Drug Interactions between Effervescent Potassium / Chloride and valsartan

If you are taking valsartan you should avoid potassium-containing salt substitutes or over-the-counter potassium supplements without first talking to your doctor. This can cause high levels of potassium in your blood. High levels of potassium can cause weakness, irregular heartbeat, confusion, tingling of the extremities, or feelings of heaviness in the legs. Call your doctor at once if you have any of these symptoms.

The use of potassium salts is contraindicated in patients with hyperkalemia, since a further increase in serum potassium concentration in such patients can lead to cardiac arrhythmias or arrest. Potassium therapy should be administered cautiously in patients with conditions predisposing to hyperkalemia, such as chronic renal failure, systemic acidosis, acute dehydration, hypoaldosteronism (e.g., due to primary adrenal insufficiency or congenital adrenal enzyme deficiency), uncontrolled diabetes mellitus, and extensive tissue breakdown (e.g., due to severe burns, intravascular hemolysis, tumor lysis syndrome, or rhabdomyolysis). Close monitoring of serum potassium concentrations is recommended, as potentially fatal hyperkalemia can develop rapidly and is often asymptomatic, manifested only by an increased potassium level (6.5 to 8 mEq/L) and characteristic electrocardiographic changes (peaking of T waves, loss of P waves, depression of ST segment, prolongation of the QT interval). Late manifestations include muscle paralysis and cardiovascular collapse from cardiac arrest (9 to 12 mEq/L). Continuous or serial electrocardiography may be appropriate in some patients during replacement therapy, particularly if given intravenously.

The use of potassium salts is contraindicated in patients with hyperkalemia, since a further increase in serum potassium concentration in such patients can lead to cardiac arrhythmias or arrest. Potassium therapy should be administered cautiously in patients with conditions predisposing to hyperkalemia, such as chronic renal failure, systemic acidosis, acute dehydration, hypoaldosteronism (e.g., due to primary adrenal insufficiency or congenital adrenal enzyme deficiency), uncontrolled diabetes mellitus, and extensive tissue breakdown (e.g., due to severe burns, intravascular hemolysis, tumor lysis syndrome, or rhabdomyolysis). Close monitoring of serum potassium concentrations is recommended, as potentially fatal hyperkalemia can develop rapidly and is often asymptomatic, manifested only by an increased potassium level (6.5 to 8 mEq/L) and characteristic electrocardiographic changes (peaking of T waves, loss of P waves, depression of ST segment, prolongation of the QT interval). Late manifestations include muscle paralysis and cardiovascular collapse from cardiac arrest (9 to 12 mEq/L). Continuous or serial electrocardiography may be appropriate in some patients during replacement therapy, particularly if given intravenously.

The use of potassium salts is contraindicated in patients with hyperkalemia, since a further increase in serum potassium concentration in such patients can lead to cardiac arrhythmias or arrest. Potassium therapy should be administered cautiously in patients with conditions predisposing to hyperkalemia, such as chronic renal failure, systemic acidosis, acute dehydration, hypoaldosteronism (e.g., due to primary adrenal insufficiency or congenital adrenal enzyme deficiency), uncontrolled diabetes mellitus, and extensive tissue breakdown (e.g., due to severe burns, intravascular hemolysis, tumor lysis syndrome, or rhabdomyolysis). Close monitoring of serum potassium concentrations is recommended, as potentially fatal hyperkalemia can develop rapidly and is often asymptomatic, manifested only by an increased potassium level (6.5 to 8 mEq/L) and characteristic electrocardiographic changes (peaking of T waves, loss of P waves, depression of ST segment, prolongation of the QT interval). Late manifestations include muscle paralysis and cardiovascular collapse from cardiac arrest (9 to 12 mEq/L). Continuous or serial electrocardiography may be appropriate in some patients during replacement therapy, particularly if given intravenously.

