Spectrum of Non diabetic kidney disease in patients with type 2 diabetes and its clinicopathological correlation.

Diabetes mellitus (DM) is the leading cause of chronic kidney disease worldwide chiefly attributable to diabetic nephropathy (DN). In these patients, non diabetic kidney disease (NDKD) can also occur either alone or superimposed on diabetic nephropathy. This study aimed to identify the prevalence and the etiology of NDKD in our center and also the clinical and laboratory parameters to help distinguish these two entities. MATERIAL: This was a cross sectional observational study. A total of 47 patients were enrolled in the study during the study period. In all the patients, kidney biopsy was done because of atypical presentations and was examined by light and immunofluorescence microscopy. The clinical & laboratory parameters and the biopsy findings were recorded in a standard proforma. OBSERVATION: A total of 47 patients (male/female: 34/13 and mean age 52.11±9.36) were included in the study. The chief co morbidity was hypertension which was present in 61.7% of patients. The most common indication of biopsy was nephrotic presentation (38.3%) followed by nephritic illness (25.5%). The prevalence of NDKD in our study cohort was 85.1% of which isolated NDKD was 57.4% and NDKD + DN was 27.7%. The most common histological lesion were membranous glomerulopathy and focal segmental glomerulosclerosis (FSGS) each with a frequency of 15% followed by chronic tubulointerstitial nephritis (CTIN), IgA nephropathy and others. There was significant difference in the median duration of diabetes in these groups and it was around 5 years less in the NDKD group. There was no difference among three groups in term of eGFR, HbA1C and proteinuria. CONCLUSION: Our study demonstrated a high prevalence of NDKD in the patients with type 2 diabetes. The duration of diabetes was the strongest predictor of NDKD. Kidney biopsy should be undertaken liberally whenever there is strong clinical suspicion especially in the presence of atypical features. The exact histological diagnosis can clarify the further treatment planning as well as the prognosis.

Desidustat in Anemia due to Non-Dialysis-Dependent Chronic Kidney Disease: A Phase 3 Study (DREAM-ND).

BACKGROUND: Desidustat, an oral hypoxia-inducible factor prolyl hydroxylase inhibitor, is being developed to treat anemia in patients with chronic kidney disease (CKD) without dialysis dependency. METHODS: In total, 588 patients with a clinical diagnosis of anemia due to CKD without dialysis need and with baseline hemoglobin of 7.0-10.0 g/dL (inclusive) were randomized in a 1:1 ratio to receive either desidustat 100 mg oral tablets thrice a week for 24 weeks or biosimilar darbepoetin subcutaneous injection 0.75 µg/kg once in 2 weeks for 24 weeks. The primary outcome was the change from baseline in hemoglobin to evaluation period of Weeks 16-24. Key secondary outcomes included the number of patients with hemoglobin response, changes in the hepcidin levels, changes in the vascular endothelial growth factor (VEGF) levels, and changes in the lipid and lipoprotein profiles. RESULTS: Hemoglobin change from baseline to Weeks 16-24 was 1.95 g/dL in the desidustat group and 1.83 g/dL in the darbepoetin group (difference: 0.11 g/dL; 95% CI: -0.12, 0.34), which met prespecified non-inferiority margin (-0.75 g/dL). The hemoglobin responders were significantly higher (p = 0.0181) in the desidustat group (196 [77.78%]) compared to the darbepoetin group (176 [68.48%]). The difference of change in hepcidin from baseline to Week 12 and Week 24 (p = 0.0032 at Week 12, p = 0.0016 at Week 24) and the difference of change in low-density lipoprotein from baseline to Week 24 (p value = 0.0269) between the two groups was statistically significant. The difference of change from baseline in VEGF to Weeks 12 and 24 between the two groups was not statistically significant. CONCLUSION: Desidustat is non-inferior to darbepoetin in the treatment of anemia due to non-dialysis dependent CKD and it is well-tolerated.

Sofosbuvir-Velpatasvir Fixed Drug Combination for the Treatment of Chronic Hepatitis C Infection in Patients With End-Stage Renal Disease and Kidney Transplantation.

