The gelatin-derived plasma substitute Gelofusine causes low-molecular-weight proteinuria by decreasing tubular protein reabsorption

• Published in: Journal of critical care 2001-09, Vol.16 (3), p.115-120
• Main Authors: ten Dam, Marc A.G.J., Branten, Amanda J.W., Klasen, Ina S., Wetzels, Jack F.M.
• Format: Article
• Language: English
• Subjects: Adult; Gelatin - adverse effects; Hemodynamics; Humans; Kidney Tubules - physiopathology; Male; Molecular Weight; Netherlands; Plasma Substitutes - adverse effects; Proteins - chemistry; Proteins - metabolism; Proteinuria - chemically induced; Succinates - adverse effects
• ISSN: 0883-9441; 1557-8615
• DOI: 10.1053/jcrc.2001.28787

Purpose: Proteinuria is frequently encountered in patients in the intensive care unit, most likely as a result of renal tubular cell injury. It has been reported that gelatin-derived plasma substitutes contribute to an increase in renal protein excretion. The aim of this study was to investigate the magnitude and the mechanism of the proteinuric effect of Gelofusine, a modified gelatin. Materials and Methods: In six healthy male subjects, renal hemodynamics and urinary protein excretion were measured before and after infusion of 330 mL of Gelofusine. Results: Gelofusine had a minor effect on blood pressure, glomerular filtration rate, effective renal plasma flow, and on urinary excretion of immunoglobulin, and albumin. In contrast, there was a major increase in the urinary excretion of the low-molecular-weight proteins β 2-microglobulin (from 0.06 ± 0.04 to 43.52 ± 11.75 μg/min; P < .01) and α 1-microglobulin (from 11 ± 8 to 72 ± 24 μg/min; P < .01). The urinary excretion of N-acetyl-β- D-glucosaminidase (β-NAG) remained unchanged, suggesting that there was no significant renal tubular cell injury. Conclusions: When analyzing proteinuria in patients in the intensive care unit it should be considered that Gelofusine increases the urinary excretion of proteins, in particular those of low molecular weight. This effect is most likely due to competitive inhibition of tubular protein reabsorption. Copyright © 2001 by W.B. Saunders Company