The use of potassium salts is contraindicated in patients with hyperkalemia, since a further increase in serum potassium concentration in such patients can lead to cardiac arrhythmias or arrest. Potassium therapy should be administered cautiously in patients with conditions predisposing to hyperkalemia, such as chronic renal failure, systemic acidosis, acute dehydration, hypoaldosteronism (e.g., due to primary adrenal insufficiency or congenital adrenal enzyme deficiency), uncontrolled diabetes mellitus, and extensive tissue breakdown (e.g., due to severe burns, intravascular hemolysis, tumor lysis syndrome, or rhabdomyolysis). Close monitoring of serum potassium concentrations is recommended, as potentially fatal hyperkalemia can develop rapidly and is often asymptomatic, manifested only by an increased potassium level (6.5 to 8 mEq/L) and characteristic electrocardiographic changes (peaking of T waves, loss of P waves, depression of ST segment, prolongation of the QT interval). Late manifestations include muscle paralysis and cardiovascular collapse from cardiac arrest (9 to 12 mEq/L). Continuous or serial electrocardiography may be appropriate in some patients during replacement therapy, particularly if given intravenously.

The use of these agents is contraindicated in patients with a history of angioedema related to previous angiotensin-converting enzyme (ACE) inhibitor or angiotensin II receptor blocker (ARB) therapy or in patients with hereditary angioedema. Patients with a history of angioedema unrelated to these agents may be at increased risk of angioedema while receiving angiotensin II receptor (AR) antagonists. Patients should be advised to immediately report any signs or symptoms suggestive of angioedema (swelling of face, extremities, eyes, lips, or tongue, or difficulty swallowing or breathing) and to stop taking the medication until otherwise directed by their physician. Emergency therapy and/or measures to prevent airway obstruction are required for angioedema involving the tongue, glottis, or larynx. Treatment with angiotensin II receptor (AR) antagonists should be discontinued permanently if angioedema develops in association with therapy.

The use of potassium salts is contraindicated in patients with hyperkalemia, since a further increase in serum potassium concentration in such patients can lead to cardiac arrhythmias or arrest. Potassium therapy should be administered cautiously in patients with conditions predisposing to hyperkalemia, such as chronic renal failure, systemic acidosis, acute dehydration, hypoaldosteronism (e.g., due to primary adrenal insufficiency or congenital adrenal enzyme deficiency), uncontrolled diabetes mellitus, and extensive tissue breakdown (e.g., due to severe burns, intravascular hemolysis, tumor lysis syndrome, or rhabdomyolysis). Close monitoring of serum potassium concentrations is recommended, as potentially fatal hyperkalemia can develop rapidly and is often asymptomatic, manifested only by an increased potassium level (6.5 to 8 mEq/L) and characteristic electrocardiographic changes (peaking of T waves, loss of P waves, depression of ST segment, prolongation of the QT interval). Late manifestations include muscle paralysis and cardiovascular collapse from cardiac arrest (9 to 12 mEq/L). Continuous or serial electrocardiography may be appropriate in some patients during replacement therapy, particularly if given intravenously.

The use of potassium salts is contraindicated in patients with hyperkalemia, since a further increase in serum potassium concentration in such patients can lead to cardiac arrhythmias or arrest. Potassium therapy should be administered cautiously in patients with conditions predisposing to hyperkalemia, such as chronic renal failure, systemic acidosis, acute dehydration, hypoaldosteronism (e.g., due to primary adrenal insufficiency or congenital adrenal enzyme deficiency), uncontrolled diabetes mellitus, and extensive tissue breakdown (e.g., due to severe burns, intravascular hemolysis, tumor lysis syndrome, or rhabdomyolysis). Close monitoring of serum potassium concentrations is recommended, as potentially fatal hyperkalemia can develop rapidly and is often asymptomatic, manifested only by an increased potassium level (6.5 to 8 mEq/L) and characteristic electrocardiographic changes (peaking of T waves, loss of P waves, depression of ST segment, prolongation of the QT interval). Late manifestations include muscle paralysis and cardiovascular collapse from cardiac arrest (9 to 12 mEq/L). Continuous or serial electrocardiography may be appropriate in some patients during replacement therapy, particularly if given intravenously.

Potassium chloride liquid suspension contains the stool softener, docusate sodium, as a dispersing agent. Clinical studies with potassium chloride liquid suspension indicate that minor changes in stool consistency may be common though usually well tolerated. However, patients may rarely experience diarrhea or cramping abdominal pain. Patients with severe or chronic diarrhea or who are dehydrated ordinarily should not be prescribed potassium chloride liquid suspension.