INTRODUCTION: India is witnessing high hepatitis C virus (HCV) infection burden in patients of chronic kidney disease. Due to unavailability of costly Kidney Disease Improving Global Outcomes-recommended directly acting antiviral drugs, a widely available pan-genotypic combination of Sofosbuvir and Velpatasvir can become an economical option. Data regarding treatment experience of sofosbuvir-velpatasvir combination in chronic kidney disease is scarce. No data from India have been published in patients on renal replacement therapies till now. METHODS: This retrospective analysis included all patients of end-stage renal disease on maintenance hemodialysis with treatment-naïve chronic HCV infection treated with sofosbuvir (400 mg) and velpatasvir (100 mg) fixed-dose combination. Pretreatment routine investigations were performed, which included HCV viral load, genotype, fibro scan, endoscopy for esophageal varices, and portal vein Doppler. The patients were followed up with HCV viral load to declare sustained virologic response. RESULT: patients were included with a mean age of 39.8 ± 10.8 years, and 77.4% were male. Genotype 1 was found to be most prevalent (67.7%), with a median viral load of 106copies/ml. Six (19.3%) patients had hepatitis B virus co-infection. Three (9.7%) patients had cirrhosis. Sustained virologic response (SVR12) was achieved in 30 (96.8%) patients, and one (3.2%) patient had relapse. Furthermore, 14 (45.2%) patients underwent renal transplantation, and none of them had relapsed. Dyspepsia (9.7%) was the most common side effect observed with no major adverse effect. CONCLUSION: Our study showed excellent efficacy with the safety profile of this drug combination in end-stage renal disease patients. However, larger prospective studies and multicenter randomized controlled trials are needed for further confirmation.

Clinicoepidemiological profile of peritonitis complicating acute peritoneal dialysis: A single-center experience.

A prospective observational study examining the incidence and microbiological aspects of peritonitis complicating acute intermittent peritoneal dialysis (IPD) was performed. A total of 145 acute IPD treatments were included involving 112 patients. The majority of patients suffered from acute kidney injury (72.3%) secondary to sepsis. Peritonitis occurred in 31 treatment sessions, giving a frequency of 21.4% of procedures performed. The mean interval between starting dialysis and the first sign of peritonitis was 2.9 days, with 58% of cases occurring in the Intensive Care Unit. Frequent catheter manipulation/repositioning and leakages were identified as significant predisposing factors for peritonitis, and the risk of peritonitis was increased with longer duration of IPD. Gram-negative infections were more common than Grampositive infections. The use of systemic antibiotics did not prevent the development of peritonitis.

Gitelman's syndrome presenting with hypocalcemic tetany and hypokalemic periodic paralysis.

Gitelman's syndrome is an autosomal recessive renal tubular disorder characterized by hypomagnesemia, hypokalemia, hypocalciuria, and metabolic alkalosis. Hypocalcemic tetany as a presentation of Gitelman's syndrome has rarely been reported in literature. We report a rare case of Gitelman's syndrome presenting with hypocalcemic tetany along with hypokalemic periodic paralysis. A 17-year-old female was admitted to our hospital with a history of perioral numbness and carpal spasms of five days duration with progressive quadriparesis developing over a period of few hours. Past history was significant for three episodes of transient lower limb weakness. On examination, blood pressure was 110/70 mm Hg. Chvostek's sign and Trousseau's sign were positive. Neurologically, she was fully oriented. She had Grade 3 power in all the four limbs with intact sensation. Laboratory tests showed hypocalcemia (7.8 mg/dL), hypokalemia (2.2 mEq/L), hypomagnesemia (0.9 mEq/L), and hypocalciuria (104 mg/day). Arterial blood gas showed mild metabolic alkalosis with respiratory compensation. Thus, a clinical diagnosis of GS was made. The patient made a remarkable recovery after the correction of electrolyte imbalance. The aim of this case report is to re-emphasize the fact that hypocalcemia can rarely occur in Gitelman's syndrome.