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indapamide 2.5 mg tablet (generic lozol)

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Like the thiazide diuretics, indapamide is used in the management of edema and salt retention associated with heart failure and other causes. Usual dosages of indapamide reportedly are about as effective as usual dosages of thiazide diuretics in patients with edema. In acute, severe left-sided heart failure, more potent diuretics such as bumetanide or furosemide should be used initially.

Although therapy with indapamide, like the thiazide diuretics, may be appropriate in the management of edema of pathologic origin during pregnancy when clearly needed, routine use of diuretics in otherwise healthy pregnant women is irrational. Use of diuretics for the management of edema of physiologic and mechanical origin during pregnancy generally is not warranted. Dependent edema secondary to restriction of venous return by the expanded uterus should be managed by elevating the lower extremities and/or by wearing support hose; use of diuretics in these pregnant women is inappropriate. In rare cases when the hypervolemia associated with normal pregnancy results in edema that produces extreme discomfort, a short course of diuretic therapy may provide relief and may be considered when other methods (e.g., decreased sodium intake, increased recumbency) are ineffective. Diuretics will not prevent the development of toxemia, nor is there evidence that diuretics have a beneficial effect on the overall course of established toxemia. For further information on precautions associated with use of indapamide during pregnancy, see Cautions: Pregnancy, Fertility, and Lactation.

Heart Failure

Indapamide is used in the management of edema associated with heart failure. Most experts state that all patients with symptomatic heart failure who have evidence for, or a history of, fluid retention generally should receive diuretic therapy in conjunction with moderate sodium restriction, an agent to inhibit the renin-angiotensin-aldosterone (RAA) system (e.g., angiotensin converting enzyme [ACE] inhibitor, angiotensin II receptor antagonist, angiotensin receptor-neprilysin inhibitor [ARNI]), a β-adrenergic blocking agent (β-blocker), and in selected patients, an aldosterone antagonist. Some experts state that because of limited and inconsistent data, it is difficult to make precise recommendations regarding daily sodium intake and whether it should vary with respect to the type of heart failure (e.g., reduced versus preserved ejection fraction), disease severity (e.g., New York Heart Association [NYHA] class), heart failure-related comorbidities (e.g., renal dysfunction), or other patient characteristics (e.g., age, race). The American College of Cardiology Foundation (ACCF) and American Heart Association (AHA) state that limiting sodium intake to 1.5 g daily in patients with ACCF/AHA stage A or B heart failure may be reasonable. While data currently are lacking to support recommendation of a specific level of sodium intake in patients with ACCF/AHA stage C or D heart failure, ACCF and AHA state that limiting sodium intake to some degree (e.g., less than 3 g daily) in such patients may be considered for symptom improvement.

Diuretics play a key role in the management of heart failure because they produce symptomatic benefits more rapidly than any other drugs, relieving pulmonary and peripheral edema within hours or days compared with weeks or months for cardiac glycosides, ACE inhibitors, or β-blockers. However, since there are no long-term studies of diuretic therapy in patients with heart failure, the effects of diuretics on morbidity and mortality in such patients are not known. Although there are patients with heart failure who do not exhibit fluid retention in the absence of diuretic therapy and even may develop severe volume depletion with low doses of diuretics, such patients are rare and the unique pathophysiologic mechanisms regulating their fluid and electrolyte balance have not been elucidated.

Most experts state that loop diuretics (e.g., bumetanide, ethacrynic acid, furosemide, torsemide) are the diuretics of choice for most patients with heart failure. However, thiazides may be preferred in some patients with concomitant hypertension because of their sustained antihypertensive effects. For additional information,


Indapamide is used in the management of hypertension. Indapamide's efficacy in hypertensive patients is similar to that of the thiazide diuretics. Indapamide has been used as monotherapy or in combination with other classes of antihypertensive agents.

For additional information on the role of diuretics in antihypertensive drug therapy and information on overall principles and expert recommendations for treatment of hypertension, .

Dosage and Administration


Indapamide is administered orally as a single daily dose.


Dosage of indapamide should be adjusted according to individual requirements and response.


The usual initial adult dosage of indapamide for the management of edema associated with heart failure is 2.5 mg daily, given as a single daily dose in the morning. If response is inadequate, dosage may be increased to 5 mg daily given as a single dose after 1 week. While higher dosages have been employed, those exceeding 5 mg daily did not appear to result in further improvement in heart failure, but were associated with an increased risk of hypokalemia. Similar dosages have been used in the management of edema from other causes. Experts state that diuretics should be administered at a dosage sufficient to achieve optimal volume status and relieve congestion without inducing an excessively rapid reduction in intravascular volume, which could result in hypotension, renal dysfunction, or both.


