ABSTRACT
Topiramato pode produzir raramente uma acidose metabólica através da inibição da anidrase carbônica no túbulo distal do néfron - acidose tubular renal do tipo 2. Relatamos o caso de mulher de 40 anos previamente saudável que desenvolveu quadro de acidose metabólica assintomática grave, sem outra etiologia identificável, durante uso de topiramato na dose de 100mg/dia por três meses. Este efeito colateral, embora infrequente, parece ser imprevisível e requer atenção cuidadosa.
Subject(s)
Female , Humans , Middle Aged , Acidosis, Renal Tubular/chemically induced , Carbonic Anhydrase Inhibitors/adverse effects , Fructose/analogs & derivatives , Acidosis, Renal Tubular/diagnosis , Fructose/adverse effectsABSTRACT
A Thai female patient developed muscular weakness, hypouricemia, hypokalemia and hyperchloremic metabolic acidosis after taking outdated tetracycline. A pathophysiologic study shows a proximal tubular defect for reabsorption of urate and bicarbonate and a distal tubular acidification defect, probably caused by outdated tetracycline.
Subject(s)
Acidosis, Renal Tubular/chemically induced , Adult , Female , Humans , Hypokalemia/chemically induced , Tetracycline/adverse effects , Uric Acid/bloodABSTRACT
We studied the kinetics of HCO-3 reabsorption in the middle proximal (MPT) and distal convoluted tubules (DCT) by measuring continuously intratubular pH with Sb-microelectrodes in stopped-flow microperfusion (HCO-3, 30 mM Ringer) experiments. Male Wistar rats (240-280 g) were injected ip with LiCl (4mEqkg-1 day-1) for 4 days (Li) and were compared to controls (C). Steady-state pH increased in MPT from 6.64 + or - 0.02(57) to 6.89 + or - 0.02(45), mean + or - SEM (number of measurements) on tissue from 13 rats in each group, and from 6.87 + or - 0.5(30) to 7.08 + or - 0.01(63) in DCT. HCO-3 reabsorption decreased from 1.32 + or - 0.08(57) to 0.96 + or - 0.4(45) nmol cm-2 s-1 in MPT and from 0.85 + or - 0.07(30) to 0.45 + or - 0.04(63) in DCT. These data indicate that lithium affected the acidification mechanism in MPT and DCT, probably through an impairment of the Na+ -H+ antiport in both tubular segments
Subject(s)
Rats , Animals , Male , Acidosis, Renal Tubular/chemically induced , Lithium/pharmacology , Sodium/metabolism , Kidney Tubules, Proximal/physiopathology , Punctures , Rats, Inbred StrainsABSTRACT
Acute metabolic acidosis potentiates the nephrotixicity of aminoglycosides by impairing the adequate excretion of ammonium and titratable acidity. The present study assesses distal tubular function after aminoglycoside administration in the rat. Two aminoglycosides, gentamicin and netilmicin were given to rats either in low doses equivalent to those used clinically (BG4 and BN5 groups) or in doses ten times higher (BG40 and BN50). The rats were subjected to acute metabolic alkalosis and the pCO2 of urine was continuously evaluated. the regression lines obtained by plotting the differences between urine and blood pCO2 as a function of urinary HCO3 in low dose models were simsilar to those obtained for the control group. However, the slopes obtained for BG40 and BN50 were significantly different from the control, suggesting an impairment of H+ secretion