KIDNEYS

Nephrotoxic Medication Exposure and Clinical Outcomes Following Acute Kidney Injury

Dr. Lincy Joseph, Dr Jatin Prajapati (Author); Dr. K. Parameswaran Namboothiri — Thu, 10 Sep 2026 00:00:00 +0000

Acute kidney injury (AKI) is a common comorbidity in patients admitted to hospitals and can also be affected by exposure to potentially nephrotoxic drugs. Medication-related and clinical predictors of adverse outcomes can be identified, which is significant to enhance risk assessment and management. An analytical study, secondary-data study was carried out on a subset of 1,000 cases of hospitalized adults with AKI based on ELAIA-2 dataset that was cleaned. ACEi/ARB, NSAIDs and PPIs exposure were evaluated in relation to AKI progression, dialysis, mortality and composite adverse outcomes. Descriptive statistics, chi-square tests, independent samples t-tests, correlation and regression were used. Crude associations between PPI exposure and AKI progression, dialysis, death, and composite outcome were significant. There were lower rates of selected outcomes with ACEi/ARB and NSAID exposure in the unadjusted analysis. Nonetheless, the composite outcome was not adjusted and independently related to individual medication classes. The overall outcome, AKI progression, death and dialysis were always predicted by the higher SOFA score. Predictors of 14-day mortality were age, and predictors of dialysis were baseline creatinine. Clinical severity and baseline renal status seemed to be more critical predictors of short-term outcomes of AKI compared to medication exposure alone. Close review of medications should thus be coupled with evaluation of severity of systemic illness and renal function.

Health-Related Quality of Life as an Early Indicator of Adverse Outcomes in Kidney Transplant Recipients

Thu, 10 Sep 2026 00:00:00 +0000

Background: Health-related quality of life (HRQoL) may provide clinically relevant prognostic information beyond conventional measures of graft function in kidney transplant recipients. This study evaluated whether baseline HRQoL could identify recipients at increased risk of adverse outcomes.
Methods: A secondary observational cohort analysis was conducted among 156 kidney transplant recipients. HRQoL was assessed using the five EQ-5D-5L dimensions and a 0–100 self-assessment score. The primary composite outcome was death or return to dialysis. Group differences were evaluated using Mann–Whitney U, chi-square, or Fisher’s exact tests. Kaplan–Meier analysis, log-rank testing, Cox proportional-hazards regression, and receiver operating characteristic analysis were performed.
Results: Twenty-nine recipients (18.6%) experienced the composite outcome. Those with adverse outcomes had lower median self-assessment scores (60 vs. 80, p < .001), greater EQ-5D-5L severity, and more affected dimensions. Lower baseline HRQoL was associated with poorer adverse-outcome-free survival. In adjusted Cox analysis, each 10-point increase in self-assessment score was associated with a 24% lower hazard of adverse outcome (HR = 0.760, 95% CI 0.595–0.972). The combined predictive model achieved an AUC of 0.814.
Conclusion: Baseline HRQoL may complement clinical indicators for early risk stratification after kidney transplantation.

Urinary Extracellular Vesicles as Molecular Fingerprints of Kidney Injury and Disease Progression

Thu, 10 Sep 2026 00:00:00 +0000

Urinary extracellular vesicles (uEVs) have emerged as promising non-invasive indicators of kidney injury and disease progression because they carry proteins, nucleic acids, lipids, metabolites, and signaling molecules derived from renal and urinary tract cells. Their molecular composition can reflect pathological alterations across glomerular, tubular, inflammatory, metabolic, and fibrotic pathways, supporting their potential use as dynamic molecular fingerprints of renal disease. This review examines the biological origin, molecular cargo, disease-associated alterations, and translational relevance of uEVs across acute kidney injury, chronic kidney disease, diabetic kidney disease, glomerular disorders, rare renal diseases, and kidney transplantation. Current evidence suggests that uEV-based signatures may support early detection, disease stratification, prognostic assessment, and longitudinal monitoring of renal dysfunction. Advances in proteomics, transcriptomics, metabolomics, mass spectrometry, Raman spectroscopy, and machine learning have further improved the characterization of multidimensional uEV profiles. However, variability in urine collection, vesicle isolation, normalization, analytical platforms, and biomarker validation continues to limit clinical implementation. Standardized workflows, larger multicenter cohorts, longitudinal validation, and integration of multi-omics data with clinical and histopathological findings are therefore required. Overall, uEV molecular fingerprinting represents a promising strategy for precision nephrology and for improving non-invasive assessment of kidney injury and disease progression.

