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Title: [Effect of protein load on kidney functions in patients with chronic glomerulonephritis]. Author: Esaian AM, Kucher AG, Kaiukov IG, Ermakov IuA, Nikogosian IuA, Riabov SI. Journal: Ter Arkh; 2002; 74(6):19-24. PubMed ID: 12136476. Abstract: AIM: To study changes in renal function in response to protein loads in patients with chronic glomerulonephritis (CGN) who have normal renal function and initial uremia. MATERIAL AND METHODS: 63 CGN patients were divided into two groups: 40 patients of group 1 (17 males, 23 females, age 16-53 years, plasma creatinine-Pcr < 0.132 mmol/l); 23 patients of group 2 (10 males, 13 females, age 18-57 years, Pcr > 0.132 mmol/l). Renal functional reserve (RFR) was assessed with oral soa isolate SUPRO 760 test (protein Techn. Int., USA), 1.0 g of protein per 1 kg of ideal body mass. By three 2-h clearance periods measurements were made of RFR, absolute and fractional excretion, concentration indices and clearances of creatinine, urea, electrolytes, osmolality. All the parameters were referred to the standard body surface. RESULTS: RFR was intact in 14 patients of group 1 and 10 patients of group 2. In CGN without uremia with intact RFR, maximal Pcr corresponded to the highest values of minute diuresis and sharp increase of urea excretion, osmotically active substances. In CGN patients with uremia and intact RFR, development of hyperfiltration was accompanied with a significant rise in Pcr, minute diuresis, absolute excretion of urea and osmotically active substances. The rise in the latter two was much less active in CGN if RFR was absent. Multiple stepwise regression analysis showed that RFR intactness depends primarily on baseline values of absolute excretion of urea and osmotically active substances. CONCLUSION: A reverse relationship exists between absolute excretion of urea, osmotically active substances and the degree of SKF in response to protein load in CGN patients both in intact nitrogen-excreting function and uremia. It is suggested that urea may be involved in regulation of intraglomerular hemodynamics by means of effect on tubular-glomerular feedback mechanism.[Abstract] [Full Text] [Related] [New Search]