Diuretics and lithium

Because CBZ can cause hyponatremia, it should be used cautiously in patients on a salt-restricted diet ( 373). Hyponatremia is rarely clinically significant when sodium values are above 125 mmol/L. Low sodium levels, as well as concomitant diuretic and lithium users, may predispose to the development of the syndrome of inappropriate ADH. Since CBZ enhances the effects of ADH, it can lead to impairment of free water clearance from the body. Older patients are at higher risk and should be closely monitored for this adverse effect which can be managed by dose reduction of CBZ. More severe cases, however, usually require switching to... 

Pyevich D, Bogenschutz MP. Herbal diuretics and lithium toxicity. Am J Psychiatr 2001 158 1329. 

Pyevich D, Bc enschutz MP Herbal diuretics and lithium toxicity Am J Psychiatry (2001) 158,1329... 

Thiazide diuretics, calcium-containing antacids, vitamin D, and lithium... 

Patients at increased risk of NSAID-induced gastrointestinal adverse effects (e.g., dyspepsia, peptic ulcer formation, and bleeding) include the elderly, those with peptic ulcer disease, coagulopathy, and patients receiving high doses of concurrent corticosteroids. Nephrotoxicity is more common in the elderly, patients with creatinine clearance values less than 50 mL/minute, and those with volume depletion or on diuretic therapy. NSAIDs should be used with caution in patients with reduced cardiac output due to sodium retention and in patients receiving antihypertensives, warfarin, and lithium. 

Lithium reduces the kidney s ability to concentrate urine and may cause a nephrogenic diabetes insipidus with low urine specific gravity and low osmolality polyuria (urine volume greater than 3 L/day). This may be treated with loop diuretics, thiazide diuretics, or triamterene. If a thiazide diuretic is used, lithium doses should be decreased by 50% and lithium and potassium levels monitored. 

Lithium toxicity can occur as a result of intentional overdose therefore, care must be taken when administering lithium to potentially suicidal patients with BPAD. Inadvertent lithium toxicity may also occur. For example, diuretics and nonsteroidal anti-inflammatory drugs such as ibuprofen (Advil, Motrin) slow the excretion of lithium and can lead to accidental toxicity. Consequently, the patient should be advised not to take such commonly available medications while treated with lithium. In addition, dehydration resulting from varied causes such as diarrhea, vomiting, and profuse sweating can lead to accidental lithium toxicity. One should advise the patient who takes lithium to be careful to remain well hydrated at all times and to contact his/her physician if any medical condition arises that may cause rapid fluid losses (e.g., stomach virus, high fevers). 

Drugs that may affect ACEIs may include antacids, capsaicin, indomethacin, phenothiazines, probenecid, and rifampin. Drugs that may be affected by ACEIs include allopurinol, digoxin, lithium, potassium preparations/potassium-sparing diuretics, and tetracycline. 

Lithium intoxication can be precipitated by the use of diuretics, particularly thiazides and metola-zone, and ACE inhibitors. NSAIDs can also precipitate lithium toxicity, mainly due to NSAID inhibition of prostaglandin-dependent renal excretion mechanisms. NSAIDs also impair renal function and cause sodium and water retention, effects which can predispose to interactions. Many case reports describe the antagonistic effects of NSAIDs on diuretics and antihypertensive drugs. The combination of triamterene and indomethacin appears particularly hazardous as it may result in acute renal failure. NSAIDs may also interfere with the beneficial effects of diuretics and ACE inhibitors in heart failure. It is not unusual to see patients whose heart failure has deteriorated in spite of increased doses of frusemide who are also concurrently taking an NSAID. 

Many interactions with lithium have been described. Thiazide and loop diuretics decrease lithium excretion predisposing to serious lithium toxicity. Also non-steroidal anti-inflammatory agents, especially indomethacin can increase the risks for lithium toxicity due to decreased renal excretion. 

Amiloride Blocks epithelial sodium channels in collecting tubules Reduces Na retention and wasting increases lithium clearance Hypokalemia from other diuretics reduces lithium-induced polyuria Orally active duration 24 h Toxicity Hyperkalemic metabolic acidosis... 

