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Calprotectin and neutrophil gelatinase–associated lipocalin in the differentiation of pre‐renal and intrinsic acute kidney injury
Author(s) -
Seibert F. S.,
Pagonas N.,
Arndt R.,
Heller F.,
Dragun D.,
Persson P.,
SchmidtOtt K.,
Zidek W.,
Westhoff T. H.
Publication year - 2013
Publication title -
acta physiologica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.591
H-Index - 116
eISSN - 1748-1716
pISSN - 1748-1708
DOI - 10.1111/apha.12064
Subject(s) - calprotectin , neutrophil gelatinase associated lipocalin , lipocalin , acute kidney injury , medicine , gelatinase , kidney , renal injury , pathology , gastroenterology , matrix metalloproteinase , disease , inflammatory bowel disease
Background Urinary calprotectin has recently been identified as a promising biomarker for the differentiation of pre‐renal and intrinsic acute kidney injury ( AKI ). This study compares the diagnostic performance of calprotectin and neutrophil gelatinase–associated lipocalin ( NGAL ) in this differential diagnosis. Methods Urinary calprotectin and NGAL concentrations were assessed in a study population of 87 subjects including 38 cases of intrinsic AKI , 24 cases of pre‐renal AKI and 25 healthy controls. Urinary tract obstruction, renal transplantation and metastatic cancer were defined as exclusion criteria. Results Mean calprotectin concentrations were significantly lower in pre‐renal (190.2 ± 205.7 ng mL −1 ) than in intrinsic AKI (6250.1 ± 7167.2 ng mL −1 , P  <   0.001). Receiver‐operating characteristic ( ROC ) analysis provided an AUC of 0.99. Mean NGAL concentrations were significantly higher in intrinsic than in pre‐renal AKI as well (458.1 ± 695.3 vs. 64.8 ± 62.1 ng mL −1 , P  = 0.001) providing an AUC of 0.82. A combination of the present study population with the cohort of the proof of concept study led to a population of 188 subjects (58 pre‐renal AKI , 90 intrinsic AKI , 40 healthy controls). ROC analyses provided an AUC of 0.97 for calprotectin and 0.76 for NGAL yielding sensitivity and specificity values of 93.3 and 94.8% (calprotectin) vs. 75.3 and 72.4% ( NGAL ). Optimal cut‐off values were 440 ng mL −1 (calprotectin) and 52 ng mL −1 ( NGAL ). Pyuria increased calprotectin concentrations independent of renal failure. Conclusion This study shows that both calprotectin and NGAL are able to differentiate between pre‐renal and intrinsic AKI after exclusion of pyuria. In the present population, calprotectin presents a higher sensitivity and specificity than NGAL .

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