Comparing cystatin C and creatinine in the diagnosis of pediatric acute renal allograft dysfunction.
Summary of "Comparing cystatin C and creatinine in the diagnosis of pediatric acute renal allograft dysfunction."
BACKGROUND:
Allograft function following renal transplantation is commonly monitored using serum creatinine. Multiple cross-sectional studies have shown that serum cystatin C is superior to creatinine for detection of mild to moderate chronic kidney dysfunction. Recent data in adults indicate that cystatin C might also be a more sensitive marker of acute renal dysfunction. This study aims to compare cystatin C and creatinine for detection of acute allograft dysfunction in children using pediatric RIFLE (risk of renal dysfunction, injury to the kidney, failure or loss of kidney function, end stage renal disease) criteria for acute kidney injury.
METHODS:
Retrospective chart review of post-transplant period in 24 patients in whom creatinine and cystatin C were measured every day. Allograft dysfunction was defined as a sustained rise in marker concentration above the mean of the three preceding measurements.
RESULTS:
In total, there were 13 episodes of allograft dysfunction. Maximum RIFLE stages with creatinine were 'R' in 7, 'I' in 4, and 'F' in 2, with cystatin C 'R' in 6, 'I' in 4 and 'F' in 3, respectively. In 9/13 cases, both markers rose simultaneously, in three, the rise in creatinine preceded cystatin C by 1-5 days (median 4). In one case, the rise in cystatin C preceded creatinine by 1 day. The time lag was not statistically different. The maximum relative rise of creatinine was significantly higher than cystatin C. By multiple linear regression analysis, the maximum rise of cystatin C was related to the maximum rise of creatinine, but independent of patient age, gender, steroid dose, and anthropometric data.
CONCLUSIONS:
In this pediatric population, cystatin C was not superior to creatinine for the detection of acute allograft dysfunction.
Affiliation
Department of Pediatric Nephrology, VU University Medical Center, Postbox 7057, 1007 MB, Amsterdam, The Netherlands.
Journal Details
This article was published in the following journal.
Name: Pediatric nephrology (Berlin, Germany)
ISSN: 1432-198X
Pages:
Links
- PubMed Source: http://www.ncbi.nlm.nih.gov/pubmed/22207347
- DOI: http://dx.doi.org/10.1007/s00467-011-2073-9
Medical and Biotech [MESH] Definitions
Kidney Failure, Acute
A severe stage of acute renal insufficiency, characterized by the sudden decrease in GLOMERULAR FILTRATION RATE to less than 15 ml per min, sometime to less than 1 to 2 ml per min. It is usually associated with OLIGURIA; EDEMA; and increase in BLOOD UREA NITROGEN and serum CREATININE concentrations.
Acute Kidney Injury
Abrupt reduction in kidney function defined as an absolute increase in serum CREATININE of more than or equal to 0.3. mg/dl, a percentage increase in serum creatinine of more than or equal to 50%, or a reduction in urine output. Acute kidney injury encompasses the entire spectrum of the syndrome including acute kidney failure; ACUTE KIDNEY TUBULAR NECROSIS; and other less severe conditions.
Cystatin C
An extracellular cystatin subtype that is abundantly expressed in bodily fluids. It may play a role in the inhibition of interstitial CYSTEINE PROTEASES.
Cystatin M
A cystatin subtype that has a diverse tissue distribution, target specificity, and functions as an endogenous inhibitor of lysosomal cysteine proteases.
Uremia
A clinical syndrome associated with the retention of renal waste products or uremic toxins in the blood. It is usually the result of RENAL INSUFFICIENCY. Most uremic toxins are end products of protein or nitrogen CATABOLISM, such as UREA or CREATININE. Severe uremia can lead to multiple organ dysfunctions with a constellation of symptoms.
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