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Natural History of Diabetic Nephropathy

  • Eli A. Friedman
Chapter
Part of the Developments in Nephrology book series (DINE, volume 9)

Abstract

Pathophysiologic and clinical manifestations of kidney damage are duration related in the type I diabetic. They appear according to a well-described sequence beginning with glomerular hyperfiltration and reversible proteinuria, progressing through fixed massive proteinuria (nephrotic syndrome), and ending in renal insufficiency. Uremia, the end result of relentless nephropathy, is usually associated with severe visual loss or blindness (renal-retinal syndrome). A similar sequence may take place in the type II diabetic. Lack of precision in establishing the onset of type II diabetes, however, prevents construction of a timed natural history. Furthermore, the type II diabetic is older and may have systemic atherosclerosis, with consequent strokes and heart attacks, obscuring the course of kidney damage. Over the past decade, in the United States and Western Europe, uremia complicating diabetic nephropathy has emerged as the most prevalent (12.2% of Medicare funded uremic patients), accurately diagnosed cause of renal failure treated by maintenance hemodialysis or renal transplantation [1]. While “glomerulonephritis” (28.4%) and “hypertension” (17.4%) are reported more frequently, these diagnoses are usually employed as synonyms for unexplained kidney failure associated with small kidneys in the majority of patients so labeled. Diabetic nephropathy is the diagnosis applied to a minimum of 20% and as many as 45% of new dialysis patients, depending on the region of the country reporting.

Keywords

Diabetic Nephropathy Plasma Renin Activity Glomerular Basement Membrane Serum Creatinine Concentration Congenital Nephrotic Syndrome 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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Copyright information

© Martinus Nijhoff Publishing, Boston 1986

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  • Eli A. Friedman

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