Clinical and Renal Function Determinants of Successful Renal Replacement Therapy Discontinuation in Acute Kidney Injury

Dr. Parampreet Singh, Dr. Rajesh Kumar, Shabnam Ain, Dr. Pritha Pal (Author) — Thu, 10 Sep 2026 00:00:00 +0000

Kidney dysfunction is a significant clinical condition which can lead to serious renal impairment, dialysis or renal replacement therapy. The purpose of this study was to assess the clinical, renal-function, and dialysis-related factors; and to determine factors associated with dialysis requirement and renal dysfunction in kidney disease patients. A quantitative, retrospective, secondary data, analytical design was used with a combined dataset of 4,304 records from two cohorts related to kidney disease. Descriptive statistics, independent-samples t-tests, chi-square tests, Pearson correlation analysis, and binary logistic regression (when appropriate) were used for the demographic, clinical, renal-function and dialysis-related variables. The clinical cohort of dialysis patients had significant renal dysfunction with high levels of serum creatinine and urea, low levels of urine output, and a significant number of severe disease patients. Within the kidney-risk group, 31 patients started dialysis and 2,273 did not. Patients who required dialysis had significantly lower GFR than patients who did not require dialysis (8.33 ± 3.31 vs. 69.78 ± 23.78, p < 0.001). The other factors that were significant were the presence of chronic kidney disease (p < 0.001) and dialysis (p < 0.001), but not age, creatinine, BUN, urine output, diabetes, or hypertension. The results show that GFR was the best renal-function predictor for dialysis. Longitudinal studies with outcomes specific to AKI and with RRT-discontinuation outcomes are warranted.

Beyond Serum Creatinine: Emerging Biomarkers for Early Detection and Prognosis of Acute Kidney Injury

Dr. Jesika Rane, Dr. Siddareddy Ankireddypalli (Author) — Thu, 10 Sep 2026 00:00:00 +0000

The diagnosis of acute kidney injury (AKI) is a major cause of morbidity and mortality as traditional markers such as serum creatinine and urine output only reflect kidney functional decline at a time when these kidneys have already sustained some degree of renal stress and injury. Emerging biomarkers provide a more biologically meaningful option by measuring damage to the tubules, cellular stress, changes in filtration, inflammation, metabolic disturbance and failure to recover at various stages of AKI. This review aims to present the latest evidence of the use of conventional and emerging biomarkers for early detection, risk stratification, clinical decision making and prognostic assessment. Special focus will be on neutrophil gelatinase-associated lipocalin, kidney injury molecule-1, cystatin C, liver-type fatty acid-binding protein, TIMP-2, IGFBP7, CCL14, soluble urokinase plasminogen activator receptor, proenkephalin, microRNAs, and metabolomic signatures, along with urinary oxygen partial pressure. Existing data suggest that these markers have the potential to supplement serum creatinine to identify subclinical injury, distinguish between reversible and irreversible injury, assess the risk of kidney replacement therapy, and predict renal recovery and kidney disease progression. The performance is however dependent on clinical setting, assay method, when the measurement is taken and patient heterogeneity. Multimarker strategies and serial biomarker profiling might therefore offer a greater diagnostic and prognostic ability than single markers. Standardization of assays, clinically validated thresholds, multicenter evaluation and demonstration of benefit of using biomarker-driven management for meaningful outcomes will be required for future progress. Combining functional, structural, stress, and molecular markers with clinical monitoring could potentially allow for earlier recognition, more accurate prognosis, personalized monitoring, and improved short and long-term outcomes in AKI in a variety of acute care and critical care settings around the world.