Administration of potassium salts in severe dehydration may predispose to renal impairment. Therapy with potassium salts should be administered cautiously in patients with acute dehydration (e.g., due to severe or prolonged diarrhea or heat stress). Close monitoring of serum potassium concentrations is recommended, as potentially fatal hyperkalemia can develop rapidly and is often asymptomatic, manifested only by an increased potassium level (6.5 to 8 mEq/L) and characteristic electrocardiographic changes (peaking of T waves, loss of P waves, depression of ST segment, prolongation of the QT interval). Late manifestations include muscle paralysis and cardiovascular collapse from cardiac arrest (9 to 12 mEq/L). Continuous or serial electrocardiography may be appropriate in some patients during replacement therapy, particularly if given intravenously.

Administration of potassium salts in severe dehydration may predispose to renal impairment. Therapy with potassium salts should be administered cautiously in patients with acute dehydration (e.g., due to severe or prolonged diarrhea or heat stress). Close monitoring of serum potassium concentrations is recommended, as potentially fatal hyperkalemia can develop rapidly and is often asymptomatic, manifested only by an increased potassium level (6.5 to 8 mEq/L) and characteristic electrocardiographic changes (peaking of T waves, loss of P waves, depression of ST segment, prolongation of the QT interval). Late manifestations include muscle paralysis and cardiovascular collapse from cardiac arrest (9 to 12 mEq/L). Continuous or serial electrocardiography may be appropriate in some patients during replacement therapy, particularly if given intravenously.

Angiotensin II receptor (AR) antagonists can cause symptomatic hypotension in patients with an activated renin-angiotensin system, such as volume- and/or sodium-depleted patients. Therapy with AR antagonists should be administered cautiously in such patients and in those predisposed to hypovolemic or hyponatremic states (e.g., patients on diuretic therapy, especially if high doses were used or if recently instituted; those on dietary salt restriction; renal dialysis patients). Volume and/or sodium depletion should be corrected prior to initiating therapy with AR antagonists, and the patient should be hemodynamically stable. Ideally, patients at risk for excessive hypotension should initiate AR antagonist therapy under close medical supervision, preferably with a lower dose, and followed closely for the first 2 weeks of treatment and whenever the dosage of AR antagonist or diuretic is increased.

The use of potassium salts is contraindicated in patients with hyperkalemia, since a further increase in serum potassium concentration in such patients can lead to cardiac arrhythmias or arrest. Potassium therapy should be administered cautiously in patients with conditions predisposing to hyperkalemia, such as chronic renal failure, systemic acidosis, acute dehydration, hypoaldosteronism (e.g., due to primary adrenal insufficiency or congenital adrenal enzyme deficiency), uncontrolled diabetes mellitus, and extensive tissue breakdown (e.g., due to severe burns, intravascular hemolysis, tumor lysis syndrome, or rhabdomyolysis). Close monitoring of serum potassium concentrations is recommended, as potentially fatal hyperkalemia can develop rapidly and is often asymptomatic, manifested only by an increased potassium level (6.5 to 8 mEq/L) and characteristic electrocardiographic changes (peaking of T waves, loss of P waves, depression of ST segment, prolongation of the QT interval). Late manifestations include muscle paralysis and cardiovascular collapse from cardiac arrest (9 to 12 mEq/L). Continuous or serial electrocardiography may be appropriate in some patients during replacement therapy, particularly if given intravenously.

The use of potassium salts is contraindicated in patients with hyperkalemia, since a further increase in serum potassium concentration in such patients can lead to cardiac arrhythmias or arrest. Potassium therapy should be administered cautiously in patients with conditions predisposing to hyperkalemia, such as chronic renal failure, systemic acidosis, acute dehydration, hypoaldosteronism (e.g., due to primary adrenal insufficiency or congenital adrenal enzyme deficiency), uncontrolled diabetes mellitus, and extensive tissue breakdown (e.g., due to severe burns, intravascular hemolysis, tumor lysis syndrome, or rhabdomyolysis). Close monitoring of serum potassium concentrations is recommended, as potentially fatal hyperkalemia can develop rapidly and is often asymptomatic, manifested only by an increased potassium level (6.5 to 8 mEq/L) and characteristic electrocardiographic changes (peaking of T waves, loss of P waves, depression of ST segment, prolongation of the QT interval). Late manifestations include muscle paralysis and cardiovascular collapse from cardiac arrest (9 to 12 mEq/L). Continuous or serial electrocardiography may be appropriate in some patients during replacement therapy, particularly if given intravenously.

The coadministration of some angiotensin II receptor blocker agents with aliskiren is contraindicated in patients with diabetes.

