Diabetic Nephropathy

Diabetic nephropathy is a chronic microvascular complication of diabetes driven by prolonged hyperglycemia and associated metabolic and hemodynamic changes within the kidney.

In early stages, hyperglycemia increases tubular reabsorption, triggering renal feedback–mediated afferent arteriolar vasodilation and glomerular hyperfiltration.

The resulting intraglomerular hypertension mechanically injures the filtration barrier.

In parallel, nonenzymatic glycation of basement membrane and mesangial proteins thickens and stiffens the glomerular basement membrane while reducing its negative charge selectivity.

This process reduces the negative charge of the glomerular basement membrane, decreasing repulsion of negatively charged proteins like albumin.

Microalbuminuria initially develops and progresses to macroalbuminuria as injury advances.

Persistent damage expands the mesangial matrix and produces diffuse and nodular glomerulosclerosis, steadily reducing the glomerular filtration rate.

This promotes sodium retention and RAAS activation, leading to hypertension and progressive nephron loss.