Prostaglandins and the kidney in diabetes

Abstract

The kidney is an active site of prostaglandin synthesis. These autacoids can influence renal haemodynamics, glomerular ultrafiltration coefficient, mesangial cell proliferation and matrix expansion. Due to these features, prostaglandins may contribute to virtually all the functional and structural alterations which characterize the different phases of diabetic nephropathy. Indeed, most of the experimental as well as clinical studies to date agree that renal hyperfiltration of early diabetes is partially dependent upon enhanced renal production of vasodilatory prostaglandins. By contrast, in long-term diabetes the reduced renal synthesis of prostaglandins and increased production of intrarenal thromboxane, be the latter derived from native glomerular cells or from infiltrating platelets or monocytes, would appear to contribute to the decline in glomerular filtration rate, glomerular basement membrane alterations and proteinuria.