The purpose of this study was to determine the prevalence and types of acute renal failure in asphyxiated full-term neonates and to evaluate the accuracy of an asphyxia morbidity score in predicting acute renal failure. Neonates admitted to one institution from 1990 through 1993 with a gestational age > or = 36 weeks and 5-min Apgar score < or = 6, without congenital malformations or sepsis, were studied retrospectively for acute renal failure in the 1st week of life. Acute renal failure was defined as serum creatinine > 1.5 mg/dl (133 mumol/l) with normal maternal renal function. Nonoliguric renal failure was defined as renal failure with urine output > 1 ml/kg per hour after the 1st day. An asphyxia morbidity scoring system was used to distinguish severe from moderate asphyxia. The score ranged from 0 to 9 and was based upon fetal heart rate, Apgar score at 5 min, and base deficit in the 1st h of life. The score for severe asphyxia was defined as 6-9 and for moderate asphyxia as 1-5. Sixty-six neonates fulfilled study criteria. Acute renal failure was present in 20 of 33 (61%) infants with severe asphyxia scores and 0 of 33 with moderate asphyxia scores (P < 0.0001). Acute renal failure was nonoliguric in 12 of 20 (60%), oliguric in 5 of 20 (25%) and anuric in 3 of 20 (15%). In conclusion 1) acute renal failure occurred in 61% of infants with severe asphyxia, 2) acute renal failure associated with severe asphyxia was predominantly nonoliguric and 3) an asphyxia morbidity score, which can be determined at 1 h of age, predicted acute renal failure in full-term infants with 100% sensitivity and 72% specificity.

A comprehensive asthma intervention program for Medicaid-insured asthmatic children can significantly improve health outcomes while reducing health care costs.asthma education, health care outcomes, Medicaid, asthma outreach, utilization.

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Obesity, which has reached epidemic proportions in the United States and other western countries, may be complicated by hypertension, an increased incidence of renal cancer or proteinuria. Patients with obesity-associated proteinuria show focal glomerulosclerosis and glomerulomegaly on biopsy, usually have minimal clinical edema and relatively normal levels of serum albumin, cholesterol and blood pressure, and can progress to end-stage renal disease. Severe obesity may also be an additive risk factor in patients with preexisting nephropathy or reduced renal mass. The pathophysiology of obesity-associated proteinuria is unclear but may include hyperfiltration, increased renal venous pressure, glomerular hypertrophy, hyperlipidemia and increased synthesis of vasoactive and fibrogenic substances, including angiotensin II, insulin, leptin and transforming growth factor-beta1. These substances may individually or interactively affect glomerular hyperfiltration, mesangial cell hypertrophy and matrix production, and the production of collagen, fibronectin, transforming growth factor-beta and other fibrogenic mediators of change. Although angiotensin-converting enzyme inhibition has proven to have an impact, perhaps temporarily, on obesity-associated proteinuria in humans, weight reduction early in the course of the disease would appear the most important therapeutic approach.

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Although nitric oxide (NO) has a well-established role in regulating renal function in the adult, recent studies point to perhaps an even more critical role for NO in maintaining basal renal blood flow (RBF) and glomerular filtration rate (GFR) in the developing kidney. The immature kidney has enhanced renal hemodynamic and functional responses to stimulation and inhibition of NO synthesis when compared with the adult, and these increased responses are not mediated by prostaglandins. Increased intrarenal activity of NO in the developing kidney counter-regulates the highly activated renin angiotensin system by modulating the angiotensin II-mediated vasoconstriction of the developing renal vasculature, the angiotensin II effects on GFR, as well as renin release. Localization studies demonstrate that NO acts on neonatal RBF and stabilization of GFR through an intrarenal distribution of the synthesizing enzyme, nitric oxide synthase, that is different from that of the adult. The developing kidney is dependent on NO to maintain RBF and GFR during periods of hypoxemia, protecting against renal injury, such as acute renal failure. In summary, NO is vital in the developing kidney to maintain normal physiological function and to protect the immature kidney during pathophysiological stress.

To determine if the developing kidney differs from the adult in the expression of the neuronal nitric oxide synthase, NOS I, these experiments measured mRNA gene expression by RNase protection assay and protein content by Western blot of NOS I in piglets at ages newborn and 3, 7, 10, 14, and 21 days and adult pigs. Whole kidney NOS I mRNA was greatest at birth and decreased progressively during renal maturation to adult levels. NOS I protein content paralleled this developmental pattern. Cortical NOS I protein was equivalent in newborn and 14-day-old piglets and was greater at both ages than the adult. Medullary NOS I protein was relatively greater than cortical in both immature ages and decreased from a peak at birth to adult levels. We conclude the following. 1) During postnatal maturation, renal NOS I mRNA and protein content show a pattern that is developmentally regulated. 2) This developmental pattern of NOS I after birth may, in part, contribute to the enhanced functional role of NO during renal maturation.