Neutrophil Gelatinase-Associated Lipocalin Is a New and Sensitive Marker of Kidney Function in Chronic Kidney Disease Patients and Renal Allograft Recipients

Małyszko, J.; Bachórzewska−Gajewska, Hanna; Poniatowski, Bogusław; Dobrzycki, Sławomir; Myśliwiec, Michał

doi:10.1016/j.transproceed.2008.10.088

Cited by 83 publications

(81 citation statements)

References 19 publications

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“…Other potentially interesting molecules include the tubular injury markers NGAL (383-385), KIM-1 (385-388), TIMP-2 (389), IGFBP7 (389) and liver-type fatty acid-binding protein (L-FABP) (390,391). The diagnostic value of these markers is well described in acute tubular injury and is being evaluated in the settings of CKD (392) or as a potential marker of ''tubular atrophy'' in allografts (384,393,394). Keratin 18, an epithelial-specific cytoskeletal protein released into urine or serum upon tubular cell death, might also be a novel marker of CKD (395).…”

Section: Serum and Urine Biomarkersmentioning

confidence: 99%

Renal Allograft Fibrosis: Biology and Therapeutic Targets

Floege

2015

American Journal of Transplantation

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Section: Serum and Urine Biomarkersmentioning

confidence: 99%

Renal Allograft Fibrosis: Biology and Therapeutic Targets

Floege

2015

American Journal of Transplantation

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“…In this study, each of the models exhibited baseline elevations in one or more urinary biomarkers that correlated with preexisting kidney injury identified in the corresponding model. Urinary biomarker elevations in these disease models were not as prominent for the specific proximal tubule biomarker, Kim-1 (Ichimura et al 2004;Prozialeck et al 2007;Rached et al 2008;Sieber et al 2009;Zhou et al 2008), as for the less specific biomarkers, Lcn-2 and Opn, that have both been associated with inflammation in multiple organs and in multiple locations within the nephron (Aigner et al 2007;Bu et al 2006;Kuwabara et al 2009;Lebkowska et al 2009;Makris et al 2009;Malyszko et al 2009;Persy et al 1999;Sieber et al 2009;Vaidya, Ferguson, and Bonventre 2008;Wang et al 2008;Wang et al 2007;Xie et al 2001). Findings of severe periarteritis nodosa in the kidneys of DSS and SHRs as well as in the livers of DSS models should encourage researchers to evaluate the relationship between biomarkers of vascular injury (Zhang, Hanig, and De Felice 2012) and CIN.…”

Section: Biomarker Monitoringmentioning

confidence: 83%

Kidney Injury Biomarkers in Hypertensive, Diabetic, and Nephropathy Rat Models Treated with Contrast Media

et al. 2012

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Contrast-induced nephropathy (CIN) refers to a decline in renal function following exposure to iodinated contrast media (CM). The present study was initiated to explore the role of known human risk factors (spontaneous hypertension, diabetes, protein-losing nephropathy) on CIN development in rodent models and to determine the effect of CM administration on kidney injury biomarkers in the face of preexisting kidney injury. Spontaneously hypertensive rats (hypertension), streptozotocin-treated Sprague Dawley rats (diabetes), and Dahl salt-sensitive rats (protein-losing nephropathy) were given single intravenous injections of the nonionic, low osmolar contrast medium, iohexol. Blood urea nitrogen (BUN), serum creatinine (sCr), and urinary biomarkers; albumin, lipocalin 2 (Lcn-2), osteopontin (Opn), kidney injury molecule 1 (Kim-1), renal papillary antigen 1 (Rpa-1), a-glutathione S-transferase (a-Gst), m-glutathione S-transferase (m-Gst), and beta-2 microglobulin (b2m) were measured in disease models and appropriate controls to determine the response of these biomarkers to CM administration. Each disease model produced elevated biomarkers of kidney injury without CM. Preexisting histopathology was exacerbated by CM but little or no significant increases in biomarkers were observed. When 1.5-fold or greater sCr increases from pre-CM were used to define true positives, receiver-operating characteristic curve analysis of biomarker performance showed sCr was the best predictor of CIN across disease models. b2m, Lcn-2, and BUN were the best predictors of histopathology defined kidney injury.

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“…The latter have shown that NGAL can be used as an early biomarker, for example, contrast-induced nep hropathy in patients with normal serum creatinine levels undergoing percutaneous coronary inter ventions, 12 kidney transplant recipients, 13 and hypertensive patients with coronary artery diseases. 14 These results show that NGAL has the potential for detecting kidney injury earlier than either serum creatinine or, perhaps, GFR estimation formulas that use static measurements of serum creatinine.…”

Section: Discussionmentioning

confidence: 99%

Untitled

Hekmat

Eshraghi²,

Esmailpour³

et al. 2017

Exp Clin Transplant

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Objectives: Kinetic glomerular filtration rate estimation may have more power and versatility than the Modification of Diet in Renal Disease or CockcroftGault formula for evaluating kidney function when plasma creatinine fluctuates rapidly. After kidney donation, glomerular filtration rate rapidly fluctuates in otherwise healthy patients. We compared 3 formulas for estimating glomerular filtration rate: kinetic, Modification of Diet in Renal Disease, and Cockcroft-Gault, for determining stages of acute kidney injury early after kidney donation. Materials and Methods: In 42 living kidney donors, we measured serum creatinine, cystatin C, neutrophil gelatinase-associated lipocalin, and glomerular filtration rates before uninephrectomy and 3 days afterward. To estimate glomerular filtration rate, we used Cockcroft-Gault, Modification of Diet in Renal Disease, and kinetic equations. We sought the most accurate formula for staging acute kidney injury according to the risk, injury, failure, loss, and end-stage criteria. Results: The kinetic glomerular filtration rate model found more cases of stage 3 acute kidney injury than did the Modification of Diet in Renal Disease or Cockcroft-Gault formula. Receiver operating characteristic curves showed that the kinetic glomerular filtration rate model had more sensitivity and specificity than the Cockroft-Gault formula for discriminating among risk, injury, failure, loss, and end-stage criteria stages of acute kidney injury, based on serum creatinine changes. On day 2 after donation, a more sensitive marker with a shorter half-life (serum neutrophil gelatinase-associated lipocalin) was more significantly correlated with kinetic glomerular filtration rate estimation. Conclusions: The kinetic glomerular filtration rate model was able to discriminate stages of acute kidney injury early after kidney donation according to risk, injury, failure, loss, and end-stage criteria better than the Modification of Diet in Renal Disease or CockcroftGault formulas. The kinetic model detected failurestage acute kidney injury ≥ 1 to 2 days earlier than the MDRD formula, CG formula detected no failure.

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Neutrophil Gelatinase-Associated Lipocalin Is a New and Sensitive Marker of Kidney Function in Chronic Kidney Disease Patients and Renal Allograft Recipients

Cited by 83 publications

References 19 publications

Renal Allograft Fibrosis: Biology and Therapeutic Targets

Renal Allograft Fibrosis: Biology and Therapeutic Targets

Kidney Injury Biomarkers in Hypertensive, Diabetic, and Nephropathy Rat Models Treated with Contrast Media

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