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Krishan Lal Gupta

Krishan Lal Gupta

PGIMER, India

Title: Nutritional therapy to prevent progression of Acute Kidney Injury to Chronic Kidney Disease: Design and Methods

Biography

Biography: Krishan Lal Gupta

Abstract

Background

Acute Kidney Injury (AKI) has been recognized as an important risk factor for Chronic Kidney Disease (CKD). In CKD, dietary protein restriction is used to mitigate its progression by reducing intra-glomerular pressure. We believe that post AKI, the kidney is vulnerable to the metabolic demands and dietary protein control may facilitate renal recovery and retard progression to CKD.

Methods

This will be a pilot, single center, open label, randomized, controlled trial of adult subjects who would be recovering from an episode of Stage 2/3 AKI at the Postgraduate Institute of Medical education and Research, Chandigarh, India. The subjects will be randomized to a low protein and KetosterilÒ (LPD-K) or ad-lib diet for 3 months. The randomization procedure will be non-stratified, using random permuted blocks of 4 subjects to guarantee groups of equal size throughout the study.  After the 3-month period, subjects will continue ad lib diet and followed for additional three months.  Clinical and laboratory investigations details would be recorded every 2 weeks for first 3 months and finally, at the end of 6 months. The primary objective is change in nutritional status (as measured by anthropometry, subjective global assessment, nutrition biomarkers and bioelectrical impedance) at 6 months. The secondary objectives are rate and degree of recovery of renal function at 3 months and proportion of patients who progress to one CKD stage higher than their baseline at 3 months and 6 months.

Relevance

Recent data suggest that when dietary compliance is achieved in CKD patients, LPD-K diet is feasible for the majority and rate of decline in glomerular filtration rate is significantly lower on LPD-K than on low protein diet alone. Protein restriction has not been studied at all in AKI. It is possible that, by the same mechanisms, LPD-K will reduce the tubular workload in the recovering kidney, ameliorate further tubular damage, and enhance recovery of renal function, or at least retard the progression to CKD. If successful, it will set the stage for a larger trial and might become one of the first interventions to decrease development of CKD following AKI.