Comparing cystatin C and creatinine in the diagnosis of pediatric acute renal allograft dysfunction

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. 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. 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. In this pediatric population, cystatin C was not superior to creatinine for the detection of acute allograft dysfunctio

Polymorphism of hypoxia-inducible factor-1 α gene in pediatric acute respiratory distress syndrome

Objective: To examine if hypoxia-inducible factor-1 α (Hif-1 α ) polymorphisms are associated with pediatric acute respiratory distress syndrome (PARDS). Methods: Twenty two patients with PARDS and 11 non-PARDS controls were examined in pediatric intensive care unit in Cukurova University Balcali Hospital. Blood polymorphism was used to assess the Hif-1 α C1772T and G1790A polymorphisms of Hif-1 α gene, and differences in genotypes between the 2 groups were compared. Results: Hif-1 α C1772T polymorphism was observed only in one case of PARDS group but non-PARDS group didn’t show any C1772T polymorphism. Particularly, the difference in number of cases with Hif-1 α G1790A polymorphism was not significant between PARDS and non-PARDS groups. In addition, Hif-1 α G1790A polymorphism was significantly related to the distribution of lung opacities in children with PARDS (P<0.05). Conclusions: Our results indicate that Hif-1 α G1790A polymorphism is related to an increased susceptibility to pulmonary for PARDS children. The detection of G1790A polymorphism could help pediatricians to predict the extensity of PARDS early in lung tissue