Retrospective clinical studies have suggested that exposure to lead in early life may result in chronic renal disease durlng adulthood. W e established an animal model to test this hypothesis. Sprague-Dowley rats received either tap water (C) ar a 1% lead acetate solution in water (E) from 3 to 9 weeks of age and were studied in pairs either 2-6 weeks or 14-18 weeks after exposure. Since no statistical differences in renal function between C and E ar a function of age were found, the results were pooled and analyzed by paired t-test. n C (ji + dRTA was documented in 2 females (Case 1 -14 yrs, Case 2 -8 mo). The diagnosis of dRTA was b~e d upon a urine pH of 6.9 for each came durlng an acute metabolic acidosis (blood pH 7.01 and 7.14), a normal HCOj threshold (fractional HCOj excretion 4.7 and 3.4%) and a low urine minus blood PC02 gradient in alkaline urine (U-B PC02 2 and 3). 'he diapnoais of NDI was suapectad became of polyuria, persiatent hypotonic urine and confirmed when investigated in detail. Mnximm spontaneous urine omolality (U Oam) for Case 1 and 2 were 139 and 93 m0sm/kg and increased slightly after infusion of antidiuretic hormone to 180 and 122 mOam1kg respectively. 2 controls given a similar infusion achieved U Oamqs ,800 mOamlkg. l h m our casea have a distal nephron which is impermeable to water and also dRTA with a low U-B PCO2. The low U-B PC02 can be due to an increased psrmeability of the distal nephron to H+ in acid urine and H2CO3 in alkaline urine. However our cases had a diatal nephron with reduced permability to Hz0 and dRTA. lherefore unless there is a selective increased permeability to H2C03 and H+ but decreased permeability to water, the low V-B PC0 observed in these cases t la more compatible with a failure of H secretion in the distal nephron. Animal studies supporting this will be presented. Cincinnati .-Ohio. While ARF following rhabdomyolyais or crush syndrome is well documented,ita pathophysiology has not been defined.Myog1obin. thought to be responsible for the pathogenesis of ARF.ia not toxic unless dehydration or acidoaia is already preaent.To elucidate the pathophysiology of ARF.8 new experimental model was established using a crude muscle extract(ME) prepared by homogenization of saline perfused rat thigh muscle followed by centrifugation and filtration.Experimenta1 rats were injected i.v. with ME and control groups with aaline.boiled ME.and myoglobin in normal rat serum.ME caused death at doaes > 1 0 mg ME protein1 100 g and ARF at 5-10 mg.0liguria.proteinuria.hemepigmenturia with an active urine sedlment.hypocomplementemia.1eucopenia and thrombocytopenia developed shortly after ME injection.Thesefindings were not present in the control groups;tranaient harmless myoglobinuria was present in the control rats given myoglobin. Involvement of the coagulation system suggested by experimental data led to studies using heparin an an anticosgulant.Ten of 10 rats pretreated with heparin before ME injection lived whereas 9 of 10 controls died.This experimental model closely resemb...
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