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Early detection of urinary NGAL and plasma CysC may prevent progression to overt acute renal failure
Author(s) -
Hakan Şarlak,
Mustafa Dınc,
Şevket Balta,
Mustafa Çakar,
Erol Arslan,
S. Demirbas
Publication year - 2014
Publication title -
schweizerische medizinische wochenschrift
Language(s) - English
Resource type - Journals
ISSN - 0036-7672
DOI - 10.4414/smw.2014.13949
Subject(s) - medicine , cystatin c , acute kidney injury , renal function , creatinine , lipocalin , urology , urinary system , biomarker , renal replacement therapy , subclinical infection , intensive care unit , kidney disease , gastroenterology , biochemistry , chemistry
We read with interest the article “Cystatin C and neutrophilgelatinase-associated lipocalin: biomarkers for acute kid-ney injury after congenital heart surgery” written by Ste-fanie Seitz et al. [1]. They concluded that, after congenitalheart surgery, urine neutrophil gelatinase-associated lipo-calin (NGAL) indicated the damaging effects of cardiopul-monary bypass and that serum cystatin C was a valuablepredictive biomarker for the resulting acute kidney injury(AKI) [1].In current practice, the standard method for renal functionmonitoring remains serum creatinine (SCr) measurement,although it is late and insensitive as there is a 24- to48-hour delay between renal insult and SCr changes [2].Furthermore, creatinine starts increasing only when morethan 50% of the glomerular filtration rate (GFR) is lost,cannot reflect GFR trends and may be diluted after aggress-ive fluid resuscitation [3]. NGAL has emerged as one of themost promising biomarkers for the early diagnosis of AKI,and a significant correlation has been found between acuterenal injury and serum NGAL concentration 2 hours aftercardiopulmonary bypass [4]. Recent investigations havevalidated the reliability of NGAL as a specific, sensitiveand early predictor of AKI after cardiac surgery, contrastadministration, septic shock and even renal transplantation[5]. Plasma NGAL (pNGAL) is less specific than its ur-inary counterpart [2]. In fact, pNGAL is already increasedin patients with chronic kidney disease or systemic ill-nesses, and increases six times less than urinary NGAL incases of renal injury [2]. Urinary NGAL was evident evenafter very mild “subclinical” renal ischaemia, despite nor-mal serum creatinine levels [3]. In intensive care settings,plasma cystatin C (pCysC) was able to detect AKI earlierand was more sensitive than SCr in detecting minor GFRreductions [2]. Unfortunately, pCysC levels may also be in-fluenced by several nonrenal factors including corticoster-oid administration, thyroid dysfunction, systemic inflam-mation, neoplasia, age and muscular mass [2]. There is anurgent need for tools allowing an early and accurate detec-tion of AKI [2]. In this regard, urinary NGAL and pCysCseem to be the most promising [2]. These early biomarkerswill also help to develop new preventive and/or therapeuticmethods for the management of AKI [2].We think that such early, rapid and simple detection of ur-inary NGAL and pCysC in patients with subtle, subclinic-al ischaemic renal injury or subclinical nephrotoxic dam-age will alert the clinician to introduce manoeuvres aimedat preventing progression to overt acute renal failure.Note from the publisher: The authors of the original articledo not wish to comment on this contribution.

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