Lisinopril, once daily, is an effective and well-tolerated antihypertensive in children aged 6 to 16 years. An initial dose of 0.07 mg/kg, administered once daily, effectively lowered BP within 2 weeks. Blood pressure was reduced in a dose-dependent fashion.

A non-immune complex-mediated glomerulonephritis associated with persistent hypocomplementemia occurred in a young boy. Measurement of complement components revealed complete factor H deficiency, inherited as an autosomal recessive trait. Evaluation of the renal lesion revealed extensive deposition of type III collagen suggestive of collagen type III glomerulopathy, a recently identified cause of chronic renal insufficiency in children and adults. This report represents the first association of inherited factor H deficiency with collagen type III glomerulopathy.

Considerable attention is directed to a surprising biologic phenomenon wherein tissues exposed to one insult acquire resistance to another. We identify a novel example of acquired resistance to acute renal failure and a mechanism that contributes to such resistance. Nephrotoxic serum, administered to rats 24 h before the induction of glycerol-induced acute renal failure, reduces functional and structural injury that occurs in this model. Since heme oxygenase, the ratelimiting enzyme in heme degradation, protects against heme protein-induced renal injury, we questioned whether induction of heme oxygenase underlies the protection afforded by nephrotoxic serum. Kidney heme oxygenase (HO-1) mRNA was induced 6 h after nephrotoxic serum and renal tubules were identified as the site of expression of heme oxygenase protein.