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      Renal neutrophil gelatinase-associated lipocalin and kidney injury molecule-1 expression in children with acute kidney injury and Henoch-Schönlein purpura nephritis

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          Abstract

          The aim of this study was to investigate the expression of neutrophil gelatinase-associated lipocalin (NGAL) and kidney injury molecule-1 (KIM-1) in the serum, urine and renal tissues of children with acute kidney injury (AKI) and Henoch-Schönlein purpura nephritis (A-on-C). A prospective single-center evaluation of the serum, urine and renal NGAL and KIM-1 levels was performed in a cohort of children. Blood and 5-ml urine samples were collected from each patient for the analysis of NGAL and KIM-1 levels using an ELISA. In addition, the expression of NGAL and KIM-1 in the kidney was examined using immunohistochemistry in patients with A-on-C and HSPN. The expression of serum cystatin C, β2-macroglobulin and serum creatinine (SCr), as well as urinary β2-MG and SCr, in the patients with A-on-C was significantly higher than that of HSPN patients, and the expression of NGAL and KIM-1 in the serum and urine in the A-on-C patients was also significantly higher than that of HSPN patients. However, there were no significant differences in the urine protein levels between the two groups. NGAL and KIM-1 were expressed in renal tubular epithelial cells, and the expression of NGAL and KIM-1 in the A-on-C patients was significantly higher than that in HSPN patients. In addition, the urine NGAL and KIM-1 levels were negatively correlated with glomerular filtration rate, but there was no significant correlation between the urine NGAL/KIM-1 and urine protein levels. The changes in serum and urine NGAL and KIM-1 levels may be applied to the diagnosis of A-on-C.

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          Incidence and mortality of acute renal failure in Medicare beneficiaries, 1992 to 2001.

          Jay L Xue, Frank Daniels, Robert Star … (2006)
          This study's objective was to determine the incidence and mortality of acute renal failure (ARF) in Medicare beneficiaries. Data were from hospitalized Medicare beneficiaries (5,403,015 discharges) between 1992 and 2001 from the 5% sample of Medicare claims. For 1992 to 2001, the overall incidence rate of ARF was 23.8 cases per 1000 discharges, with rates increasing by approximately 11% per year. Older age, male gender, and black race were strongly associated (P < 0.0001) with ARF. The overall in-hospital death rate was 4.6% in discharges without ARF, 15.2% in discharges with ARF coded as the principal diagnosis, and 32.6% in discharges with ARF as a secondary diagnosis. In-hospital death rates were 32.9% in discharges with ARF that required renal dialysis and 27.5% in those with ARF that did not require dialysis. Death within 90 d after hospital admission was 13.1% in discharges without ARF, 34.5% in discharges with ARF coded as the principal diagnosis, and 48.6% in discharges with ARF as a secondary diagnosis. Discharges with ARF were more (P < 0.0001) likely to have intensive care and other acute organ dysfunction than those without ARF. For discharges both with and without ARF, rates for death within 90 d after hospital admission showed a declining trend. In conclusion, the incidence rate of ARF in Medicare beneficiaries has been increasing. Those of older age, male gender, and black race are more likely to have ARF. These data show ARF to be a major contributor to morbidity and mortality in hospitalized patients.
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            Urinary kidney injury molecule-1: a sensitive quantitative biomarker for early detection of kidney tubular injury.

            Norma Bobadilla, Victoria Ramírez, Joseph V. Bonventre … (2006)
            Sensitive and specific biomarkers are needed to detect early kidney injury. The objective of the present work was to develop a sensitive quantitative urinary test to identify renal injury in the rodent to facilitate early assessment of pathophysiological influences and drug toxicity. Two mouse monoclonal antibodies were made against the purified ectodomain of kidney injury molecule-1 (Kim-1), and these were used to construct a sandwich Kim-1 ELISA. The assay range of this ELISA was 50 pg/ml to 5 ng/ml, with inter- and intra-assay variability of <10%. Urine samples were collected from rats treated with one of three doses of cisplatin (2.5, 5, or 7.5 mg/kg). At one day after each of the doses, there was an approximately three- to fivefold increase in the urine Kim-1 ectodomain, whereas other routinely used biomarkers measured in this study [plasma creatinine, blood urea nitrogen (BUN), urinary N-acetyl-beta-glucosaminidase (NAG), glycosuria, proteinuria] lacked the sensitivity to show any sign of renal damage at this time point. When rats were subjected to increasing periods (10, 20, 30, or 45 min) of bilateral ischemia, there was an increasing amount of urinary Kim-1 detected. After only 10 min of bilateral ischemia, Kim-1 levels on day 1 were 10-fold higher (5 ng/ml) than control levels, whereas plasma creatinine and BUN were not increased and there was no glycosuria, increased proteinuria, or increased urinary NAG levels. Thus urinary Kim-1 levels serve as a noninvasive, rapid, sensitive, reproducible, and potentially high-throughput method to detect early kidney injury in pathophysiological studies and in preclinical drug development studies for risk-benefit profiling of pharmaceutical agents.
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              Tubular kidney injury molecule-1 (KIM-1) in human renal disease.

