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==Pathophysiology==
==Pathophysiology==
* The first renal abnormality seen in patients with diabetic nephropathy is [[hyperfiltration]] and intraglomerular hypertension.
* The first renal abnormality seen in patients with diabetic nephropathy is [[hyperfiltration]] and intraglomerular hypertension.
* [[Microalbuminuria]] (serum albumin level:30 - 300 mg/dl) is the earliest abnormality noted in the urine. This change first appears approximately 5 years after diagnosis of [[diabetes mellitus]]. Although uncontrolled [[systemic hypertension]], sustained high [[blood glucose]] levels and high [[serum cholesterol]] levels contribute to faster progression of damage to [[nephrons]] and earlier appearance of [[albumin]] in urine.
* [[Microalbuminuria]] ([[serum albumin]] level:30 - 300 mg/dl) is the earliest abnormality noted in the urine. This change first appears approximately 5 years after diagnosis of [[diabetes mellitus]]. Although uncontrolled [[systemic hypertension]], sustained high [[blood glucose]] levels and high [[serum cholesterol]] levels contribute to faster progression of damage to [[nephrons]] and earlier appearance of [[albumin]] in urine.
* This [[microalbuminuria]] is not detectable on routine protein dipstick.
* This [[microalbuminuria]] is not detectable on routine protein dipstick.
* As the nephropathy progresses, more albumin is filtered across the glomerular membrane and ultimately reaches [[nephrotic syndrome|nephrotic]] range.
* As the nephropathy progresses, more [[albumin]] is filtered across the glomerular membrane and ultimately reaches [[nephrotic syndrome|nephrotic]] range within the next 5 to 10 years.
*
 
==References==
==References==



Revision as of 00:53, 21 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

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