Joseph Palmisano

Absence of Anion Gap Metabolic Acidosis in Severe Methanol Poisoning: A Case Report and Review of the Literature

Methanol poisoning in humans is characterized by a latent period with subsequent development of anion gap metabolic acidosis and blindness. We describe a patient with potentially lethal methanol ingestion as evidenced by an admission serum methanol level of 403 mg/dL and sustained serum methanol levels greater than 50 mg/dL for more than 18 hours after ingestion, despite hemodialysis therapy. That anion gap metabolic acidosis or visual impairment did not develop in this patient was attributed to documented prior ethanol ingestion (admission serum ethanol level of 158 mg/dL) and continued ethanol administration during hospitalization (sustained serum ethanol levels greater than 100 mg/dL). This case demonstrates the ability of ethanol to inhibit the metabolism of methanol to formic acid in humans. This inhibition was achieved without induction of lactic acidosis. Thus this case documents the efficacy of ethanol therapy in patients with methanol poisoning.

Disorders of Proton Secretion by the Kidney

Rapid advances have been made in the understanding of the cellular mechanisms of proton transport in urinary epithelia. The polar epithelial cells of the kidney tubules as well as various urinary bladder preparations are made up of apical and basolateral cell membranes with very different properties. The site of H + secretion is at the apical membrane and for each H + secreted a HCO3- ion is generated and transported across the basolateral cell membrane. In the proximal renal tubule, H + secretion at the brush border occurs primarily via a Na + /H + exchanger; in the tight epithelia of the turtle and toad bladder and, probably, the mammalian collecting tubules, the luminal membrane contains an electrogenic proton pump which appears to be a H + -translocating ATPase. The efflux of HC03- across the basolateral cell membranes of both leaky and tight epithelia appears to occur either via an anion exchanger or a conductive channel, but is not coupled directly to metabolic energy.

Twenty-year follow-up: an unusual case of nephropathy of antiphospholipid syndrome.

Nephropathy of antiphospholipid antibody syndrome (NAPS) is an increasingly well-recognized aspect of antiphospholipid syndrome. The most characteristic histopathology is that of thrombotic microangiopathy, and thrombosis occurring in the renal vasculature is thought to be the initiating event. Other less common pathologies have been reported, and the mechanisms of these are unclear. Therapy has been largely empiric. We report a case of NAPS in a patient with atypical pathology, who has declined therapy with immunosuppressive agents and anticoagulants and who has maintained normal renal function in 20 years of follow-up.