Introduction:Thrombotic microangiopathy (TMA) as a cause of snake-bite-induced acute kidney injury (AKI) is rarely reported. Very little is known about the clinical course, optimal management, and prognosis of this entity. We describe a series of snake-bite-induced TMA and compare their outcomes with those without TMA.Methods:This was a single-center retrospective study of patients with AKI following snake envenomation admitted between January 2012 and December 2017. Demographic profile, clinical parameters, and outcomes were studied. TMA was diagnosed based on presence of triad of microangiopathic hemolytic anemia, thrombocytopenia, and AKI, and groups with and without TMA were compared.Results:Of 103 patients with AKI following snake bite, 19 (18.5%) had clinical evidence of TMA. All patients with TMA had advanced azotemia (mean peak serum creatinine 9.5 ± 3.0 mg/dL), with 18 (95%) requiring renal replacement therapy (RRT). Thirteen (68%) had either complete or partial recovery of renal functions, two (10%) progressed to end-stage renal disease, and one died (three patients were lost to follow-up). Age ≥50 years, presence of oliguria/anuria, anti-snake venom dose ≥10 vials, and urea ≥80 mg/dL at presentation were independently associated with TMA (P < 0.05). RRT requirement (95% vs. 57%), mean number of RRT sessions (18 vs. 4.5 sessions), and hospital stay ≥7 days (84% vs. 58%) were higher in patients with TMA (P < 0.05), but patient outcomes did not differ.Conclusions:In conclusion, TMA was seen in 18.5% of patients with snake-bite-related AKI in our study and was associated with almost universal need for RRT, longer duration on RRT, and hospital stay compared with patients without TMA.

Aim A significant proportion of patients with minimal change disease (MCD) and focal segmental glomerulosclerosis (FSGS) are either steroid dependent or steroid resistant, requiring long‐term calcineurin inhibitors (CNI) use. Rituximab has more favourable safety profile. The present study was undertaken to evaluate the efficacy and safety of rituximab in CNI‐dependent patients. Methods This was a prospective observational study conducted from July 2014 to February 2018. Steroid‐dependent nephrotic syndrome or steroid‐resistant nephrotic syndrome (biopsy proven MCD/FSGS), who were CNI dependent were enrolled. Mean age at enrolment was 22.77 ± 7.45 years. All patients received rituximab at a dose of 375 mg/m2 at entry in the study. CD‐19 levels were monitored monthly and patients having CD‐19 levels >5/μL and/or > 1% received additional low‐dose (100 mg) of rituximab. Results A total of 24 patients were followed up for 12 months. At the end of 6 and 12 months, 87.5% and 79.16% of the patients achieved remission, respectively. Eight (33.33%) patients developed relapse. The mean dose of rituximab in the first year was 791 mg. The average cost of rituximab in the first year was 487.17$. Rituximab was well‐tolerated, with mild infusion reactions, respiratory tract infection and oral candidiasis in 5 (20.83%), 5 (20.83%) and 1 (4.17%) patient, respectively. Conclusions CD‐19 targeted rituximab is a safe and cost‐effective agent in remission maintenance in adults with CNI dependent. Over three‐fourths of the patients with CNI‐dependent podocytopathy maintain clinical remission with CD‐19 targeted rituximab therapy.

