Amiloride Trimethoprim

There is a risk of acute renal failure when iodi-nated contrast material that is used for radiological studies is administered with metformin. Metformin therapy is stopped for 48 hours before and after radiological studies using iodinated material. Alcohol, amiloride, digoxin, morphine, procainamide, quini-dine, quinine ranitidine, triamterene, trimethoprim, vancomycin, cimetidine, and furosemide all increase the risk of hypoglycemia. There is an increased risk of lactic acidosis when metformin is administered with the glucocorticoids. 

Drugs that can precipitate lactic acidosis in patients taking metformin include ACE inhibitors, thiazide diuretics, NSAIDs, and drugs such as furosemide, nifedipine, cimetidine, amiloride, triamterene, trimethoprim, and digoxin, which are all secreted in the renal tubules, compete with metformin, and can contribute to increased plasma metformin concentrations (76). 

This interaction may be due to an amiloride-like diuretic effect of trimethoprim, causing lithium retention. 

Trimethoprim has the same effect on the kidney as amiloride, whose combined use with lithium can cause a raised serum lithium concentration. 

Trimethoprim (SED-14, 675) is structurally similar to amiloride and can cause severe hyperkalemia if co-prescribed with potassium-sparing diuretics (10). This is a particularly important interaction in patients with AIDS. 

The use of fixed combination of a thiazide and a potassium-sparing drug, often Moduretic (hydrochlorothiazide 50 mg with amiloride 5 mg), has been consistently implicated in diuretic-induced hyponatremia. Treatment with chlorpropamide (200-800 mg/day) along with Moduretic has precipitated hyponatremia in several cases (96). Simultaneous use of Moduretic with trimethoprim has also been reported to increase the risk (97). The mechanism appears to be impairment of the clearance of free water, resulting in dilutional hyponatremia. Whether... 

Concurrent acidosis in patients with trimethoprim-induced hyperkalemia is uncommon, which could be explained if the action of trimethoprim, like that of amiloride, is hmited to the cortical collecting tubule but does not affect the medullary collecting tubule, which has a large capacity to secrete hydrogen ions and may therefore prevent the development of acidosis. Predisposing factors for the rare adverse effect of renal tubular acidosis in this case may have been aldosterone deficiency or resistance, medullary dysfunction of sickle cell anemia, and renal insufficiency. All these factors could contribute to impaired renal handling of secretion of hydrogen ions (72). 

Transporter absorptive effects predominant Examples. Acyclovir, Amiloride -, Amoxicillin Atenolol Atropine, Bidisomide Bisphosphonates Captoprit, Cefazolin Cetirizine Cimetidine Ciprofloxacin, Cloxacillin Dicloxacillin Erythromycin - -, Famotidine Fexofenadine Folinic acid Furosemide, Ganciclovir Hydrochlorothiazide, Lisinopril Metformin Methotrexate, Nadolol Penicillins Pravastatin Ranitidine Tetracycline Trimethoprim Valsartan Zalcitabine... 

Excessively low sodium levels have been seen in a few patients taking hydrochlorothiazide with amiloride or triamterene when they were given trimethoprim or co-trimoxazole. Trimethoprim may cause hyperkalaemia and this may be additive with potassium-sparing diuretics, including the aldosterone antagonists. 

A 75-year-old woman with multiple medical conditions taking methyl-dopa, levothyroxine and co-amilozide (hydrochlorothiazide with amiloride) developed nausea and anorexia, and was found to have hyponatraemia (plasma sodium 107 mmol/L), within 4 days of starting to take trimethoprim 200 mg twice daily. The problem resolved when the diuretics and trimethoprim were stopped. When re-challenged 4 months later with trimethoprim, hyponatraemia did not occur, but it developed rapidly when co-amilozide was also restarted. The authors of this report say that they have seen several other patients who developed hyponatraemia within 4 to 12 days of starting trimethoprim or co-trimoxazole, all of whom were elderly and all but one of whom were taking a diuretic [unnamed]. ... 

Not established. Thiazide diuretics combined with potassium-sparing diuretics are said to be particularly liable to cause hyponatraemia. Trimethoprim can also cause hyperkalaemia , by blocking amiloride-sensitive sodium channels in the collecting duct (this produces a similar effect to that of a potassium-sparing diuretic). It seems likely that these adverse effects can be additive with the effects of other drugs. 

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