In patients with renal diseases characterized by proteinuria,the initial insult to the kidney is usually followed by a progressivedecline in the glomerular filtration rate. This decline hasbeen thought to be due to changes in renal hemodynamics initiatedby the loss of nephrons.1 When renal mass is reduced in rats,the remaining nephrons undergo sudden hypertrophy, with a concomitantlowering of arteriolar resistance and an increase in glomerularplasma flow.2,3 Afferent arteriolar tone decreases more thanefferent arteriolar tone, and therefore, the hydraulic pressurein glomerular capillaries rises4 and the amount of filtrateformed by each nephron increases. . . . [Full Text of this Article]
Activation of Local Hormones and Inflammatory Chemokines by Filtered Protein
Evidence from Animal Studies
Evidence from Animal Models of Human Diseases
Limiting Protein Filtration
Protein-Dependent Interstitial Inflammation in Nephropathies
Ratio of Urinary Protein to Creatinine as a Predictor of End-Stage Renal Disease
Effect of Reducing Protein Excretion on the Decline in the Glomerular Filtration Rate
Role of Blood-Pressure Reduction
Conclusions
Source Information
From the Mario Negri Institute for Pharmacological Research and the Nephrology Unit, Ospedali Riuniti di Bergamo both in Bergamo, Italy.
Address reprint requests to Dr. Remuzzi at the Mario Negri Institute for Pharmacological Research, Via Gavazzeni 11, 24125 Bergamo, Italy.
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