Glomerulosclerosis diabetic

In the interstitium, angiotensin II induces proliferation of mesangial cells and fibroblasts and the synthesis of collagen and other matrix molecules by these cells via the ATI receptor. Moreover, by the concomitant stimulation of chemoattractant cytokines, inflammation is induced. These processes are mediated by endothelin, transforming growth factor(3, and reactive oxygen species, and finally lead to interstitial fibrosis and glomerulosclerosis observed in hypertension and diabetes. 

Nephrotic syndrome may complicate the course of many primary and secondary glomerulopathies. Diabetic nephropathy is the most common cause of nephrotic proteinuria (not always accompanied by full-blown nephrotic syndrome). Lupus nephritis and renal amyloidosis are much rarer secondary glomerulopathies resulting in nephrotic syndrome. The prevalence of primary glomerulopathies differs between Blacks and Whites (focal segmental glomerulosclerosis is more common... 

Several reports have linked renal dysfunction with nifedipine. In a study of hypertensive diabetics with renal insufficiency, nifedipine increased proteinuria and worsened renal function (SEDA-16, 196). Others have reported mild reversible renal impairment in patients with chronic renal insufficiency taking nifedipine for angina or hypertension a biopsy in one of the patients, who had heavy proteinuria, showed focal and segmental glomerulosclerosis (30). Immune-complex nephritis was reported in a patient taking nifedipine, but the proteinuria persisted (and indeed worsened) on changing to verapamil (31). 

Zatz R, Dunn BR, Meyer TW, Anderson S, Rennke HG, and Brenner BM. 1986. Prevention of diabetic glomerulosclerosis by pharmacological amelioration of glomeular capillary hypertension. / Clin Invest 77 925- 930. 

Microvascular complications of diabetes 1 Focal segmental glomerulosclerosis 3... 

Nodular glomerulosclerosis, first described by Kimmelstiel and Wilson in 1936, appears to be specific for juvenile onset or islet cell antibody-positive diabetes mellitus. The nodular lesion is found in the intercapillary tissue or mesangium (19). 

Glomerulosclerosis with basement membrane thickening is characteristic of diabetic microangiopathy involving small blood vessels in the kidney and other organs, such as the skin, muscles, and retina. The reduction of the width of the capillary basement membrane in controlled diabetics is evidence that basement membrane thickening is related to hyperglycemia. 

Proteinuria is characteristic of diabetic nephropathy (20). Patients with diabetes mellitus may have massive proteinuria and the nephrotic syndrome. Some of these patients never develop glomerulosclerosis. Hypertension develops but is rarely malignant. Plasma renin activity is normal or decreased. More commonly, hypo-reninemic hypoaldosteronism with hyperkalemia and mild hyperchloremic metabolic acidosis is found. 

Wendt TM, Tanji N, Guo J, et al. RAGE drives the development of glomerulosclerosis and implicates podocyte activation in the pathogenesis of diabetic nephropathy. Am J Pathol 2003 162 1123-1137. 

Fig. 8-28. Nodular diabetic glomerulosclerosis. Deposits form in the mesangial regions of glomerular lobules as described by Kimmelstiel and Wilson. Hematoxylin and eosin stain (supplied by Harrison Latta)...

Churg, J., Dachs, S. Diabetic renal disease arteriosclerosis and glomerulosclerosis. Path. Annu. 1, 148-171 (1966)... 

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