Dietary protein as casein (CAS) augments intrinsic acid production, induces endothelin-mediated kidney acidification, and promotes kidney injury. We tested the hypothesis that dietary CAS induces endothelin-mediated kidney injury through augmented intrinsic acid production. Munich-Wistar rats ate minimum electrolyte diets from age 8 to 96 weeks with 50 or 20% protein as either acid-inducing CAS or non-acid-inducing SOY. Urine net acid excretion and distal nephron net HCO3 reabsorption by in vivo microperfusion (Net J(HCO3)) were higher in 50 than 20% CAS but not 50 and 20% SOY. At 96 weeks, 50% compared the 20% CAS had higher urine endothelin-1 excretion (U(ET-1)V) and a higher index of tubulo-interstitial injury (TII) at pathology (2.25+/-0.21 vs 1.25+/-0.13 U, P<0.03), but each parameter was similar in 50 and 20% SOY. CAS (50%) eating NaHCO3 to reduce intrinsic acid production had lower Net J(HCO3), lower U(ET-1)V, and less TII. By contrast, 50% SOY eating dietary acid as (NH4)2SO4 had higher Net J(HCO3), higher U(ET-1)V, and more TII. Endothelin A/B but not A receptor antagonism reduced Net J(HCO3) in 50% CAS and 50% SOY+(NH4)2SO4 animals. By contrast, endothelin A but not A/B receptor antagonism reduced TII in each group. The data support that increased intake of acid-inducing dietary protein induces endothelin B-receptor-mediated increased Net J(HCO3) and endothelin A-receptor-mediated TII through augmented intrinsic acid production.

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to June 30, 2004, were reviewed and data were collected. Results: 486 infants of 30-33 weeks gestation had screening cranial US performed. IVH occurred in 22 of 486 (4.5%). Of the 22 infants, 4 infants had significant IVH (grade III and/or grade IV). Of the 4 infants with significant IVH, 2 were 30 weeks and 2 were 31 weeks gestation. All 4 infants had either significant risk factors for brain injury (abruption, asphyxia) or clinical symptoms (seizures) that would warrant US during their hospital course. Of the 486 infants who had US, 5 additional infants (1%) had PVL, and 2 of these 5 had risk factors (abruption, shock) that warranted obtaining a sonogram. There was a statistically significant trend towards fewer abnormal sonograms from 33 weeks to 30 weeks gestation (p = .04).