Usual Dosage

The panel members appointed to the Eighth Joint National Committee on the Prevention, Detection, and Treatment of High Blood Pressure (JNC 8 expert panel) state that evidence-based dosing information (i.e., dosages shown in randomized controlled trials to reduce complications of hypertension) should be used when available to determine target dosages of antihypertensive agents. Based on such information, an initial adult indapamide dosage of 1.25 mg once daily and a target dosage of 1.25-2.5 mg once daily are recommended. The manufacturer states that the usual initial adult dosage of indapamide for the management of hypertension is 1.25 mg daily, given as a single daily dose in the morning; if response is inadequate, dosage may be increased at 4-week intervals to 2.5 mg daily and subsequently to 5 mg daily. While higher dosages have been employed, those exceeding 5 mg daily did not appear to result in further improvement in blood pressure control, but were associated with an increased risk of hypokalemia. Target dosages of antihypertensive agents generally can be achieved within 2-4 weeks, but it may take up to several months. Antihypertensive therapy should be titrated until goal blood pressure is achieved.

If an adequate blood pressure response is not achieved with indapamide monotherapy, another antihypertensive agent with demonstrated benefit may be added; if goal blood pressure is still not achieved with the use of 2 antihypertensive agents at optimal dosages, a third drug may be added.

When concomitant therapy with other antihypertensive agents is required, the usual dose of the other agent may need to be reduced initially by up to 50%; subsequent dosage adjustments should be based on blood pressure response.

In patients who experience intolerable adverse effects with indapamide, dosage reduction should be considered; if adverse effects worsen or fail to resolve, it may be necessary to discontinue the diuretic and switch to another class of antihypertensive agent.

Blood Pressure Monitoring and Treatment Goals

Careful monitoring of blood pressure during initial titration or subsequent upward adjustment in dosage of indapamide is recommended.

The goal of hypertension management and prevention is to achieve and maintain optimal control of blood pressure; specific target levels of blood pressure should be individualized based on consideration of multiple factors, including patient age and comorbidities, and the currently available evidence from clinical studies.

For additional information on initiating and adjusting indapamide dosage in the management of hypertension, .

Dosage in Renal Impairment

Adjustment of indapamide dosage in patients with renal impairment does not appear to be necessary; however, additional experience with the drug in these patients is needed.


Indapamide shares many of the toxic potentials of the thiazide diuretics and the usual precautions of these agents should be observed. In therapeutic dosage, indapamide usually is well tolerated and has a low incidence of adverse effects. The incidence and severity of adverse reactions may occasionally be obviated by a reduction in dosage. Adverse reactions requiring discontinuance of indapamide therapy occur in 2-10% of patients.

Fluid, Electrolyte, and Renal Effects

Indapamide-induced diuresis may result in fluid and electrolyte disturbances.

One of the most common adverse effects of indapamide is hypokalemia. In most patients, hypokalemia is not severe or progressive but reportedly causes symptoms in 3-7% of patients receiving the drug. Electrolyte disturbances are particularly likely to occur in patients receiving parenteral fluids, those experiencing excessive vomiting and/or diarrhea, those whose salt intake is restricted, and those with diseases subject to electrolyte disorders (e.g., heart failure, renal diseases, hepatic cirrhosis and ascites). Potassium depletion is particularly likely to occur in patients with hyperaldosteronism, hepatic cirrhosis and ascites, low dietary-potassium intake, or potassium-losing renal diseases; in patients receiving potassium-depleting drugs (e.g., corticosteroids, corticotropin); when large dosages of indapamide (i.e., greater than 5 mg daily) are used; or when diuresis is brisk. Hypokalemia may require particular attention in geriatric patients, in patients receiving a cardiac glycoside (e.g., digoxin) concomitantly, and in those with a history of ventricular arrhythmias or other conditions in which hypokalemia is considered to represent a risk. Supplemental therapy with potassium chloride (including potassium-containing salt substitutes) may be necessary for prevention of hypokalemia and/or metabolic alkalosis in some patients receiving indapamide. The manufacturer states that the safety and efficacy of concurrent use of a potassium-sparing diuretic (e.g., amiloride, triamterene) for the prevention of hypokalemia have not been determined to date.

