Abstract
As the prevalence of obesity rises in the United States, so does the incidence of obesity-related kidney disease. Obesity itself is an independent risk factor for chronic kidney disease where the pathophysiology is complex, involving altered hemodynamics, renin-angiotensin-aldosterone system overactivation, and adipokines leading to inflammation and fibrosis. Obesity-related kidney disease comprises both obesity-related glomerulopathy and fatty kidney disease. Obesity-related glomerulopathy is a consequence of glomerular hyperfiltration and often presents clinically with subnephrotic proteinuria and pathologically with glomerulomegaly with or without focal glomerulosclerosis. Fatty kidney disease is the effect of renal ectopic fat contributing to chronic kidney disease. Whether the renal ectopic fat is a distinct clinical entity or a pathologic mechanism contributing to obesity-related glomerulopathy, the treatment paradigm of weight and proteinuria reduction remains the same. We present the pathophysiology behind obesity-related kidney disease, clinical outcomes, and treatment strategies, which include lifestyle interventions, use of renin-angiotensin-aldosterone system inhibitors, glucagon-like peptide 1 receptor agonists, sodium-glucose co-transporter-2 inhibitors, and bariatric surgery. With old and novel therapeutics, we are attempting to stave off the silent epidemic that obesity-related kidney disease is becoming.
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