Administration of potassium salts in severe dehydration may predispose to renal impairment. Therapy with potassium salts should be administered cautiously in patients with acute dehydration (e.g., due to severe or prolonged diarrhea or heat stress). Close monitoring of serum potassium concentrations is recommended, as potentially fatal hyperkalemia can develop rapidly and is often asymptomatic, manifested only by an increased potassium level (6.5 to 8 mEq/L) and characteristic electrocardiographic changes (peaking of T waves, loss of P waves, depression of ST segment, prolongation of the QT interval). Late manifestations include muscle paralysis and cardiovascular collapse from cardiac arrest (9 to 12 mEq/L). Continuous or serial electrocardiography may be appropriate in some patients during replacement therapy, particularly if given intravenously.

Potassium chloride liquid suspension contains the stool softener, docusate sodium, as a dispersing agent. Clinical studies with potassium chloride liquid suspension indicate that minor changes in stool consistency may be common though usually well tolerated. However, patients may rarely experience diarrhea or cramping abdominal pain. Patients with severe or chronic diarrhea or who are dehydrated ordinarily should not be prescribed potassium chloride liquid suspension.

Administration of potassium salts in severe dehydration may predispose to renal impairment. Therapy with potassium salts should be administered cautiously in patients with acute dehydration (e.g., due to severe or prolonged diarrhea or heat stress). Close monitoring of serum potassium concentrations is recommended, as potentially fatal hyperkalemia can develop rapidly and is often asymptomatic, manifested only by an increased potassium level (6.5 to 8 mEq/L) and characteristic electrocardiographic changes (peaking of T waves, loss of P waves, depression of ST segment, prolongation of the QT interval). Late manifestations include muscle paralysis and cardiovascular collapse from cardiac arrest (9 to 12 mEq/L). Continuous or serial electrocardiography may be appropriate in some patients during replacement therapy, particularly if given intravenously.

The use of all solid oral formulations of potassium is contraindicated in patients with arrested or delayed gastrointestinal (GI) transit, whether due to structural, pathological, or pharmacological causes. Potassium is irritating to the GI mucosa and may cause ulcerative and/or stenotic lesions during prolonged physical contact. Based on spontaneous adverse reaction reports, the frequency of small bowel lesions associated with enteric-coated preparations of potassium chloride is 40 to 50 per 100,000 patient-years, while that for wax matrix controlled-release formulations is less than one per 100,000 patient years. Esophageal ulceration has also been reported following administration of controlled-release formulations of potassium chloride in cardiac patients with esophageal compression due to enlarged left atrium. Potassium supplementation should be administered as a liquid preparation or as an aqueous suspension in patients with esophageal obstruction and/or delayed gastrointestinal transit time.

Because of ulcerogenic effects, oral potassium should be administered cautiously in patients with peptic ulcers or other upper gastrointestinal diseases associated with inflammation, bleeding, or perforation. Patients should be advised not to crush, chew, or break potassium tablets or capsules, and to take them with meals and a full glass of water or other liquid. Potassium liquids should be diluted prior to consumption.

The use of all solid oral formulations of potassium is contraindicated in patients with arrested or delayed gastrointestinal (GI) transit, whether due to structural, pathological, or pharmacological causes. Potassium is irritating to the GI mucosa and may cause ulcerative and/or stenotic lesions during prolonged physical contact. Based on spontaneous adverse reaction reports, the frequency of small bowel lesions associated with enteric-coated preparations of potassium chloride is 40 to 50 per 100,000 patient-years, while that for wax matrix controlled-release formulations is less than one per 100,000 patient years. Esophageal ulceration has also been reported following administration of controlled-release formulations of potassium chloride in cardiac patients with esophageal compression due to enlarged left atrium. Potassium supplementation should be administered as a liquid preparation or as an aqueous suspension in patients with esophageal obstruction and/or delayed gastrointestinal transit time.

Because of ulcerogenic effects, oral potassium should be administered cautiously in patients with peptic ulcers or other upper gastrointestinal diseases associated with inflammation, bleeding, or perforation. Patients should be advised not to crush, chew, or break potassium tablets or capsules, and to take them with meals and a full glass of water or other liquid. Potassium liquids should be diluted prior to consumption.

Administration of potassium salts may precipitate attacks in familial hyperkalemic periodic paralysis or paramyotonia congenita. Therapy with potassium preparations should be administered cautiously in patients with these conditions.

