Diabetic nephropathy(DN), also known as diabetic kidney disease, is the chronic loss of kidney function occurring in those with diabetes mellitus. Diabetic nephropathy is one of the leading causes of chronic kidney disease (CKD) and end-stage renal disease (ESRD) globally. Protein loss in the urine due to damage to the glomeruli may become massive, and cause a low serum albuminwith resulting generalized body swelling (edema)and result in the nephrotic syndrome. Likewise, the estimated glomerular filtration rate(eGFR) may progressively fall from a normal of over 90 ml/min/1.73m2to less than 15, at which point the patient is said to have end-stage kidney disease(ESKD). It usually is slowly progressive over years.
Pathophysiologic abnormalities in DN begin with long-standing poorly controlled blood glucose levels. This is followed by multiple changes in the filtration units of the kidneys, the nephrons. (There are normally about 750,000–1.5 million nephrons in each adult kidney). Initially, there is constriction of the efferent arteriolesand dilation of afferent arterioles, with resulting glomerular capillary hypertension and hyperfiltration; this gradually changes to hypofiltration over time.Concurrently, there are changes within the glomerulus itself: these include a thickening of the basement membrane, a widening of the slit membranes of the podocytes, an increase in the number of mesangial cells, and an increase in mesangial matrix. This matrix invades the glomerular capillaries and produces deposits called Kimmelstiel-Wilson nodules. The mesangial cells and matrix can progressively expand and consume the entire glomerulus, shutting off filtration.