Renal Function and Proteinuria as Indicators of Adverse Outcomes in Biopsy-Confirmed Diabetic Kidney Disease

Thu, 10 Sep 2026 00:00:00 +0000

Diabetic kidney disease (DKD) is a major cause of chronic kidney disease and adverse renal outcomes. Renal function and proteinuria are routinely assessed markers, but their prognostic importance in biopsy-confirmed DKD requires further evaluation. To assess renal function and proteinuria, compare these parameters between patients with and without adverse outcomes and determined their association with adverse clinical outcomes in biopsy-confirmed DKD. A retrospective secondary-data-based observational study was conducted using a publicly available dataset of 168 patients with biopsy-confirmed DKD. Renal function markers included estimated glomerular filtration rate (eGFR), serum creatinine, and blood urea nitrogen, while proteinuria was assessed using 24-hour urinary protein and urinary microalbumin. Adverse outcome was defined as a composite of all-cause mortality, initiation of regular dialysis, or renal transplantation. Descriptive statistics, independent-samples t-test, chi-square test, correlation analysis, and logistic regression were applied. Patients with adverse outcomes showed significantly lower eGFR and higher serum creatinine, blood urea nitrogen, 24-hour urinary protein, and urinary microalbumin. eGFR was negatively correlated with proteinuria, while serum creatinine showed positive correlations with urinary protein measures. Univariate regression identified several renal markers and serum albumin as significant factors. In multivariable analysis, eGFR remained independently associated with adverse outcome, while 24-hour urinary protein lost statistical significance after adjustment. Serum albumin also remained independently protective. Reduced renal function and increased proteinuria were associated with adverse outcomes in biopsy-confirmed DKD, with eGFR emerging as the strongest independent renal indicator.

Keywords: Diabetic kidney disease; eGFR; Proteinuria; Renal function; Adverse outcomes

Mitochondrial Dysfunction in Kidney Transplantation: A Mechanistic Link Between Ischemic Injury and Chronic Allograft Damage

Dr. Avina Kharat (Author) — Thu, 10 Sep 2026 00:00:00 +0000

Kidney transplantation remains the preferred treatment for end-stage kidney disease, yet ischemia–reperfusion injury continues to compromise early graft recovery and long-term allograft survival. The concept of mitochondrial dysfunction has come to play a key role in the understanding of the relationship between peri-transplant ischemic injury and chronic allograft damage. Warm and cold ischemia leads to impaired oxidative phosphorylation, ATP depletion, calcium imbalance and metabolic disruption that destabilize renal tubular cells and endothelial cells. Excessive generation of ROS, membrane depolarization, permeability transition, defective mitophagy, and activation of apoptosis, necroptosis and ferroptosis are further exacerbated during reperfusion. CGAS–STING activation, activation of the NLRP3 inflammasome, endothelial inflammation, recruitment of leukocytes, and alloimmune responses are also promoted by damaged mitochondria releasing mitochondrial DNA and other damage associated molecular patterns. The lack of mitochondrial homeostasis can perpetuate tubular and endothelial dysfunction, promote maladaptive reparative response, induce fibroblast activation and present a risk of interstitial fibrosis, tubular atrophy, microvascular rarefaction, delayed graft function, and chronic allograft dysfunction. New mitochondrial biomarkers such as circulating and urinary mitochondrial DNA, metabolic signatures and respiratory parameters could help to better evaluate the graft and to better stratify the risk. There are several promising strategies to protect the graft such as those using antioxidants targeted to the mitochondria, metabolic modulators, mitophagy-directed therapies, and machine-perfusion strategies. Targeting mitochondrial dysfunction may therefore provide an integrated strategy to reduce ischemic injury and preserve long-term kidney allograft function.