              Dania van der Meer, V Bailly, Sjoerd Burg … (2007)
              KIM-1, a transmembrane tubular protein with unknown function, is undetectable in normal kidneys, but is markedly induced in experimental renal injury. The KIM-1 ectodomain is cleaved, detectable in urine, and reflects renal damage. KIM-1 expression in human renal biopsies and its correlation with urinary KIM-1 (uKIM-1) is unknown. In biopsies from various renal diseases (n = 102) and controls (n = 7), the fraction of KIM-1 positive tubules and different renal damage parameters were scored. Double labelling was performed for KIM-1 with macrophages (MØ), alpha-smooth muscle actin (alpha-SMA), proximal (aquaporin-1) and distal (E-cadherin) tubular markers and a dedifferentiation marker (vimentin). uKIM-1 at the time of biopsy (n = 53) was measured by ELISA. Renal KIM-1 was significantly increased in all diseases versus controls (p < 0.05), except minimal change. KIM-1 was primarily expressed at the luminal side of dedifferentiated proximal tubules, in areas with fibrosis (alpha-SMA) and inflammation (MØ). Independent of the disease, renal KIM-1 correlated positively with renal damage, negatively with renal function, but not with proteinuria. uKIM-1 was increased in renal patients versus controls (p < 0.001), including minimal change, and correlated positively with tissue KIM-1 and MØ, negatively with renal function, but not with proteinuria. In conclusion, KIM-1 is upregulated in renal disease and is associated with renal fibrosis and inflammation. uKIM-1 is also associated with inflammation and renal function, and reflects tissue KIM-1, indicating that it can be used as a non-invasive biomarker in renal disease. Copyright 2007 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Exp Ther Med
                Journal ID (iso-abbrev): Exp Ther Med
                Journal ID (publisher-id): ETM
                Title: Experimental and Therapeutic Medicine
                Publisher: D.A. Spandidos
                ISSN (Print): 1792-0981
                ISSN (Electronic): 1792-1015
                Publication date (Print): May 2014
                Publication date (Electronic): 28 February 2014
                Publication date PMC-release: 28 February 2014
                Volume: 7
                Issue: 5
                Pages: 1130-1134
                Affiliations
                Department of Pediatric Nephrology, Shengjing Hospital of China Medical University, Shenyang, Liaoning 110004, P.R. China
                Author notes
                Correspondence to: Dr Yue Du, Department of Pediatric Nephrology, Shengjing Hospital of China Medical University, 36 Sanhao Street, Peace Region, Shenyang, Liaoning 110004, P.R. China, E-mail: duyue_nephrology@ 123456163.com
                Article
                Publisher ID: etm-07-05-1130
                DOI: 10.3892/etm.2014.1595
                PMC ID: 3991550
                PubMed ID: 24940398
                SO-VID: 02d3e067-097c-4ad7-9bb4-77abff4606d4
                Copyright © Copyright © 2014, Spandidos Publications
                License:

                This is an open-access article licensed under a Creative Commons Attribution-NonCommercial 3.0 Unported License. The article may be redistributed, reproduced, and reused for non-commercial purposes, provided the original source is properly cited.

                History
                Date received : 04 August 2013
                Date accepted : 13 December 2013
                Categories
                Subject: Articles

                ScienceOpen disciplines: Medicine
                Keywords: renal neutrophil gelatinase-associated lipocalin,injury molecule-1,acute kidney injury,henoch-schönlein purpura nephritis,children
                Data availability:
                ScienceOpen disciplines: Medicine
                Keywords: renal neutrophil gelatinase-associated lipocalin, injury molecule-1, acute kidney injury, henoch-schönlein purpura nephritis, children

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