Hypochloremic alkalosis may occur with hypokalemia, especially in patients with renal or liver disease, but usually is mild and requires no specific treatment. Patients with other losses of potassium and chloride such as those with vomiting, diarrhea, GI drainage, excessive sweating, paracentesis, or potassium-losing renal diseases may be at particular risk for developing metabolic alkalosis.

Dilutional hyponatremia may occasionally occur or be aggravated during indapamide therapy. Such hyponatremia usually develops insidiously during chronic therapy and is asymptomatic and of modest degree, and, in such cases, serum sodium concentrations return rapidly to within the normal range following withdrawal of the diuretic, water restriction, and potassium and/or magnesium supplementation. However, severe hyponatremia (serum sodium concentration less than 120 mEq/L) can occur rarely. Geriatric patients, especially females who are underweight, have poor oral intake of fluid and electrolytes, and/or excessive intake of low-sodium nutritional supplements, may be at increased risk of dilutional hyponatremia induced by diuretics. Dilutional hyponatremia most commonly occurs in patients with edematous disorders and usually is treated by restriction of fluid intake (e.g., 500 mL/day) and withdrawal of the diuretic. Sodium chloride should not be administered unless the hyponatremia is life threatening or actual sodium depletion is documented. If sodium chloride is administered to correct severe, symptomatic hyponatremia, care should be taken to avoid early overcorrection to normonatremia or hypernatremia since resultant rapid osmolar changes may be associated with the development of central pontine myelinolysis. Therefore, although prognosis appears to depend on rapid correction of severe hyponatremia during the first 1 or 2 days, such correction initially should only be to a state of mild hyponatremia.

Increases in serum creatinine concentration have occurred in less than 5% of patients receiving indapamide but were not clinically important. Increased BUN also has been reported in less than 5% of patients and appears to be associated with dehydration. Although slight increases in BUN and serum creatinine concentration have been reported in hypertensive patients with renal impairment receiving the drug, these changes were not substantially different from placebo.

Hyperuricemia occurs in some patients receiving indapamide. Hyperuricemia secondary to diuretic therapy usually is asymptomatic and rarely leads to clinical gout. If therapy is required, hyperuricemia and gout may be treated with a uricosuric agent.

Metabolic Effects

Although indapamide appears to have little effect on serum triglyceride, total cholesterol, high-density lipoprotein (HDL), very low-density lipoprotein (VLDL), and low-density lipoprotein (LDL) concentrations, the drug has increased serum total cholesterol in some patients and long-term data are limited. Thiazide diuretics cause a modest long-term increase in serum total cholesterol, low-density lipoprotein-cholesterol, and triglyceride concentrations and, although there is no evidence to date that similar increases occur during long-term indapamide therapy, the possibility that these increases could occur during long-term indapamide therapy should be considered.

Hyperglycemia and glycosuria have been reported in less than 5% of patients receiving indapamide. The drug has been associated with decreased glucose tolerance in a few patients. The possibility that indapamide, like thiazide diuretics, may impair glucose tolerance should be considered during therapy with the drug. Diabetes may become manifest during therapy with indapamide in patients with a history of impaired glucose tolerance (latent diabetes).(See Cautions: Precautions and Contraindications.)

Other Adverse Effects

Adverse effects of indapamide other than electrolyte and metabolic disturbances are infrequent. Adverse nervous system effects, including headache, dizziness, fatigue, weakness, lethargy, muscle cramps or spasm, numbness of the extremities, nervousness, tension, anxiety, irritability, and agitation, occur in 5% or more of patients receiving indapamide. Lightheadedness, drowsiness, vertigo, insomnia, depression, tingling of the extremities, and blurred vision occur in less than 5% of patients.

Dermatologic reactions occurring in less than 5% of patients receiving indapamide include rash (e.g., erythematous, maculopapular, morbilliform), urticaria, pruritus, and vasculitis. In some cases, rash was accompanied by fever and/or dysuria. Rash generally resolves within 2 weeks after discontinuance of the drug, usually without specific therapy, although antihistamines occasionally have been used. Erythema multiforme and epidermal necrolysis have been reported rarely.

GI reactions reported with indapamide include anorexia, abdominal pain or cramps, constipation, diarrhea, gastric irritation, nausea, and vomiting. These GI reactions occur in less than 5% of patients. Orthostatic hypotension, premature ventricular depolarizations, irregular heart beat, and palpitation have been reported in less than 5% of patients receiving indapamide. Frequency of urination, nocturia, and polyuria also have been reported in less than 5% of patients receiving the drug.