Administration of potassium salts may precipitate attacks in familial hyperkalemic periodic paralysis or paramyotonia congenita. Therapy with potassium preparations should be administered cautiously in patients with these conditions.

The use of all solid oral formulations of potassium is contraindicated in patients with arrested or delayed gastrointestinal (GI) transit, whether due to structural, pathological, or pharmacological causes. Potassium is irritating to the GI mucosa and may cause ulcerative and/or stenotic lesions during prolonged physical contact. Based on spontaneous adverse reaction reports, the frequency of small bowel lesions associated with enteric-coated preparations of potassium chloride is 40 to 50 per 100,000 patient-years, while that for wax matrix controlled-release formulations is less than one per 100,000 patient years. Esophageal ulceration has also been reported following administration of controlled-release formulations of potassium chloride in cardiac patients with esophageal compression due to enlarged left atrium. Potassium supplementation should be administered as a liquid preparation or as an aqueous suspension in patients with esophageal obstruction and/or delayed gastrointestinal transit time.

Because of ulcerogenic effects, oral potassium should be administered cautiously in patients with peptic ulcers or other upper gastrointestinal diseases associated with inflammation, bleeding, or perforation. Patients should be advised not to crush, chew, or break potassium tablets or capsules, and to take them with meals and a full glass of water or other liquid. Potassium liquids should be diluted prior to consumption.

The use of all solid oral formulations of potassium is contraindicated in patients with arrested or delayed gastrointestinal (GI) transit, whether due to structural, pathological, or pharmacological causes. Potassium is irritating to the GI mucosa and may cause ulcerative and/or stenotic lesions during prolonged physical contact. Based on spontaneous adverse reaction reports, the frequency of small bowel lesions associated with enteric-coated preparations of potassium chloride is 40 to 50 per 100,000 patient-years, while that for wax matrix controlled-release formulations is less than one per 100,000 patient years. Esophageal ulceration has also been reported following administration of controlled-release formulations of potassium chloride in cardiac patients with esophageal compression due to enlarged left atrium. Potassium supplementation should be administered as a liquid preparation or as an aqueous suspension in patients with esophageal obstruction and/or delayed gastrointestinal transit time.

Because of ulcerogenic effects, oral potassium should be administered cautiously in patients with peptic ulcers or other upper gastrointestinal diseases associated with inflammation, bleeding, or perforation. Patients should be advised not to crush, chew, or break potassium tablets or capsules, and to take them with meals and a full glass of water or other liquid. Potassium liquids should be diluted prior to consumption.

The use of all solid oral formulations of potassium is contraindicated in patients with arrested or delayed gastrointestinal (GI) transit, whether due to structural, pathological, or pharmacological causes. Potassium is irritating to the GI mucosa and may cause ulcerative and/or stenotic lesions during prolonged physical contact. Based on spontaneous adverse reaction reports, the frequency of small bowel lesions associated with enteric-coated preparations of potassium chloride is 40 to 50 per 100,000 patient-years, while that for wax matrix controlled-release formulations is less than one per 100,000 patient years. Esophageal ulceration has also been reported following administration of controlled-release formulations of potassium chloride in cardiac patients with esophageal compression due to enlarged left atrium. Potassium supplementation should be administered as a liquid preparation or as an aqueous suspension in patients with esophageal obstruction and/or delayed gastrointestinal transit time.

Because of ulcerogenic effects, oral potassium should be administered cautiously in patients with peptic ulcers or other upper gastrointestinal diseases associated with inflammation, bleeding, or perforation. Patients should be advised not to crush, chew, or break potassium tablets or capsules, and to take them with meals and a full glass of water or other liquid. Potassium liquids should be diluted prior to consumption.

Angiotensin II receptor (AR) antagonists can cause symptomatic hypotension in patients with an activated renin-angiotensin system, such as volume- and/or sodium-depleted patients. Therapy with AR antagonists should be administered cautiously in such patients and in those predisposed to hypovolemic or hyponatremic states (e.g., patients on diuretic therapy, especially if high doses were used or if recently instituted; those on dietary salt restriction; renal dialysis patients). Volume and/or sodium depletion should be corrected prior to initiating therapy with AR antagonists, and the patient should be hemodynamically stable. Ideally, patients at risk for excessive hypotension should initiate AR antagonist therapy under close medical supervision, preferably with a lower dose, and followed closely for the first 2 weeks of treatment and whenever the dosage of AR antagonist or diuretic is increased.