Purpose Arteriovenous fistula(AVF) is preferred vascular access for hemodialysis but has primary failure in 20–60%. Studying predictors of AVF failure would help plan appropriate management.We studied AVF outcomes, clinical and vascular factors predicting their failure in patients requiring hemodialysis. Methods Retrospective study of patients with AVF creation from January 2017 to December 2018. Outcomes studied were immediate (< 72 h), primary (3 months) AVF failure, six-month/one-year patency, analyzed for predictive clinical, vascular factors as assessed using Pre-operative Doppler Ultrasound(DUS). Results Of 530 AVFs in 460 patients, DUS was done in 426/530 (80.4%), 349/460 (75.8%) were males, mean age was 53.10 ± 14.54 (18–91), 215/460(46.7%) had Diabetes mellitus(DM), 423/460(92%) hypertension. AVFs were radiocephalic in 79/530 (14.9%), brachiocephalic 418/530 (78.9%), brachiobasilic 33/530 (6.2%). AVF Immediate/Primary failure was seen in 64/530 (12.1%), 90/352 (25.6%); Patency at six months/one year in 253/352(71.8%),191/305 (62.6%), respectively. Older age had less immediate failures (AOR 0.97, CI 0.95–0.99, p 0.03). Feeding arterial diameter predicted immediate and primary failure on univariate analysis [OR 0.64 (95% CI 0.49–0.83), 0.62 (95% CI 0.47–0.89), respectively], but not multivariate. Artery diameter of > 4.0 mm had less failures [immediate (p 0.01), primary (p 0.02)], < 2.0 mm had specificity 95.9% and 95.4% for immediate, primary failure respectively. Conclusion AVF failure is 12.1%, immediately; 25.6% three months after construction, Patency at 6 months is 71.8%, one year 62.6%. Immediate failures decrease with age. Artery diameters > 4.0 mm had less, < 2.0 mm had more failures.

Acute kidney injury in cirrhosis of liver carries high in-hospital mortality. Pre-renal AKI has a better survival compared to ATN and HRS. The higher stage of AKI at presentation and the presence of oliguria are two important predictors of in-hospital mortality.

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The global burden of diabetic kidney disease (DKD) is escalating, and it remains as a predominant cause of the end-stage renal disease (ESRD). DKD is associated with increased cardiovascular disease and morbidity in all types of diabetes. Prediction of progression with albuminuria and eGFR is challenging in DKD, especially in non-proteinuric DKD patients. The pathogenesis of DKD is multifactorial characterized by injury to all components of the nephron, whereas albuminuria is an indicator of only glomerular injury. The limits in the diagnostic and prognostic value of urine albumin demonstrate the need for alternative and clinically significant early biomarkers, allowing more targeted and effective diabetic treatment, to reduce the burden of DKD and ESRD. Identification of biomarkers, based on multifactorial pathogenesis of DKD can be the crucial paradigm in the treatment algorithm of DKD patients. This review focuses on the potential biomarkers linked to DKD pathogenesis, particularly with the hope of broadening the diagnostic window to identify patients with different stages of DKD progression.

Purpose: Diabetic kidney disease (DKD) represents a unique subset of patients with chronic kidney disease (CKD). Acute kidney injury (AKI) is implicated in DKD progression; however, their interplay is not studied well. We studied risk factors for AKI and the effect of AKI on disease progression in a homogeneous group of patients with DKD. Patients and Methods: We conducted a retrospective open cohort study of patients with DKD at a single tertiary care centre between August 2016-August 2019. Patients with a minimum follow-up of 2 years were included in the study. The incidence, etiology and risk factors for AKI were studied. The primary outcome studied was the effect of AKI on reduction in estimated glomerular filtration rate (eGFR) in DKD. Loss in eGFR by 50% and need for renal replacement therapy or reaching CKD stage V were studied as secondary outcomes. Results: Two hundred and ninety-two DKD patients meeting the study criteria with a follow-up of 29.57 (±4.3) months were included. The incidence of AKI was 31.1%. Sepsis was the most common etiology (61%). Proteinuria was an independent risk factor for AKI after adjusting for covariates (adjusted OR-1.158; 95% CI (1.018-1.316); p=0.025). In patients with AKI, median decline in eGFR was 10.29 mL/min/1.73m 2 /year (IQR-5.58-13.84) which was significantly higher compared to patients with no AKI [eGFR 7.25 (IQR 5.06-11.38); p-0.014]. On subgroup analysis, sepsis-induced AKI (versus non-sepsis AKI; p<0.001) and higher AKI stage (stage 2/3 versus stage 1; p=0.019) were associated with a faster decline in eGFR. Conclusion: AKI is common in patients with DKD with sepsis being the most common etiology. AKI in diabetic kidney disease is associated with a faster decline in eGFR. Baseline proteinuria is an independent risk factor for AKI.