Drug Interactions Other antihypertensive agents Carbamazepine (vasodilators, ACE inhibitors, Rifampin diuretics, and beta-blockers) Phenobarbital Digoxin Cyclosporine Disopyramide Theophylline Flecainide Inhalation anesthetics Quinidine Neuromuscular blocking agents Cimetidine Lithium ... 

Lithium + diuretics — reduced lithium clearance and raised plasma lithium concentration thereby enhancing toxicity. 

Before the introduction of specific vasopressin receptor antagonists, pharmacological treatments for hyponatremia centered on the use of loop diuretics and nonspecific inhibitors of vasopressin signaling, such as lithium carbonate and demeclocycline.11 The utility of such therapies has been limited by a range of sideeffects. Loop diuretic use can result in electrolyte imbalances and suffers from poor response predictability.11 Lithium carbonate suffers from a low therapeutic index and a risk of renal damage as well as limited effectiveness in many patients. Lithium carbonate has therefore been nearly completely supplanted by demeclocycline, a tetracycline antibiotic, in the treatment of chronic hyponatremia.12 Demeclocycline use is itself limited by its nephrotoxicity (particularly in cirrhotic patients), ability to cause reversible uremia, and ability to induce photosensitivity.1,11... 

Stokke ES, Ostensen J, Hartmann A, Kiil F. Loop diuretics reduce lithium reabsorption without affecting bicarbonate and phosphate reabsorption. Acta Physiol Scand 1990 140(l) lll-8. 

LOOP DIURETICS ANTIDEPRESSANTS-LITHIUM t plasma concentrations of lithium, with risk of toxic effects L renal excretion of lithium Monitor clinically and by measuring blood lithium levels for lithium toxicity. Loop diuretics are safer than thiazides... 

Acetazolamide, and probably other diuretics which inhibit carbonic anhydrase, cause a strong inhibition of proximal NaHCOg reabsorption and lithium reabsorption. However, unlike loop diuretics, acetazolamide does not interfere with tubuloglomerular feedback and causes a 20% decrease in glomerular filtration rate. The increase in absolute lithium excretion is somewhat lower than that caused by loop diuretics [22]. Colussi et al. [25] reported the effect of furosemide and acefazola-mide to be additive, indicating a dual site of action (i.e., inhibition of lithium reabsorption in both the proximal tubule and the loop of Henle). 

Michimata M, Fujita S, ArakiT, Mizukami K, Kazama I, Muramatsu Y, Suzuki M, kImuraT, Sasaki Ss, Imal Y, Matsubara M. Reverse pharmacological effect of loop diuretics and altered rBSCl expression In rats with lithium nephropathy. Kidney Int 2003 63(1 ) 165-171. 

Forrest J Jr. Lithium-induced polyuria cellular mechanisms and response to diuretics. In Lithium - controversies and unresolved Issues. Cooper TB, Gershon S, Kline NS (editors). Excerpta Medica, Amsterdam 1979 p. 632-641. 

Many drugs and other chemicals can adversely affect renal function by directly or indirectly affecting the reabsorption of electrolytes and water in the kidney. Chlorpropamide can enhance the secretion of ADH and promote the water conservation actions of the hormone, while lithium use can lead to a nephrogenic diabetes insipidus. NSAIDs block the formation of renal prostaglandins, which can result in hyperkalemia. Hyperkalemia may also result from the use of beta blockers, potassium-sparing diuretics, and cyclosporine. 

Ibuprofen reduces the excretion of lithium and can raise plasma concentrations to toxic levels. It may also antagonise the diuretic and antihypertensive effects of diuretics, and should not be recommended to patients taking these drugs. 

Traveler s diarrhea is identified by multiple names depending on where the disease occurs, but all describes the clinical syndrome manifested by malaise, anorexia, and abdominal cramps followed by the sudden onset of diarrhea that incapacitates many travelers. In particular, an increased risk lies with North Americans and northern Europeans traveling to Latin America, southern Europe, Africa, and Asia. The highest risk is observed with patients with immunocompromised conditions, achlorhydria, or inflammatory bowel disease and people taking diuretics, digoxin, lithium, or insulin (because of the need for appropriate hydration). Overall, an estimated 20% to 50% of people traveling to high-risk areas will develop the illness. 

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