John Cijan He

Published on: , , , , APOL1 research is driving precision nephrology, but prediction gaps and equity challenges still limit clinical impact. A decade and a half after APOL1 was linked to kidney disease, clinicians are still grappling with misdiagnosis, unpredictable progression, and uneven access to genetic insight, just as targeted therapies begin to emerge.

An evolving understanding of podocyte injury in glomerular disease is being driven by advances in genetics, targeted therapeutics, and biomarker development, signaling a shift beyond traditional immunosuppression. Recently, John Cijiang He, MD, PhD, Professor of Medicine and Pharmacological Sciences and Chief of the Division of Nephrology at the Icahn School of Medicine at Mount Sinai, spoke with HCPLive at the World Congress of Nephrology (WCN).

Podocyte injury plays a central role as the shared mechanism driving proteinuria and progressive kidney dysfunction across both primary and secondary glomerular diseases, including focal segmental glomerulosclerosis (FSGS) and diabetic kidney disease. Diabetic kidney disease affects approximately 30% to 40% of patients with diabetes, remaining a leading cause of kidney failure worldwide. FSGS accounts for an estimated 20% to 25% of adult nephrotic syndrome cases in the United States.