Diabetes mellitus, type I or type II.
The glomerular and vascular pathology is linked to hyperglycemia.
Nonenzymatic glycosylation to glomerular proteins results in accumulation of irreversible advanced glycosylation end products in the glomerular mesangium and glomerular basement membrane . This alteration leads to proteinuria and eventually glomerulosclerosis.,
The epidemiology is that of diabetes mellitus, type I or type II.
|General Gross Description|
The kidneys may be grossly normal in appearance, but with advancing disease the kidneys may become larger rather than smaller.
|General Microscopic Description|
The glomeruli show diffuse expansion of the mesangial regions, more by matrix material than by cells.
These mesangial regions take on a rounded, nodular appearance with sparse cellularity and appear as sclerotic nodules in central regions of glomerular lobules.
The capillary loops around the centrilobular sclerosis usually remain patent.
On direct immunofluorescence the capillary basement membranes show smooth linear fluorescence for albumin.
Electron microscopy of the peripheral capillary loops show homogenous thickening of the glomerular basement membranes.
Additional lesions seen microscopically in diabetes are hyaline thickening of the glomerular arterioles, insudative large proteinaceous deposits occluding some capillary loops and hyaline proteinaceous droplets attached to Bowman's capsule.
Cotran RS, Kumar V, Robbins SL: Robbins Pathologic Basis of Disease. 5th ed. Philadelphia, W.B. Saunders, 1994, pp. 961-963.
Rose B. Renal Pathophysiology the essentials. Baltimore: Williams and Wilkins. 1994. Ch. 9.
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||Synopsis by: Harold Yamase M.D. (T71200M00028)