The use of potassium salts is contraindicated in patients with hyperkalemia, since a further increase in serum potassium concentration in such patients can lead to cardiac arrhythmias or arrest. Potassium therapy should be administered cautiously in patients with conditions predisposing to hyperkalemia, such as chronic renal failure, systemic acidosis, acute dehydration, hypoaldosteronism (e.g., due to primary adrenal insufficiency or congenital adrenal enzyme deficiency), uncontrolled diabetes mellitus, and extensive tissue breakdown (e.g., due to severe burns, intravascular hemolysis, tumor lysis syndrome, or rhabdomyolysis). Close monitoring of serum potassium concentrations is recommended, as potentially fatal hyperkalemia can develop rapidly and is often asymptomatic, manifested only by an increased potassium level (6.5 to 8 mEq/L) and characteristic electrocardiographic changes (peaking of T waves, loss of P waves, depression of ST segment, prolongation of the QT interval). Late manifestations include muscle paralysis and cardiovascular collapse from cardiac arrest (9 to 12 mEq/L). Continuous or serial electrocardiography may be appropriate in some patients during replacement therapy, particularly if given intravenously.

The use of potassium salts is contraindicated in patients with hyperkalemia, since a further increase in serum potassium concentration in such patients can lead to cardiac arrhythmias or arrest. Potassium therapy should be administered cautiously in patients with conditions predisposing to hyperkalemia, such as chronic renal failure, systemic acidosis, acute dehydration, hypoaldosteronism (e.g., due to primary adrenal insufficiency or congenital adrenal enzyme deficiency), uncontrolled diabetes mellitus, and extensive tissue breakdown (e.g., due to severe burns, intravascular hemolysis, tumor lysis syndrome, or rhabdomyolysis). Close monitoring of serum potassium concentrations is recommended, as potentially fatal hyperkalemia can develop rapidly and is often asymptomatic, manifested only by an increased potassium level (6.5 to 8 mEq/L) and characteristic electrocardiographic changes (peaking of T waves, loss of P waves, depression of ST segment, prolongation of the QT interval). Late manifestations include muscle paralysis and cardiovascular collapse from cardiac arrest (9 to 12 mEq/L). Continuous or serial electrocardiography may be appropriate in some patients during replacement therapy, particularly if given intravenously.

The use of all solid oral formulations of potassium is contraindicated in patients with arrested or delayed gastrointestinal (GI) transit, whether due to structural, pathological, or pharmacological causes. Potassium is irritating to the GI mucosa and may cause ulcerative and/or stenotic lesions during prolonged physical contact. Based on spontaneous adverse reaction reports, the frequency of small bowel lesions associated with enteric-coated preparations of potassium chloride is 40 to 50 per 100,000 patient-years, while that for wax matrix controlled-release formulations is less than one per 100,000 patient years. Esophageal ulceration has also been reported following administration of controlled-release formulations of potassium chloride in cardiac patients with esophageal compression due to enlarged left atrium. Potassium supplementation should be administered as a liquid preparation or as an aqueous suspension in patients with esophageal obstruction and/or delayed gastrointestinal transit time.

Because of ulcerogenic effects, oral potassium should be administered cautiously in patients with peptic ulcers or other upper gastrointestinal diseases associated with inflammation, bleeding, or perforation. Patients should be advised not to crush, chew, or break potassium tablets or capsules, and to take them with meals and a full glass of water or other liquid. Potassium liquids should be diluted prior to consumption.

The use of potassium salts is contraindicated in patients with hyperkalemia, since a further increase in serum potassium concentration in such patients can lead to cardiac arrhythmias or arrest. Potassium therapy should be administered cautiously in patients with conditions predisposing to hyperkalemia, such as chronic renal failure, systemic acidosis, acute dehydration, hypoaldosteronism (e.g., due to primary adrenal insufficiency or congenital adrenal enzyme deficiency), uncontrolled diabetes mellitus, and extensive tissue breakdown (e.g., due to severe burns, intravascular hemolysis, tumor lysis syndrome, or rhabdomyolysis). Close monitoring of serum potassium concentrations is recommended, as potentially fatal hyperkalemia can develop rapidly and is often asymptomatic, manifested only by an increased potassium level (6.5 to 8 mEq/L) and characteristic electrocardiographic changes (peaking of T waves, loss of P waves, depression of ST segment, prolongation of the QT interval). Late manifestations include muscle paralysis and cardiovascular collapse from cardiac arrest (9 to 12 mEq/L). Continuous or serial electrocardiography may be appropriate in some patients during replacement therapy, particularly if given intravenously.

