Journal
SCANDINAVIAN JOURNAL OF CLINICAL & LABORATORY INVESTIGATION
Volume 75, Issue 4, Pages 333-340Publisher
INFORMA HEALTHCARE
DOI: 10.3109/00365513.2015.1025427
Keywords
Beta-trace protein; creatinine; cystatin C; glomerular filtration rate; kidney diseases; beta 2-microglobulin; retinol-binding proteins
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Funding
- Alfred Osterlund Foundation
- Greta and Johan Kock Foundation
- Medical Faculty of the University of Lund
- Region Skane
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The plasma levels of cystatin C, beta(2)-microglobulin, beta-trace protein, retinol binding protein (RBP) and creatinine were determined in plasma samples from 111 randomly selected patients with eGFR(cystatin C) <= 60% of eGFR(creatinine) and from 55 control patients with 0.9eGFR(creatinine) <= eGFR(cystatin C) <= 1.1eGFR(creatinine) (eGFR(cystatin C) approximate to eGFR(creatinine)). The concentration ratios of cystatin C/creatinine, beta(2)-microglobulin/creatinine, beta-trace protein/creatinine and RBP/creatinine were significantly higher in patients with eGFR(cystatin C) < 60% of eGFR(creatinine) than in patients with eGFR(cystatin C) approximate to eGFR(creatinine). When the patients were divided into three groups with different estimated GFR intervals (<= 40, 40-60 and >= 60 mL/min/1.73m(2)) the concentration ratios of cystatin C/creatinine, beta(2)-microglobulin/creatinine, and beta-trace protein/creatinine were significantly higher in patients with eGFR(cystatin C) <= 60% of eGFR(creatinine) than in patients with eGFR(cystatin C) approximate to eGFR(creatinine) for all GFR intervals. Similar results were obtained when the population without pregnant women was studied as well as the subpopulations of men or of non-pregnant women. Populations of pre-eclamptic women and pregnant women in the third trimester display similar results. Since the production of these four proteins with sizes similar to that of cystatin C is not co-regulated, the most likely explanation for the simultaneous increase of their creatinine-ratios in patients with eGFR(cystatin C) <= 60% of eGFR(creatinine) is that their elimination by glomerular filtration is decreased. We suggest that this is due to a reduction in pore diameter of the glomerular membrane and propose the designation 'Shrunken pore syndrome' for this pathophysiological state.
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