Senescent Cells in Kidney Transplantation: Hidden Drivers of Graft Aging, Inflammation, and Long-Term Dysfunction

Dr Sanath patil (Author); Dr. Prabin Kumar Majhi, Agnibha Dutta — Thu, 10 Sep 2026 00:00:00 +0000

Although kidney transplantation is the best option for ESRD, many issues have been identified that can affect long-term success, such as progressive graft aging and chronic allograft dysfunction. Persistent inflammation, decreased tissue repair and fibrotic remodeling have become clear mechanisms linking transplantation-associated injury to cellular senescence. Renal tissue senescent cells are generated via donor aging, ischemia–reperfusion injury, oxidative and mitochondrial stress, alloimmune response, and treatment-related insult. These cells, although permanently arrested in the cell cycle, continue to be metabolically active, and exhibit a senescence-associated secretory phenotype that can lead to propagation of inflammation, modification of immune-cell function, induce secondary senescence and promote extracellular matrix remodeling. In this review, the molecular mechanisms and transplant-specific mechanisms of renal senescence, its relationship to immune dysregulation, fibrosis, progressive graft dysfunction, and what methods are available to detect the presence of senescence in kidney allografts are discussed. It also reviews the predictive capacity of senescence markers and novel senolytic and senomorphic therapies. The ability to comprehend and therapeutically modulate graft senescence may offer novel means to maintain graft function and enhance long-term transplant survival.

Acute Kidney Injury Severity And Its Impact On Clinical Outcomes In Critically Ill Patients.

Aygun Aliyarbayova (Author); Albert Ulutorti Green, Sampa Stanley — Thu, 17 Sep 2026 00:00:00 +0000

Acute kidney damage (AKI), which is linked to higher morbidity, mortality, and the need for organ support, is a frequent consequence in critically sick patients. This study evaluated AKI severity and its relationship with major clinical outcomes. A retrospective secondary-data-based observational study was conducted using data from 144 critically ill patients. Patients were classed as either AKI or non-AKI, and KDIGO Stages 1-3 were used to classify the severity of AKI. In-hospital mortality, mechanical ventilation, usage of vasoactive drugs, dialysis, ARDS, and length of hospital stay were among the clinical outcomes. Binary logistic regression, correlation analysis, independent t-test, chi-square test, frequency, and percentage were all used. AKI occurred in 41 patients (28.5%), with KDIGO Stage 3 being the most frequent severity category. Patients with AKI were older and had significantly higher APACHE II and IGS2/SAPS II scores. Mortality, mechanical ventilation, vasoactive drug use, dialysis requirement, and ARDS were significantly more frequent among AKI patients. Dialysis requirement increased significantly with advancing KDIGO stage. KDIGO severity correlated positively with AKI creatinine and negatively with urine output. AKI continued to be independently linked to in-hospital mortality in adjusted regression (adjusted OR=3.657, 95% CI: 1.225–10.915, p=0.020). Higher mortality, more organ support needs, and a more severe disease were all linked to AKI. Identification of critically sick individuals at increased risk of unfavorable outcomes may be aided by early detection and careful monitoring of renal impairment.

Ferroptosis and Tubular Injury: Molecular Drivers of Renal Damage, Maladaptive Repair, and Disease Progression

Vaishali singla (Author); Akshit Singh — Sat, 19 Sep 2026 00:00:00 +0000

Ferroptosis has been shown to be a significant regulated cell death mechanism that associates renal tubular injury with maladaptive repair and progressive renal dysfunction. This review will discuss the molecular mechanism of ferroptosis in tubular epithelial cells and the role of ferroptosis in both acute and chronic renal damage. Collectively, iron dysregulation, lipid peroxidation, depletion of glutathione, impairment of GPX4, ferroptinophagy, and disruption of NRF2 signaling all contribute to the susceptibility of the tubules to ferroptotic injury. On-going ferroptotic stress can disrupt epithelial regeneration, induce cell cycle arrest, further enhance inflammatory and profibrotic signals, and lead to tubulointerstitial fibrosis. These mechanisms link acute kidney injury, inadequate tubular recovery, the transition from acute to chronic kidney disease, diabetic kidney disease, and the loss of nephrons. Therapeutics based on iron homeostasis, lipid peroxidation, GSH–GPX4 axis, and other alternative antioxidant pathways hold promise for the prevention of renal damage associated with ferroptosis. There is a need for validated ferroptosis-specific biomarkers, better patient stratification, clinically representative models, and well-defined therapeutic windows to translate insights into mechanisms into effective renal intervention in the future.