Other adverse reactions attributed to indapamide in less than 5% of patients include impotence, reduced libido, rhinorrhea, flushing, weight loss, and dry mouth. Hepatitis, which resolved following discontinuance of the drug, has been reported in at least one patient during indapamide therapy.

The possibility that other adverse effects associated with thiazide diuretic therapy may occur during indapamide therapy should be considered. These include jaundice (intrahepatic cholestatic type), sialadenitis, xanthopsia, photosensitivity, purpura, necrotizing angiitis, fever, respiratory distress (including pneumonitis), anaphylactoid reactions, hematologic reactions (e.g., agranulocytosis, leukopenia, thrombocytopenia, aplastic anemia), and hypercalcemia and hypophosphatemia.

Precautions and Contraindications

Electrolyte disturbances such as hyponatremia, hypokalemia, or hypochloremic alkalosis may occur during indapamide therapy. Patients receiving the drug should be observed carefully for electrolyte depletion, especially hypokalemia. Patients should be informed of the signs and symptoms of electrolyte imbalance and instructed to contact their physician if dryness of mouth, thirst, weakness, lethargy, drowsiness, restlessness, oliguria, hypotension, tachycardia, GI disturbance, or muscle pains or cramps occur. Periodic determinations of serum electrolyte concentrations (particularly potassium, sodium, chloride, and bicarbonate) should be performed and measures to maintain normal serum concentrations should be instituted if necessary. Supplemental therapy with potassium chloride may be used if necessary to prevent or treat hypokalemia and/or metabolic alkalosis.

Prevention of hypokalemia is particularly important when large dosages of indapamide are used (i.e., 5 mg or more daily) or diuresis is brisk; for patients receiving cardiac glycosides or potassium-depleting drugs (e.g., corticosteroids, corticotropin) concomitantly; and for those with hepatic cirrhosis and ascites or with hyperaldosteronism, potassium-losing renal diseases, or other conditions (e.g., history of ventricular arrhythmias) in which hypokalemia is considered to represent a risk. Periodic determination of serum electrolyte concentrations is particularly important in patients experiencing excessive vomiting and/or diarrhea, those receiving parenteral fluids, those with diseases subject to electrolyte disorders, and those with restricted sodium intake. Patients with edematous conditions are at increased risk of developing dilutional hyponatremia.

Indapamide should be used with caution in patients with severe renal diseases, because reduced plasma volume accompanied by decreases in glomerular filtration rate may precipitate azotemia. If progressive renal impairment becomes evident as indicated by rising nonprotein nitrogen, BUN, or serum creatinine concentrations, consideration should be given to interrupting or discontinuing indapamide therapy. Periodic determinations of renal function (e.g., BUN, serum creatinine) should be performed in patients receiving the drug.

Indapamide also should be used with caution in patients with impaired hepatic function or progressive liver disease, particularly when serum potassium deficiency exists, since drug-induced alterations in fluid and electrolyte balance may precipitate hepatic coma.

Blood glucose concentration should be determined periodically during indapamide therapy, especially in patients with known or suspected (e.g., marginally impaired glucose tolerance) diabetes mellitus.(See Cautions: Metabolic Effects.)

Like the thiazide diuretics, indapamide should be used with caution in patients with hyperparathyroidism or thyroid disorders. Although indapamide has not been shown to cause clinically important changes in calcium or phosphate excretion or serum protein-bound iodine concentrations, these changes have been observed with thiazide diuretics and the possibility that they may occur with indapamide should be considered. If hypercalcemia and hypophosphatemia occur during indapamide therapy, the drug should be discontinued before parathyroid function tests are performed. Because thiazide diuretics may exacerbate systemic lupus erythematosus, the possibility of this adverse effect occurring with indapamide should be considered. Indapamide also should be used with caution in sympathectomized patients, since the hypotensive effect of the drug may be enhanced in these patients.

Indapamide is contraindicated in patients with anuria and in those who are allergic to indapamide or other sulfonamide derivatives.

Pediatric Precautions

Safety and efficacy of indapamide in children have not been established. For information on overall principles and expert recommendations for treatment of hypertension in pediatric patients, .

Mutagenicity and Carcinogenicity

It is not known whether indapamide is mutagenic or carcinogenic in humans. There was no evidence of carcinogenicity in lifetime (21-24 months) studies in mice and rats at oral dosages up to 100 mg/kg daily. In vitro tests to determine the mutagenic potential of the drug have not been performed to date.

