Diabetic nephropathy pathophysiology: Difference between revisions
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* As the nephropathy progresses, systemic blood pressure more [[albumin]] is filtered across the glomerular membrane and ultimately reaches [[nephrotic syndrome|nephrotic]] range within the next 5 to 10 years. | * As the nephropathy progresses, systemic blood pressure more [[albumin]] is filtered across the glomerular membrane and ultimately reaches [[nephrotic syndrome|nephrotic]] range within the next 5 to 10 years. | ||
* Accumulation of glycosylated proteins also damage the renal tubular epithelium causing type IV [[renal tubular acidosis]], resulting in [[hyperkalemia]]. | * Accumulation of glycosylated proteins also damage the renal tubular epithelium causing type IV [[renal tubular acidosis]], resulting in [[hyperkalemia]]. | ||
==Pathology== | |||
==References== | ==References== | ||
Revision as of 01:02, 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
- 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.
- This microalbuminuria is not detectable on routine protein dipstick.
- As the nephropathy progresses, systemic blood pressure more albumin is filtered across the glomerular membrane and ultimately reaches nephrotic range within the next 5 to 10 years.
- Accumulation of glycosylated proteins also damage the renal tubular epithelium causing type IV renal tubular acidosis, resulting in hyperkalemia.