The use of potassium salts is contraindicated in patients with hyperkalemia, since a further increase in serum potassium concentration in such patients can lead to cardiac arrhythmias or arrest. Potassium therapy should be administered cautiously in patients with conditions predisposing to hyperkalemia, such as chronic renal failure, systemic acidosis, acute dehydration, hypoaldosteronism (e.g., due to primary adrenal insufficiency or congenital adrenal enzyme deficiency), uncontrolled diabetes mellitus, and extensive tissue breakdown (e.g., due to severe burns, intravascular hemolysis, tumor lysis syndrome, or rhabdomyolysis). Close monitoring of serum potassium concentrations is recommended, as potentially fatal hyperkalemia can develop rapidly and is often asymptomatic, manifested only by an increased potassium level (6.5 to 8 mEq/L) and characteristic electrocardiographic changes (peaking of T waves, loss of P waves, depression of ST segment, prolongation of the QT interval). Late manifestations include muscle paralysis and cardiovascular collapse from cardiac arrest (9 to 12 mEq/L). Continuous or serial electrocardiography may be appropriate in some patients during replacement therapy, particularly if given intravenously.

Angiotensin II receptor (AR) antagonists can cause symptomatic hypotension in patients with an activated renin-angiotensin system, such as volume- and/or sodium-depleted patients. Therapy with AR antagonists should be administered cautiously in such patients and in those predisposed to hypovolemic or hyponatremic states (e.g., patients on diuretic therapy, especially if high doses were used or if recently instituted; those on dietary salt restriction; renal dialysis patients). Volume and/or sodium depletion should be corrected prior to initiating therapy with AR antagonists, and the patient should be hemodynamically stable. Ideally, patients at risk for excessive hypotension should initiate AR antagonist therapy under close medical supervision, preferably with a lower dose, and followed closely for the first 2 weeks of treatment and whenever the dosage of AR antagonist or diuretic is increased.

The use of all solid oral formulations of potassium is contraindicated in patients with arrested or delayed gastrointestinal (GI) transit, whether due to structural, pathological, or pharmacological causes. Potassium is irritating to the GI mucosa and may cause ulcerative and/or stenotic lesions during prolonged physical contact. Based on spontaneous adverse reaction reports, the frequency of small bowel lesions associated with enteric-coated preparations of potassium chloride is 40 to 50 per 100,000 patient-years, while that for wax matrix controlled-release formulations is less than one per 100,000 patient years. Esophageal ulceration has also been reported following administration of controlled-release formulations of potassium chloride in cardiac patients with esophageal compression due to enlarged left atrium. Potassium supplementation should be administered as a liquid preparation or as an aqueous suspension in patients with esophageal obstruction and/or delayed gastrointestinal transit time.

Because of ulcerogenic effects, oral potassium should be administered cautiously in patients with peptic ulcers or other upper gastrointestinal diseases associated with inflammation, bleeding, or perforation. Patients should be advised not to crush, chew, or break potassium tablets or capsules, and to take them with meals and a full glass of water or other liquid. Potassium liquids should be diluted prior to consumption.

The use of potassium salts is contraindicated in patients with severe renal impairment characterized by oliguria, anuria, or azotemia. Since potassium is excreted by the kidney, the administration of potassium salts in such patients, particularly by the intravenous route, may produce hyperkalemia and cardiac arrhythmias or arrest. Therapy with potassium salts should be administered cautiously in patients with diminished renal function or other conditions which impairs potassium excretion (e.g. adrenal insufficiency). Close monitoring of serum potassium concentrations is recommended, as potentially fatal hyperkalemia can develop rapidly and is often asymptomatic, manifested only by an increased potassium level (6.5 to 8 mEq/L) and characteristic electrocardiographic changes (peaking of T waves, loss of P waves, depression of ST segment, prolongation of the QT interval). Late manifestations include muscle paralysis and cardiovascular collapse from cardiac arrest (9 to 12 mEq/L). Continuous or serial electrocardiography may be appropriate in some patients during replacement therapy, particularly if given intravenously.

