Mechanisms of progression and regression of renal lesions of chronic nephropathies and diabetes
Giuseppe Remuzzi, … , Ariela Benigni, Andrea Remuzzi
Giuseppe Remuzzi, … , Ariela Benigni, Andrea Remuzzi
Published February 1, 2006
Citation Information: J Clin Invest. 2006;116(2):288-296. https://doi.org/10.1172/JCI27699.
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Mechanisms of progression and regression of renal lesions of chronic nephropathies and diabetes

Abstract

The incidence of chronic kidney diseases is increasing worldwide, and these conditions are emerging as a major public health problem. While genetic factors contribute to susceptibility and progression of renal disease, proteinuria has been claimed as an independent predictor of outcome. Reduction of urinary protein levels by various medications and a low-protein diet limits renal function decline in individuals with nondiabetic and diabetic nephropathies to the point that remission of the disease and regression of renal lesions have been observed in experimental animals and even in humans. In animal models, regression of glomerular structural changes is associated with remodeling of the glomerular architecture. Instrumental to this discovery were 3D reconstruction studies of the glomerular capillary tuft, which allowed the quantification of sclerosis volume reduction and capillary regeneration upon treatment. Regeneration of capillary segments might result from the contribution of resident cells, but progenitor cells of renal or extrarenal origin may also have a role. This review describes recent advances in our understanding of the mechanisms and mediators underlying renal tissue repair ultimately responsible for regression of renal injury.

Authors

Giuseppe Remuzzi, Ariela Benigni, Andrea Remuzzi

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Progression of nephropathy in type 2 diabetes. Following 10 years of sta...
Progression of nephropathy in type 2 diabetes. Following 10 years of stable renal function and normal UAE rate (<20 μg/min or <30 mg/d), UAE increases in 20–40% of type 2 diabetic patients. UAE persistently in the range of 20–200 μg/min or 30–300 mg/d (microalbuminuria) heralds the onset of incipient nephropathy. If left untreated, 20–40% of patients progress to overt nephropathy, a syndrome of macroalbuminuria (UAE rate >200 μg/min or >300 mg/d), declining glomerular filtration rate, and increased cardiovascular morbidity. With the onset of macroalbuminuria renal function progressively declines, and ESRDs eventually develop, requiring RRT with dialysis or transplantation. Diabetics with overt proteinuria have a higher risk of dying from cardiovascular disease (122).