Diabetic nephropathy pathophysiology: Difference between revisions
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==Overview== | ==Overview== | ||
Thickening of [[glomerular basement membrane]], accumulation of eosinophilic material in the mesangium and intraglomerular hypertension are the major pathophysiologic changes taking place in the nephrons in long standing [[diabetes mellitus]]. | |||
==Pathophysiology== | ==Pathophysiology== | ||
The earliest detectable change in the course of diabetic nephropathy is a thickening in the glomerulus. At this stage, the kidney may start allowing more [[serum albumin]] (plasma protein) than normal in the [[urine]] ([[albuminuria]]), and this can be detected by sensitive [[medical test]]s for albumin. This stage is called "microalbuminuria". It can appear 5 to 10 years before other symptoms develop. As diabetic nephropathy progresses, increasing numbers of glomeruli are destroyed by nodular glomerulosclerosis. Now the amounts of albumin being excreted in the urine increases, and may be detected by ordinary [[urinalysis]] techniques. At this stage, a kidney [[biopsy]] clearly shows diabetic nephropathy. | The earliest detectable change in the course of diabetic nephropathy is a thickening in the glomerulus. At this stage, the kidney may start allowing more [[serum albumin]] (plasma protein) than normal in the [[urine]] ([[albuminuria]]), and this can be detected by sensitive [[medical test]]s for albumin. This stage is called "microalbuminuria". It can appear 5 to 10 years before other symptoms develop. As diabetic nephropathy progresses, increasing numbers of glomeruli are destroyed by nodular glomerulosclerosis. Now the amounts of albumin being excreted in the urine increases, and may be detected by ordinary [[urinalysis]] techniques. At this stage, a kidney [[biopsy]] clearly shows diabetic nephropathy. | ||
==References== | ==References== | ||
Revision as of 03:30, 20 January 2013
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aarti Narayan, M.B.B.S [2]
Overview
Thickening of glomerular basement membrane, accumulation of eosinophilic material in the mesangium and intraglomerular hypertension are the major pathophysiologic changes taking place in the nephrons in long standing diabetes mellitus.
Pathophysiology
The earliest detectable change in the course of diabetic nephropathy is a thickening in the glomerulus. At this stage, the kidney may start allowing more serum albumin (plasma protein) than normal in the urine (albuminuria), and this can be detected by sensitive medical tests for albumin. This stage is called "microalbuminuria". It can appear 5 to 10 years before other symptoms develop. As diabetic nephropathy progresses, increasing numbers of glomeruli are destroyed by nodular glomerulosclerosis. Now the amounts of albumin being excreted in the urine increases, and may be detected by ordinary urinalysis techniques. At this stage, a kidney biopsy clearly shows diabetic nephropathy.