Pregnancy, Fertility, and Lactation


Indapamide should not be used routinely in pregnant women with mild edema who are otherwise healthy. Risks to the fetus associated with use of indapamide may include fetal or neonatal jaundice or thrombocytopenia and possibly other adverse effects associated with use of the drug in adults. There are no adequate and controlled studies to date using indapamide in pregnant women, and the drug should be used during pregnancy only when clearly needed.(See Uses: Edema.)

Diuretics are considered second-line agents for control of chronic hypertension in pregnant women; if initiation of antihypertensive therapy is necessary during pregnancy, other antihypertensive agents (i.e., methyldopa, nifedipine, labetalol) are preferred.

Diuretics are not recommended for prevention or management of gestational hypertension or preeclampsia.


Reproduction studies in rats, mice, and rabbits at dosages up to 6250 times the usual human dosage have not revealed evidence of impaired fertility or harm to the fetus.


It is not known whether indapamide is distributed into human milk. The manufacturers state that if use of indapamide is considered essential in lactating women, nursing should be discontinued; however, the drug is considered to be compatible with breastfeeding.

Drug Interactions

Drugs Affected by or Causing Potassium Depletion

In patients receiving a cardiac glycoside (e.g., digoxin), electrolyte disturbances produced by indapamide (principally hypokalemia) predispose the patient to digitalis toxicity. Therefore, it is particularly important that hypokalemia be prevented in patients receiving indapamide and a cardiac glycoside concomitantly. Periodic electrolyte determinations should be performed in patients receiving a thiazide and a cardiac glycoside, and correction of hypokalemia undertaken if warranted.

Some drugs such as corticosteroids, corticotropin, and amphotericin B also cause potassium loss, and severe potassium depletion may occur when one of these drugs is administered during indapamide therapy.


Indapamide, like the thiazide diuretics, may reduce renal lithium clearance. Diuretic-induced reductions in renal lithium clearance may result in increased serum lithium concentrations and lithium toxicity. When thiazide diuretics are used concurrently with lithium, most clinicians recommend reducing lithium dosage by about 50% and carefully monitoring serum lithium concentrations. Indapamide and lithium generally should not be used concomitantly because of the increased risk of lithium toxicity. If concomitant therapy is necessary, serum lithium concentrations should be monitored carefully and dosage adjusted accordingly.

Hypotensive Agents

The hypotensive effects of most other hypotensive agents are increased by indapamide. This effect usually is used to therapeutic advantage in antihypertensive therapy, but patients should be observed for the possibility of potentiation of postural hypotension associated with other antihypertensive drugs. Dosage of the other hypotensive agent, and possibly both drugs, should be reduced when indapamide is added to an existing antihypertensive regimen.

Other Drugs

A decrease in arterial responsiveness to vasopressors (e.g., norepinephrine) may occur during indapamide therapy; however, the clinical importance of this interaction has not been established and the decrease is not sufficient to preclude effective therapeutic use of vasopressors.



Indapamide is rapidly and completely absorbed from the GI tract. In healthy adults, peak blood concentrations of 230-260 ng/mL are achieved within 2-2.5 hours after oral administration of a single 5-mg dose (as two 2.5-mg tablets) of indapamide. Absorption of the drug is not substantially affected by food or antacids.


Indapamide is lipophilic and widely distributed into body tissues. The drug reportedly has an apparent volume of distribution of approximately 25 L when calculated from blood concentrations or 60-110 L when calculated from plasma concentrations. Approximately 71-79% of indapamide is bound to plasma proteins. The drug preferentially and reversibly distributes into erythrocytes; the whole blood/plasma ratio is about 6 at the time of peak concentrations and about 3.5 eight hours after administration. The drug competitively and reversibly binds to carbonic anhydrase in erythrocytes.(See Pharmacology: Metabolic Effects.)

It is not known whether indapamide is distributed into milk or crosses the placenta in humans.


Blood concentrations of indapamide appear to decline in a biphasic manner. In adults with normal renal function, the drug has a terminal half-life (t½β) of 14-18 hours. The half-life of the drug is not prolonged in patients with impaired renal function.

Indapamide is extensively metabolized in the liver, principally to glucuronide and sulfate conjugates. Approximately 60% of a dose of the drug is excreted in urine within 48 hours; only 7% of a dose is excreted unchanged. Approximately 16-23% of the drug is excreted in feces, probably via biliary elimination.

Indapamide is not removed from circulation by hemodialysis.

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