Clinical diabetic nephropathy in man is the consequence of the development of a specific constellation of glomerular, tubular, vascular, and interstitial structural abnormalities accompanied by highly characteristic immunohistochemical alterations that, together, are unique to diabetes. Because changes resembling the specific pathology of diabetes do not develop in patients with conditions that lead to long-standing glomerular hyperfunction (such as unilateral nephrectomy), it is unlikely that glomerular hemodynamic abnormalities per se can be the cause of diabetic nephropathy. Whether hemodynamic abnormalities represent a risk factor that, in the presence of the diabetic state, can accelerate the rate of development of the basic lesions of diabetic nephropathy is currently unclear. However, there is considerable evidence that when the renal lesions of diabetes are far advanced, factors such as systemic hypertension can determine the rate of renal functional deterioration in diabetes as in other disorders. Although the diabetic rat may be a useful model for the study of aspects of the pathogenesis of diabetic nephropathy, much confusion has resulted from the inclusion of focal segmental glomerularsclerosis as a diabetic lesion. Similarly, the acceptance of all increases in urinary protein excretions in this model as resulting from or reflecting of diabetic nephropathology can be misleading. It is concluded that treatment aimed at manipulating renal hemodynamics in diabetic patients without evidence of renal disease should remain in the realm of clinical research.
|Original language||English (US)|
|Number of pages||10|
|Journal||American Journal of Kidney Diseases|
|State||Published - 1992|
Bibliographical noteFunding Information:
From the Departments of Pediatrics and Laboratory Medicine and Pathology, University of Minnesota Medical School, Minneapolis, MN. Received May 8, 1992; accepted in revised form July J 7, 1992. Supported in part by the National Institutes of Health (Grants No. AMl3083, AM20742, AM17697, and M01-RR00400), and by the Juvenile Diabetes Foundation International. Address reprint requests to S. Michael Mauer, MD, Department of Pediatrics, University of Minnesota, Box 491 UMHC, 515 Delaware St SE, Minneapolis, MN 55455. © 1992 by the National Kidney Foundation, Inc. 0272-6386/ 92/ 2006-0003$3.00/0
- renal biopsy