). CAR showed the highest AUC (0.80), followed by LAR (0.79), BAR (0.78), and ACR (0.76). Incorporating all four ratios improved model discrimination (C-statistic 0.872 vs. 0.823; Δ = +0.049, p < 0.001) and reclassification (NRI = 0.162; IDI = 0.052). Conclusions: BAR, CAR, LAR, and ACR are independent and complementary predictors of short-term mortality in ICU patients with chronic comorbidities. Among them, CAR exhibited the best discriminative power. The combined use of these ratios enhanced risk prediction beyond traditional severity scores, suggesting their utility as simple, cost-effective markers for early mortality assessment. Because these indices are calculated from routinely measured laboratory parameters, they may represent practical and widely accessible tools for mortality risk stratification in routine ICU practice. Full article

Diabetic kidney disease (DKD) persists as the leading cause of chronic kidney disease (CKD) and often leads to end-stage renal disease (ESRD). Worldwide, 30–50% of patients with diabetes are affected by DKD, while DKD contributes to about half of ESRD. Previously, DKD had been defined based on overt proteinuria—that is, a urine albumin-to-creatinine ratio (UACR) above 300 mg/g—after a stage of microalbuminuria (UACR 30–300 mg/g). However, emerging data suggest that a significant number of patients develop renal functional decline without albuminuria, suggesting that DKD can occur in the absence of protein excretion. This phenotype of normoalbuminuric or non-proteinuric DKD (NA-DKD or NP-DKD) is emerging as an important clinical entity. It is characterized by a gradual decline in renal function, commonly with an annual reduction in estimated glomerular filtration rate (eGFR) > 3 mL/min/1.73 m² or an eGFR < 60 mL/min/1.73 m², while the UACR remains < 30 mg/g. Growing rates of NP-DKD expose limitations inherent in traditional models of DKD pathogenesis and underscore the need for diagnostic and therapeutic paradigms that are not reliant on albuminuria-only criteria. Here, we present a comprehensive review of the NP-DKD to guide a more inclusive model of DKD pathogenesis, its diagnosis, and therapy. Full article

Background: Acute compartment syndrome (ACS), a condition characterized by elevated pressure within an enclosed compartment, leads to ischemia and organ failure, and is hence a surgical emergency. Renal compartment syndrome (RCS) is a disease in which there is an increase in the pressure within the native kidney’s compartment due to peri-renal or subcapsular fluid collection, causing acute kidney injury. To our knowledge, the diagnosis of bilateral traumatic renal compartment syndrome (BTRCS) due to trauma has not been previously described in the literature. Case Presentation: The patient is a 20-year-old female presenting as a case of blunt trauma due to a severe motor vehicle collision. Initially, investigations showed multiple injuries, including a femur fracture that was managed accordingly. Postoperatively, she remained stable with no signs of complications. However, after 10 days, she began complaining of abdominal pain. Further workup revealed an acute drop in hemoglobin, elevated serum creatinine, and bilateral perinephric hematomas. BTRCS was diagnosed and was surgically managed by open laparotomy and bilateral capsulotomy, with the return of robust urine production. The patient recovered successfully and was consequently discharged. Conclusions: This paper reports a case of renal compartment syndrome that was diagnosed and treated appropriately. Doppler ultrasound and CT scan, along with renal function tests, are the investigations of choice. Although there can be a role for conservative management, open surgical decompression remains the definitive treatment in patients with progressive renal dysfunction. To our knowledge, this represents the first reported case applying the term “bilateral traumatic renal compartment syndrome (BTRCS)” involving native kidneys following blunt trauma, successfully treated with bilateral surgical decompression and rapid physiological recovery. Full article