Antikaliuretic action of trimethoprim is minimized by raising urine pH.

  title={Antikaliuretic action of trimethoprim is minimized by raising urine pH.},
  author={Martin Schreiber and Lynn E. Schlanger and Chi-hong B. Chen and Mahbob Lessan-Pezeshki and Mitchell L. Halperin and A Patnaik and Brian N. Ling and Thomas R. Kleyman},
  journal={Kidney international},
  volume={49 1},
This study was designed to test the hypothesis that the antikaliuresis caused by trimethoprim could be diminished by alkalinizing the luminal fluid in the CCD, thereby converting trimethoprim from its cationic, active form to an electroneutral, inactive, form. Trimethoprim-induced inhibition of transepithelial Na+ transport was examined in A6 distal nephron cells by analysis of short circuit current. The voltage-dependence of the trimethoprim-induced block of Na+ channels was examined with… 
Reversal of trimethoprim-induced antikaliuresis.
It is suggested that acute administration of TMP inhibits the amiloride-sensitive Na(+)-channel and K+ secretion in the distal nephron and can abrogate TMP's antikaliuretic effect due, in part, to an increase of the low TTKG observed with TMP.
Trimethoprim-Induced Hyperkalaemia
In circumstances where continued treatment with trimethoprim is required, induction of high urinary flow rates with intravenous fluids and a loop diuretic, as well as alkalinisation of the urine, have been shown to block the antikaliuretic effect of trimethOPrim on distal nephron cells.
Reversal of Trimethoprim-Induced Antikaliuresis in an HIV Patient With Pneumocystis Pneumonia
A case of a patient with severe PJP causing respiratory failure treated with high-dose trimethoprim-sulfamethaxazole who experienced hyperkalemia was successfully managed with a combination of fludrocortisone and furosemide allowing completion of antibiotic course.
Iatrogenic hyperkalaemia--points to consider in diagnosis and management.
  • K. SiamopoulosM. ElisafK. Katopodis
  • Medicine
    Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association
  • 1998
Three cases of iatrogenic hyperkalaemia with ECG changes secondary to drug therapy are described and the appropriate sium excretion is discussed, based on these cases, with clinical management of this problem.
Drug-induced hyperkalemia: old culprits and new offenders.
  • M. Perazella
  • Medicine, Biology
    The American journal of medicine
  • 2000
Fluid, electrolyte and acid–base disorders associated with antibiotic therapy
The mechanisms that disrupt renal tubular function are described and Integrated with the physiology of each successive nephron segment, the receptors, transporters, channels or pores that are affected by antibiotics are discussed.
An approach to the patient with severe hypokalaemia: the potassium quiz.
The objective of this teaching session with Professor McCance is to develop an approach to the management of patients with a very low plasma potassium (K(+)) concentration (P(K)). The session begins
Expression of the Cystic Fibrosis Phenotype in a Renal Amphibian Epithelial Cell Line*
The data suggest that the regulation of Na+ channels by CFTR is not limited to respiratory epithelia and to epithelial cells in culture overexpressing CFTR and epithelial Na- channel Po, when compared with forskolin-stimulated controls.
Trimethoprim related Hyperkalaemia in a patient with Renal Tubular Acidosis Type 4.
This case illustrates the vulnerability of patients with pre-existing renal tubular acidosis type 4 to medications that further inhibit renin-aldosterone action and the danger of keeping entirely separate case notes between different hospital disciplines.
The Collagen IV Nephropathies
Inherited disorders of type IV collagen account for a significant percentage of patients with persistent hematuria and hereditary angiopathy associated with nephropathy, aneurysms, and muscle cramps is caused by mutations that affect a glomerular basement network that consists of α( alpha)1(IV) and α(alpha)2( IV) chains.


K(+)-sparing diuretic actions of trimethoprim: inhibition of Na+ channels in A6 distal nephron cells.
Investigation of the effect of TMP on the 4 pS, highly selective Na+ channel in the apical membrane of A6 cells grown on permeable supports in the presence of 1.5 microM aldosterone found the appearance of a new closed state after apical TMP treatment was revealed.
A Mechanism for Pentamidine-Induced Hyperkalemia: Inhibition of Distal Nephron Sodium Transport
Two well-established models of cortical collecting tubule ion transport were investigated to investigate the effects of pentamidine on renal tubular Na+ reabsorption and, therefore, K+ secretion and the causes of hyperkalemia.
Trimethoprim-Sulfamethoxazole Induces Reversible Hyperkalemia
A retrospective analysis comparing a cohort of HIV-infected patients who received high dose trimethoprim-sulfamethoxazole (Tmp-Smx) therapy with those who did not, finding that the hyperkalemia was often associated with hyponatremia and mild azotemia and universally resolved after discontinuation of Tmp- Smx.
The transtubular potassium concentration in patients with hypokalemia and hyperkalemia.
Importance of guanidinium groups of blocking sodium channels in epithelia.
The evidence is consistent with the view that sodium entry into the epithelium is dependent on an acid grouping, which behaves as a singly ionizable grouping with a pKa of around 5.5.
Effect of amiloride and some of its analogues of cation transport in isolated frog skin and thin lipid membranes
The inhibition of short-circuit current (Isc) in isolated frog skin and the induction of surface potentials in lipid bilayer membranes produced by the diuretic drug amiloride and a number of its
Hyperkalemia with high-dose trimethoprim-sulfamethoxazole therapy.
  • S. GreenbergI. ReiserS. Chou
  • Medicine, Biology
    American journal of kidney diseases : the official journal of the National Kidney Foundation
  • 1993
Development of a test to evaluate the transtubular potassium concentration gradient in the cortical collecting duct in vivo.
The TTKG fell to unity when amiloride was given, consistent with an abolition of the apparent TEPD in vivo by this drug, and results were obtained in non-diuretic rats.
The mechanism of action of amiloride.
Amiloride induces a mild natriuresis as well as antikaliuretic effect and this effect is most likely a result of hyperpolarization of the apical plasma membrane and decrease in the electrochemical driving force for potassium movement across the apICAL membrane into the urinary space.
Brief report: trimethoprim-induced hyperkalemia in a patient with AIDS.
It is found that hyperkalemia develops in 20 to 53 percent of patients with AIDS while they are receiving high doses of trimethoprim in combination with sulfamethoxazole or dapsone for the treatment of Pneumocystis carinii pneumonia.