(Journal Article): Structural and functional changes in diabetic glomerulopathy.
Schleicher E, Kolm V, Ceol M, Nerlich A (Abteilung fur Innere Medizin IV, Eberhard-Karls-Universitat, Tubingen, Germany.)
IN:
Kidney Blood Press Res
1996; 19:305-315
Impact Factor(s) of Kidney Blood Press Res: 1.067 (2004), 0.968 (2002), 1.885 (2001)
ABSTRACT: Diabetic nephropathy is characterized by glomerular basement membrane thickening and mesangial expansion. Immunohistochemical studies of diabetic kidneys showed an increased collagen type IV synthesis and deposition in the mesangial matrix, while the glomerular heparan sulfate proteoglycan content was decreased. In nodular glomerulosclerosis massive deposition of collagens III and VI appears, possibly indicating irreversibility of the pathological process. These structural changes seem to be the underlying cause for the alterations of renal functions like persistent albuminuria and proteinura. In a recent study significant glomerular infiltration by macrophages at all stages of glomerulosclerosis was observed. The pathogenesis of the multitude of cellular, structural, and functional abnormalities in diabetic nephropathy is likely to be multifactorial, involving chronic hyperglycemia as well as genetic determinants. In vitro studies with cultured glomerular cells have indicated that hyperglycemia induces transforming growth factor beta, a matrix-producing cytokine. The hyperglycemia-induced cytokine production may involve protein kinase C activation and/or the formation of advanced glucosylation end products. The elucidation of the pathogenesis of diabetic nephropathy may suggest new ways for therapeutic interventions.
TYPE OF PUBLICATION: Original article
Articles citing this article:
|
||
(Journal Article): Renal structure and function in insulin-dependent diabetes mellitus and type I membranoproliferative glomerulonephritis in humans.
Mauer SM, Lane P, Hattori M, Fioretto P, Steffes MW (Department of Pediatrics, University of Minnesota Medical School, Minneapolis.)
IN:
J Am Soc Nephrol
1992; 2:S181-S184
Impact Factor(s) of J Am Soc Nephrol: 6.644 (2004), 7.499 (2003), 6.337 (2001)
ABSTRACT: Renal pathological changes of diabetes include thickening of all renal extracellular basement membranes and the mesangial matrix and, to a lesser extent, mesangial cell expansion. Two renal lesions appear critical in diabetic nephropathy. Mesangial expansion out of proportion to the size of the glomerulus is related to proteinuria, hypertension, and declining GFR. Arteriolar hyalinosis is related to global glomerulosclerosis, and both are correlated with the clinical features of nephropathy. By the time renal dysfunction is clinically detectable, these lesions tend to be advanced. Interstitial volume may be increased in insulin-dependent diabetes mellitus, particularly in areas containing sclerotic glomeruli or marked tubular atrophy. Parallel findings were documented for type I membranoproliferative glomerulonephritis in which the increased mesangial volume fraction was related to decreased GFR, increased glomerular permeability to protein, and hypertension. As in diabetes, the cortical interstitial volume fraction is correlated with functional abnormalities in type I membranoproliferative glomerulonephritis. Thus, in both of these chronic glomerular disorders, mesangial expansion and interstitial expansion are associated with disordered renal function. Thus, it is not true that glomerular structural changes correlate poorly with glomerular function. Whether it is the glomerular or interstitial pathology or both that is causally responsible for the dysfunction requires further study.
TYPE OF PUBLICATION: Original article
Articles citing this article:
|
||
|
||