Topiramate and carbonic anhydrase inhibition

Abstract

Topiramate (TPM) is a newly anticonvulsivant, which has been aproved as an adjunct therapy in partial seizures and secondarily generalized seizures in adults, with expanding uses for neuropathic pain relief and migraine prophylaxis.
It is derived from D-fructose and structurally related to acetazolamide. TPM is also a weak inhibitar of carbonic anydrase (CA) and may result in hyperchloremic metabolic acidosis.
This adverse event is infrequent and usually asymptomatico The CA plays an essential role in the reabsorption of ultrafiltered bicarbonate by the proximal tubule and the net urinary acidification by alfa-type intercalated cells of the distal nephron. Deficiency in CA is associated with a mixed proximal and distal renal tubular acidosis (RTA) type 3. We report a 76-year-old man presenting with hyperchloremic metabolic acidosis (RTA, type II), which resolved after withdrawal of TPM. We recommend evaluation of the acid-base balance befare starting TPM and advise regular monitoring in these patients.

How to cite this article:

López Gastón O, Pastorino ML, Alfonso A, Varela J, Giannaula R. [Topiramate and carbonic anhydrase inhibition]. Rev Nefrol Dial Traspl. 2009;29(2):69-73.