Pediatric nephrology : journal of the International Pediatric Nephrology Association
-
Outcomes in critically ill neonates have improved over the past three decades, yet high residual mortality and morbidity rates exist. Acute kidney injury (AKI) is not just an innocent by-stander in the critically ill patient. Research on incidence and outcomes of AKI in the critically ill neonatal population is scarce. ⋯ Large prospective studies are needed to test definitions and to better understand risk factors, incidence, independent outcomes, and mechanisms that lead to poor short- and long-term outcomes. Early biomarkers of AKI need to be explored in critically ill neonates. Infants with AKI need to be followed for sequelae after AKI.
-
Acute kidney injury (AKI) (previously called acute renal failure) is characterized by a reversible increase in the blood concentration of creatinine and nitrogenous waste products and by the inability of the kidney to regulate fluid and electrolyte homeostasis appropriately. The incidence of AKI in children appears to be increasing, and the etiology of AKI over the past decades has shifted from primary renal disease to multifactorial causes, particularly in hospitalized children. Genetic factors may predispose some children to AKI. ⋯ Children who have suffered AKI from any cause are at risk for late development of kidney disease several years after the initial insult. Therapeutic interventions in AKI have been largely disappointing, likely due to the complex nature of the pathophysiology of AKI, the fact that the serum creatinine concentration is an insensitive measure of kidney function, and because of co-morbid factors in treated patients. Improved understanding of the pathophysiology of AKI, early biomarkers of AKI, and better classification of AKI are needed for the development of successful therapeutic strategies for the treatment of AKI.
-
Nitric oxide (NO), produced by nitric oxide synthase (NOS), critically counteracts angiotensin-II-enhanced vascular resistance in the immature kidney, perhaps due to the developmental regulation of NOS expression and function in the postnatal preglomerular resistance vessels (PRV). Our experiments measured the messenger ribonucleic acid (mRNA) gene expression of neuronal NOS (nNOS), endothelial NOS (eNOS), and components of the renin-angiotensin system (renin, AT1 and AT2 receptors), by real-time RT-PCR, as well as NOS enzymatic activity by citrulline assay in PRVs (afferent, interlobular, and arcuate arterioles) obtained from swine ages newborn, 7 and 21 days, and adult. NOS enzymatic activity was upregulated in PRVs immediately after birth but decreased to adult levels with maturation. ⋯ In contrast, eNOS and AT1 receptor expression were downregulated at birth but increased to the highest levels in the adult. Upregulated NOS enzymatic activity in newborn PRVs supports the critical neonatal role for NO renal vascular vasodilation. Upregulated nNOS gene expression, concomitant with downregulated eNOS gene expression in neonatal PRVs, suggests that the nNOS isoform may be responsible for counteracting angiotensin II increased vascular resistance in immature porcine PRVs.