Early glycosilation products induce glomerular hyperfiltration in normal rats

• Published in: Kidney international Vol. 42; no. 4; pp. 875 - 881
• Main Authors: Sabbatini, Massimo, Sansone, Gennaro, Uccello, Francesco, Giliberti, Antonella, Conte, Giuseppe, Andreucci, Vittorio E.
• Format: Journal Article Conference Proceeding
• Language: English
• Published: New York, NY Elsevier Inc 01-10-1992; Nature Publishing
• Subjects: Biological and medical sciences; Medical sciences; Nephrology. Urinary tract diseases; Animal model; Vertebrata; Mammalia; Glomerular filtration; Renal function; Rat; Animal; Diabetes mellitus; Rodentia; Glycosylation; Kidney
• ISSN: 0085-2538; 1523-1755
• DOI: 10.1038/ki.1992.363

Early glycosilation products induce glomerular hyperfiltration in normal rats. The effects of early glycosilation products (Amadori Products, AP) were investigated in male Munich-Wistar rats to establish whether AP play a role in the pathogenesis of glomerular hyperfiltration of early diabetic nephropathy. To mimic such a condition, normal rats were transfused with blood containing in vitro glycated serum (Group GLYC) to achieve plasma levels of Amadori products similar to those measured in rats with streptozotocin-induced diabetes. Rats transfused with normal blood were used as control (Group CON). Glomerular hemodynamics was evaluated in basal condition (B) and during acute hyperglycemia (HG). Blood transfusion did not alter basal hemodynamics. In Group CON, HG determined a rise of single nephron GFR (41.4 ± 3.2 vs. 32.1 ± 1.8 nl/min, P < 0.005), secondary to the increase of afferent effective filtration pressure (EFPa, +19% vs. B, P < 0.01). Rats of Group GLYC, in B, had values of SNGFR higher than those of Group CON B (46.8 ± 3 nl/min, P < 0.05, ANOVA). This increase was mediated by a significant reduction of glomerular afferent arteriole (Ra, -38% vs. Group CON B, P < 0.05), a rise in hydrostatic gradient pressure in glomerular capillaries (ΔP, +17%, P < 0.05) and of EFPa (+31%, P < 0.05). During HG, a further increase of SNGFR (58.3 ± 2.6, P < 0.005 vs. all groups) was detected in rats of Group GLYC, due to a significant rise in glomerular plasma flow (P < 0.05 vs. CON B and CON HG), in P (P < 0.05 vs. all the groups) and EFPa (P < 0.05 vs. all the other groups). In conclusion, this study demonstrates that glomerular hyperfiltration can be reproduced in normal rats by increasing the plasma concentration of Amadori Products to the values observed in diabetic rats. The pattern of modifications in glomerular hemodynamics resembles that commonly described in diabetic hyperfiltering rats.