Background While fibrosis seems to be prognostic for adverse outcomes in adults with idiopathic dilated cardiomyopathy (IDC), little is known about the prevalence and development of fibrosis in pediatric IDC hearts. We hypothesize there is less activation of fibrosis at a molecular level in pediatric IDC hearts than in the failing adult heart. Methods and Results Pediatric hearts were analyzed histologically to determine the prevalence of fibrosis. Left ventricular tissue from adult and pediatric IDC hearts and adult and pediatric non-failing (NF) hearts were subjected to qRT-PCR to study the expression of important mRNAs that affect fibrosis. We found age-specific differences between IDC and NF hearts in regulation of non-coding galectin 3, Corin, MMP-2, MMP-9, TIMP-2, and TIMP-3. We also found markers that were similarly altered in both adult and pediatric IDC (ST2L, TIMP-1, and TIMP-4). Finally, microRNAs 29a-c were significantly decreased in the pediatric IDC patients. Conclusion Pediatric IDC patients demonstrate age-specific differences in the molecular pathways implicated in fibrosis in the adult heart. At the ultrastructural level the unique gene expression pattern appears to limit fibrosis in the failing pediatric heart.

Acute kidney injury is common after the Norwood procedure. Correcting creatinine for fluid balance revealed new cases of AKI. Use of an mBTS and higher VIS on POD 0 were associated with increased risk of AKI.

Fluid corrected AKI was independently associated with the development of a postoperative infection. These findings support the notion that AKI is an immunosuppressed state that increases the risk of infection.

Background Severe acute kidney injury (AKI) is associated with subsequent infection. Whether AKI followed by a return to baseline creatinine is associated with incident infection is unknown. Objective We hypothesized that risk of both short and long term infection would be higher among patients with AKI and return to baseline creatinine than in propensity score matched peers without AKI in the year following a non-infectious hospital admission. Design Retrospective, propensity score matched cohort study. Participants We identified 494 patients who were hospitalized between January 1, 1999 and December 31, 2009 and had AKI followed by return to baseline creatinine. These were propensity score matched to controls without AKI. Main Measures The predictor variable was AKI defined by International Classification of Diseases , Ninth Revision ( ICD-9 ) codes and by the Kidney Disease Improving Global Outcomes definition, with return to baseline creatinine defined as a decrease in serum creatinine level to within 10% of the baseline value within 7 days of hospital discharge. The outcome variable was incident infection defined by ICD-9 code within 1 year of hospital discharge. Results AKI followed by return to baseline creatinine was associated with a 4.5-fold increased odds ratio for infection (odds ratio 4.53 [95% CI, 2.43–8.45]; p<0.0001) within 30 days following discharge. The association between AKI and subsequent infection remained significant at 31–60 days and 91 to 365 days but not during 61–90 days following discharge. Conclusion Among patients from an integrated health care delivery system, non-infectious AKI followed by return to baseline creatinine was associated with an increased odds ratio for infection in the year following discharge.