Serum cystatin C is a poor biomarker for diagnosing acute kidney injury in critically-ill children.

BACKGROUND: Accurate diagnosis of acute kidney injury (AKI) is problematic especially in critically-ill patients in whom renal function is in an unsteady state. AIM: Our aim was to evaluate the role of serum (S.) cystatin C as an early biomarker of AKI in critically-ill children. SUBJECTS AND METHODS: S. creatinine and S. cystatin C were measured in 32 critically-ill children who were at risk for developing AKI. AKI was defined by both: Risk,-injury,-failure,-loss, and-endstage renal disease (RIFLE) classification and glomerular filtration rate (GFR) <80 ml/min/1.73 m(2). GFR was estimated by both Schwartz formula and S. cystatin C-based equation. RESULTS: S. cystatin C was not statistically higher in AKI patients compared with non-AKI by RIFLE classification (median 1.48 mg/l vs. 1.16 mg/l, P = 0.1) while S. creatinine was significantly higher (median 0.8 mg/dl vs. 0.4 mg/dl, P = 0.001). On estimating GFR by the two equations we found, a lag between rise of S. cystatin C and creatinine denoted by lower GFR by Schwartz formula in four patients, on other hand, six patients had elevated S. cystatin C with low GFR despite normal creatinine and GFR, denoting poor concordance between the two equations and the two markers. The ability of S. creatinine in predicting AKI was superior to S. cystatin with area under the curve (AUC) 0.95 with sensitivity and specificity (100% and 84.6%, respectively) using the RIFLE classification. The same findings were found when using Schwartz formula. CONCLUSION: S. cystatin C is a poor biomarker for diagnosing AKI in critically-ill children.

Tumor necrosis factor-α -308 A/G gene polymorphism in children with juvenile idiopathic arthritis: relation to disease activity, damage, and functional status.

The study aims to evaluate the clinical significance of serum levels of tumor necrosis factor alpha (TNF-α) and -308 A/G promoter polymorphism in juvenile idiopathic arthritis (JIA) patients and find any association to the subsets, clinical and laboratory features, disease activity, and damage as well as functional disability. Forty-eight JIA children and 30 controls were included in the present study. Juvenile arthritis disease activity score in 27 joints (JADAS-27) was calculated, juvenile arthritis damage index (JADI) was assessed, and Childhood Health Assessment Questionnaire (CHAQ) measured the functional status. Serum TNF-α was assayed by ELISA and gene (-308) promoter polymorphism was determined by polymerase chain reaction. The 48 JIA children (mean age 11.5 ± 2.8 years) were 13 systemic, 17 oligoarticular, and 18 polyarticular onset. The serum TNF-α was significantly higher in patients (90.4 ± 6.3 ng/ml) compared to control (3.5 ± 2.6 ng/ml) (p < 0.0001) with a tendency to be higher in the polyarticular subtype. All controls had TNF-α -308 GG alleles. The frequency of GG genotype tended to be higher in systemic onset compared to oligoarticular and polyarticular subtypes. The serum TNF-α significantly correlated with JADAS-27 (r = 0.32, p = 0.03) and CHAQ (r = 0.37, p = 0.01) and negatively with the presence of GG alleles (r = -0.48, p = 0.001). The GG alleles were significantly negatively associated with C-reactive protein (r = -0.32, p = 0.03) with a tendency to negatively correlate with JADAS-27, CHAQ, and JADI-extrarticular (r = -0.28, p = 0.06; r = -0.25, p = 0.09 and r = -0.25, p = 0.09, respectively). There is evidence of a possible influence of the -308 SNP promoter position on the production of TNF-α, the severity of JIA which may consequently influence the response to anti-TNF-α treatment.

Is Neck Circumference an Indicator for Metabolic Complication of Childhood Obesity?

BACKGROUND: The possible role of neck circumference (NC) for screening childhood obesity and its complication is not well characterized. AIM: To assess NC and to explore its increase as risk factor with metabolic syndrome (MS) variables. METHODS: Cross sectional case-control study included 50 obese children (BMI ≥95(th) percentile) and 50 healthy (BMI 15(th)-<85(th) percentile). All were subjected to clinical examination, measuring blood pressure (BP), body weight, height, NC, waist (WC) and hip (HC)., fasting blood glucose, insulin and lipid profile. RESULTS: MS was detected among 52% of obese participants, but not among controls (0%). Clinical parameters and most of the laboratory values were higher in subjects with MS than in non-metabolic subjects, with statistical significance only in blood pressure and triglycerides. Among obese without MS, NC showed significantly positive correlations with age, weight, height, WC, HC and negative with LDL. While among Obese with MS, NC showed significantly positive correlations with age, weight, height, BMI-SDS, WC, HC and DBP. CONCLUSION: NC can be considered as a good indicator and predictor for obesity, especially central obesity. However, NC has no relation with lipid profile or fasting blood sugar.

The potential role of insulin-like growth factor 1, insulin-like growth factor binding protein 3 and bone mineral density in patients with chronic hepatitis C virus in Cairo, Egypt.

Insulin-like growth factor 1 (IGF-1) levels have been found to correlate with measurements of bone mineral density (BMD) in liver diseases. This study investigated the relationship between IGF-1, insulin-like growth factor binding protein 3 (IGFBP-3) and BMD in patients with chronic hepatitis C virus. This study was conducted for 30 patients with chronic hepatitis C virus infection (16 patients without and 14 patients with cirrhosis) and 11 healthy controls. Serum levels of IGF-1 and IGFBP-3 and BMD of the proximal femur and lumbar spine were measured in all subjects. Osteoporosis of the proximal femur and lumbar spine was found in 42.9% and 21.4%, respectively, of the patients with cirrhosis. Patients with liver cirrhosis and osteoporosis of the proximal femur and lumbar spine had lower IGF-1 (P<0.001, P=0.04, P=0.04 respectively). BMD of the proximal femur was lower in cirrhotic patients compared with controls (P<0.01). Patients with liver cirrhosis had lower IGFBP-3 than patients without cirrhosis and controls (P<0.001). Patients with osteoporosis of the proximal femur had lower IGFBP-3 than those without osteoporosis (P<0.01). IGF-1 and IGFBP-3 levels were lower in patients with liver cirrhosis. IGF-1 and IGFBP-3 may play a role in hepatic osteoporosis.