29
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Reduction in glomerular pore size is not restricted to pregnant women. Evidence for a new syndrome: ‘Shrunken pore syndrome’

      research-article

      Read this article at

      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          The plasma levels of cystatin C, β 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 ≈ eGFR creatinine). The concentration ratios of cystatin C/creatinine, β 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 ≈ 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, β 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 ≈ 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.

          Related collections

          Most cited references45

          • Record: found
          • Abstract: found
          • Article: not found

          Detection of chronic kidney disease with creatinine, cystatin C, and urine albumin-to-creatinine ratio and association with progression to end-stage renal disease and mortality.

          A triple-marker approach for chronic kidney disease (CKD) evaluation has not been well studied. To evaluate whether combining creatinine, cystatin C, and urine albumin-to-creatinine ratio (ACR) would improve identification of risks associated with CKD compared with creatinine alone. Prospective cohort study involving 26,643 US adults enrolled in the Reasons for Geographic and Racial Differences in Stroke (REGARDS) study from January 2003 to June 2010. Participants were categorized into 8 groups defined by estimated glomerular filtration rate (GFR) determined by creatinine and by cystatin C of either <60 or ≥60 mL/min/1.73 m(2) and ACR of either <30 or ≥30 mg/g. All-cause mortality and incident end-stage renal disease with median follow-up of 4.6 years. Participants had a mean age of 65 years, 40% were black, and 54% were women. Of 26,643 participants, 1940 died and 177 developed end-stage renal disease. Among participants without CKD defined by creatinine, 24% did not have CKD by either ACR or cystatin C. Compared with those with CKD defined by creatinine alone, the hazard ratio for death in multivariable-adjusted models was 3.3 (95% confidence interval [CI], 2.0-5.6) for participants with CKD defined by creatinine and ACR; 3.2 (95% CI, 2.2-4.7) for those with CKD defined by creatinine and cystatin C, and 5.6 (95% CI, 3.9-8.2) for those with CKD defined by all biomarkers. Among participants without CKD defined by creatinine, 3863 (16%) had CKD detected by ACR or cystatin C. Compared with participants who did not have CKD by any measure, the HRs for mortality were 1.7 (95% CI, 1.4-1.9) for participants with CKD defined by ACR alone, 2.2 (95% CI, 1.9-2.7) for participants with CKD defined by cystatin C alone, and 3.0 (95% CI, 2.4-3.7) for participants with CKD defined by both measures. Risk of incident end-stage renal disease was higher among those with CKD defined by all markers (34.1 per 1000 person-years; 95% CI, 28.7-40.5 vs 0.33 per 1000 person-years; 95% CI, 0.05-2.3) for those with CKD defined by creatinine alone. The second highest end-stage renal disease rate was among persons missed by the creatinine measure but detected by both ACR and cystatin C (rate per 1000 person-years, 6.4; 95% CI, 3.6-11.3). Net reclassification improvement for death was 13.3% (P < .001) and for end-stage renal disease was 6.4% (P < .001) after adding estimated GFR cystatin C in fully adjusted models with estimated GFR creatinine and ACR. Adding cystatin C to the combination of creatinine and ACR measures improved the predictive accuracy for all-cause mortality and end-stage renal disease.
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            The revised Lund-Malmö GFR estimating equation outperforms MDRD and CKD-EPI across GFR, age and BMI intervals in a large Swedish population.

            The performance of creatinine-based glomerular filtration rate (GFR) estimating equations may vary in subgroups defined by GFR, age and body mass index (BMI). This study compares the performance of the Modification of Diet in Renal Disease (MDRD) study and Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) equations with the revised Lund-Malmö equation (LM Revised), a new equation that can be expected to handle changes in GFR across the life span more accurately.
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              RBP4: a controversial adipokine.

              Adipose tissue is an endocrine organ secreting biologically active factors called adipokines that act on both local and distant tissues. Adipokines have an important role in the development of obesity-related comorbidities not only in adults but also in children and adolescents. Retinol binding protein 4 (RBP4) is a recently identified adipokine suggested to link obesity with its comorbidities, especially insulin resistance, type 2 diabetes (T2D), and certain components of the metabolic syndrome. However, data, especially resulting from the clinical studies, are conflicting. In this review, we summarize up-to-date knowledge on RBP4's role in obesity, development of insulin resistance, and T2D. Special attention is given to studies on children and adolescents. We also discuss the role of possible confounding factors that should be taken into account when critically evaluating published studies or planning new studies on this exciting adipokine.
                Bookmark

                Author and article information

                Journal
                Scand J Clin Lab Invest
                Scand. J. Clin. Lab. Invest
                ICLB
                iclb20
                Scandinavian Journal of Clinical and Laboratory Investigation
                Taylor & Francis
                0036-5513
                1502-7686
                19 May 2015
                2 June 2015
                : 75
                : 4
                : 333-340
                Affiliations
                [ a ]Department of Clinical Chemistry, Skåne University Hospital , Lund, Sweden
                [ b ]Department of Clinical Chemistry, Skåne University Hospital , Malmö, Sweden
                [ c ]Intensive Care Unit , Centralsjukhuset, Kristianstad, Sweden
                [ d ]Department of Nephrology, Skåne University Hospital , Lund, Sweden
                [ e ]Department of Nephrology, Skåne University Hospital , Malmö, Sweden
                Author notes
                Correspondence: Anders Grubb, Department of Clinical Chemistry, Skåne University Hospital , SE-22185 Lund, Sweden. Tel: + 46 70 239 3773. E-mail: anders.grubb@ 123456med.lu.se
                Article
                1025427
                10.3109/00365513.2015.1025427
                4487590
                25919022
                bd158f30-8530-4776-83a0-1be82ec59d6e
                © 2015 Informa UK Ltd

                This is an open-access article distributed under the terms of the CC-BY-NC-ND 3.0 License which permits users to download and share the article for non-commercial purposes, so long as the article is reproduced in the whole without changes, and provided the original source is credited.

                History
                : 10 December 2014
                : 26 February 2015
                Page count
                Figures: 0, Tables: 5, Equations: 0, References: 51, Pages: 8
                Categories
                Original Article

                Clinical chemistry
                beta-trace protein,creatinine,cystatin c,glomerular filtration rate,kidney diseases,beta 2-microglobulin,retinol-binding proteins

                Comments

                Comment on this article