Pediatric nephrology : journal of the International Pediatric Nephrology Association
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Many different drugs and agents may cause nephrotoxic acute kidney injury (AKI) in children. Predisposing factors such as age, pharmacogenetics, underlying disease, the dosage of the toxin, and concomitant medication determine and influence the severity of nephrotoxic insult. In childhood AKI, incidence, prevalence, and etiology are not well defined. ⋯ Direct pathophysiological mechanisms of nephrotoxicity include constriction of intrarenal vessels, acute tubular necrosis, acute interstitial nephritis, and-more infrequently-tubular obstruction. Furthermore, AKI may also be caused indirectly by rhabdomyolysis. Frequent therapeutic measures consist of avoiding dehydration and concomitant nephrotoxic medication, especially in children with preexisting impaired renal function.
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Acute kidney injury (AKI), previously referred to as acute renal failure (ARF), represents a persistent problem in clinical medicine. Despite significant improvements in therapeutics, the mortality and morbidity associated with AKI remain high. A major reason for this is the lack of early markers for AKI, akin to troponins in acute myocardial disease, and hence an unacceptable delay in initiating therapy. ⋯ As they represent sequentially expressed biomarkers, it is likely that the AKI panels will be useful for timing the initial insult and assessing the duration of AKI. Based on the differential expression of the biomarkers, it is also likely that the AKI panels will distinguish between the various types and etiologies of AKI. It will be important in future studies to validate the sensitivity and specificity of these biomarker panels in clinical samples from large cohorts and from multiple clinical situations.
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Pigment nephropathy accounts for approximately 3% of all cases of acute renal failure (ARF) in children. Studies of risk factors associated with ARF and the need for renal replacement therapy (RRT) in children with rhabdomyolysis-associated pigment nephropathy consist of retrospective case series with variable inclusion criteria. Our objective was to evaluate clinical and laboratory characteristics, etiology, initial fluid therapy, prevalence of ARF and the requirement for RRT in pediatric patients with acute rhabdomyolysis. ⋯ Most of these factors are related to the level of renal insufficiency and degree of muscle injury. There was no difference in admission and peak creatine kinase (CK) levels between those who did or did not require RRT. However, all who required RRT had a peak CK level > 5000 U/L.
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The purpose of this retrospective cohort study was to describe the outcome of 107 patients with chronic kidney disease (CKD) admitted to a pre-dialysis interdisciplinary management program from 1990 to 2006. The events of interest were progression to CKD stage 5 (renal survival), patient survival, hypertension, and somatic growth. Survival was studied by the Kaplan-Meier method. ⋯ The glomerular diseases group showed a median rate of GFR deterioration of 10 ml/min per 1.73 m(2) per year (IQ range -24 to -5.7), whereas the median rate of GFR deterioration for the groups with cystic diseases, congenital nephro-uropathies, and miscellanea were 2.5 ml/min (IQ range -10 to +0.34), 2.2 ml/min (IQ range -5.0 to -0.52), and 0.36 ml/min (IQ range -2.5 to +2.6), respectively (P < 0.001). The results of this study support the view that children and adolescents with glomerular diseases present a faster deterioration of renal function. Therefore, patients with glomerular diseases need to be referred early to a pediatric nephrology center so that suboptimal pre-dialysis care might possibly be avoided.
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Proteomic analysis has revealed potential early biomarkers of acute kidney injury (AKI) in children undergoing cardiopulmonary bypass (CPB), the most prominent one with a mass-to-charge ratio of 6.4 kDa. The objective of this study was to identify this protein and test its utility as a biomarker of AKI. Trypsin-digested protein bands were analyzed by tandem mass spectrometry (MS/MS) to identify the protein in urine samples. ⋯ By multivariate analysis, the urinary aprotinin level 2 h after CPB was an independent predictor of AKI (beta = 0.001, P < 0.0001). The 2 h urinary aprotinin level correlated with serum creatinine, duration of AKI, and length of hospital stay. We concluded that urinary aprotinin levels 2 h after initiation of CPB predict the development of AKI and adverse clinical outcomes.