The most important aspect of treating drug-induced acute interstitial nephritis (AIN) is timely discontinuation of the offending drug. Steroids, oral as well as intravenous (IV), are used in the treatment of drug-induced AIN. The present study was undertaken to compare the efficacy of oral prednisolone versus IV suprapharmacological doses of corticosteroids in the treatment of drug-induced AIN. This prospective randomized controlled study included drug-induced AIN diagnosed on histopathology over a period of two years. Patients were randomized to oral prednisolone (Group A) 1 mg/kg for two weeks or pulse methylprednisolone (Group B) 30 mg/kg for three days (maximum 1 g) followed by oral prednisolone 1 mg/kg for two weeks, tapered over two weeks. Response was reported as complete remission (CR) [improvement in estimated glomerular filtration rate (eGFR) to ≥60 mL/min/1.73 m], partial remission (PR) (improvement but eGFR <60 mL/min/1.73 m), or nonresponders to steroids (no CR/PR). Steroid therapy was instituted to 31 biopsy-proven AIN cases (Group A - 16 and Group B - 15). Drugs implicated in the causation of AIN included pantoprazole, diclofenac, rifampicin, naproxen, aspirin, imipenem, piroxicam, cefixime, lornoxicam, Chinese herbs, etoricoxib, ciprofloxacin, and phenytoin. There was no difference in the baseline parameters between the two groups. At the end of follow-up, 58.06% achieved CR and 41.93% achieved PR. In Group A, nine (56.2%) achieved CR and seven (43.7%) achieved PR. In Group B, nine (60%) achieved CR and six (40%) achieved PR. There was no significant difference between the two groups. Pulses of high doses of corticosteroids have a significant but transient anti-inflammatory effect. Both oral and IV suprapharmacological doses of corticosteroids are equally effective in the treatment of drug-induced AIN, if used early.

Vitamin D deficiency state is endemic in the Kashmir valley of the Indian subcontinent. Clinicians frequently treat patients with Vitamin D for diverse clinical symptoms to improve the general health and to reduce the frailty of elderly and these doses may at times be inappropriately high. Vitamin D toxicity-induced acute kidney injury (AKI), often considered rare, can be life-threatening and associated with substantial morbidity if not identified promptly. We aimed to describe clinical and biochemical features, risk factors, and management of AKI patients with Vitamin D toxicity seen at a single tertiary care centre in Sher-i-Kashmir Institute of Medical Sciences, Srinagar, India, between January 2014 and January 2016. Evaluation included detailed clinical history and biochemical tests including serum calcium, phosphorus, creatinine, intact parathyroid hormone, and 25-hydroxyvitamin D [25(OH)D]. Nineteen patients with Vitamin D toxicity-induced AKI could be identified. Clinical manifestations included nausea, vomiting, altered sensorium, constipation, pancreatitis, AKI, acute on chronic kidney disease, and weight loss. Median (range) age was 64 (45-89) years. Median (range) serum 25(OH)D level and median (range) total serum calcium level were 99 (190-988) ng/mL and 139 (119-152) mg/dL, respectively. Overdose of Vitamin D caused by prescription of megadoses of Vitamin D was the cause of AKI in all cases. Median (range) cumulative Vitamin D dose was 6,000,000 (3,600,000-9,000,000) IU. On three- and six-month follow-up, the creatinine and estimated glomerular filtration rate normalized and returned to baseline in all patients except three cases who had underlying chronic kidney disease. Three patients needed rehospitalization for another episode of AKI. Our data demonstrate an emergence of Vitamin D toxicity as a cause of AKI in this part of the world. Irrational use of Vitamin D in megadoses resulted in AKI in all cases. Persistence of Vitamin D in the body for longer time resulted in rehospitalization of patients with AKI. Awareness among health-care providers regarding the toxic potential of high doses of Vitamin D and cautious use of Vitamin D supplements can have immense value to prevent this AKI.

IgA nephropathy (IgAN) remains one of the most common glomerular lesions, which has a striking geographic distribution and is the most common form of primary glomerular disease in Asia. However, the exact prevalence or clinicopathological spectrum of IgAN in India is not well documented. This retrospective study analyzed the presentation in 126 patients of primary IgAN out of 298 native kidney biopsies (42.28%) performed over a period of three years (2013-2015). The patients were followed up for three months. This is the second highest prevalence recorded in the world after Japan. Among the clinical features of our cohort, the mean age was 31 years, with a male-to-female ratio of 2:1, with the highest incidence observed in the third decade of life in both sexes. The majority of our patients (47%) presented with renal failure with a mean serum creatinine value of 3.1 mg/dL and with burnt out morphology on histo-pathology; 72.2% of patients were hypertensive at presentation. On histopathology, Haas class V (35.5%) had the highest frequency followed by class IV (25.8%). The Oxford MEST score was not applicable in 36 patients because of advanced sclerosis (>50%). In the remaining ninety patients, majority had tubular atrophy and interstitial fibrosis of varying degrees. At three months of follow-up, the patients who had presented with renal failure (47.6%), settled in chronic kidney disease stage III (25.4%) followed by stage IV (18.6%) and stage V (11.8%). Our study in Kashmir suggests that IgAN is more common in the younger age group, with a significant number of patients presenting with advanced renal failure and, on morphology, showing a burnt out disease, with many developing end-stage renal disease. Studies evaluating the underlying factors can have immense importance in dealing with the disease.

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