The use of potassium salts is contraindicated in patients with severe renal impairment characterized by oliguria, anuria, or azotemia. Since potassium is excreted by the kidney, the administration of potassium salts in such patients, particularly by the intravenous route, may produce hyperkalemia and cardiac arrhythmias or arrest. Therapy with potassium salts should be administered cautiously in patients with diminished renal function or other conditions which impairs potassium excretion (e.g. adrenal insufficiency). Close monitoring of serum potassium concentrations is recommended, as potentially fatal hyperkalemia can develop rapidly and is often asymptomatic, manifested only by an increased potassium level (6.5 to 8 mEq/L) and characteristic electrocardiographic changes (peaking of T waves, loss of P waves, depression of ST segment, prolongation of the QT interval). Late manifestations include muscle paralysis and cardiovascular collapse from cardiac arrest (9 to 12 mEq/L). Continuous or serial electrocardiography may be appropriate in some patients during replacement therapy, particularly if given intravenously.

Hypokalemia in patients with metabolic acidosis should be treated with an alkalinizing potassium salt (i.e. acetate, bicarbonate, citrate, or gluconate) rather than potassium chloride, since alkali therapy helps to promote cellular uptake of potassium. Close monitoring of acid-base balance, serum electrolytes, electrocardiogram, and clinical status is recommended.

Hypokalemia in patients with metabolic or respiratory alkalosis should generally be treated with potassium chloride rather than an alkalinizing potassium salt (i.e. acetate, bicarbonate, citrate, or gluconate), since alkali therapy may exacerbate the condition. In addition, hypochloremia may accompany alkalosis, which is best treated with potassium chloride. Close monitoring of acid-base balance, serum electrolytes, electrocardiogram, and clinical status is recommended.

Valsartan is primarily eliminated by biliary excretion, and a minority is excreted in the urine. Dosage adjustments are not necessary in patients with renal impairment unless they are also volume-depleted, in which case therapy should be initiated under medical supervision. Likewise, patients with mild to moderate hepatic impairment or biliary obstruction generally do not require a dosage adjustment. The manufacturer recommends administering valsartan therapy with caution in patients with impaired renal and/or liver function, particularly if these conditions are severe.

Angiotensin II receptor (AR) antagonists can cause renal impairment in patients whose renal function depends on the activity of the renin-angiotensin-aldosterone system. In addition, symptomatic hypotension can occur in susceptible individuals, which may compromise renal and myocardial perfusion. In patients with severe congestive heart failure (CHF), treatment with AR antagonists has been associated with oliguria and/or progressive azotemia and, rarely, renal failure, myocardial ischemia, and death. Therapy with AR antagonists should be initiated cautiously in patients with severe CHF, especially when accompanied by volume and/or sodium depletion. In patients who experience a decline in renal function, discontinuation of AR antagonist therapy is usually not required provided there is symptomatic improvement of the heart failure and renal deterioration is well-tolerated. Transient hypotension is also not a contraindication to further treatment with AR antagonists, since therapy can usually be reinstated without difficulty after blood pressure stabilizes.

Drugs that inhibit the renin-angiotensin, such as angiotensin II receptor antagonist system can cause hyperkalemia. Concomitant use of these agents with drugs that increase potassium levels may increase the risk of hyperkalemia. Use caution when using these agents together and monitor serum potassium periodically.

Valsartan is primarily eliminated by biliary excretion, and a minority is excreted in the urine. Dosage adjustments are not necessary in patients with renal impairment unless they are also volume-depleted, in which case therapy should be initiated under medical supervision. Likewise, patients with mild to moderate hepatic impairment or biliary obstruction generally do not require a dosage adjustment. The manufacturer recommends administering valsartan therapy with caution in patients with impaired renal and/or liver function, particularly if these conditions are severe.

Alkalinizing agents act as proton acceptors and/or dissociate to provide bicarbonate ions. Elimination of bicarbonate is decreased in patients with renal impairment and can result in metabolic alkalosis. Symptoms of metabolic alkalosis include hyperirritability or tetany, arrhythmia, and/or seizures (altered pH = altered calcium), or lactic acidosis due to impaired oxygen release. Therapy with alkalinizing agents should be administered with extreme caution in patients with compromised renal function. Clinical monitoring of renal function, acid/base balance and electrolytes is recommended.

Valsartan is primarily eliminated by biliary excretion, and a minority is excreted in the urine. Dosage adjustments are not necessary in patients with renal impairment unless they are also volume-depleted, in which case therapy should be initiated under medical supervision. Likewise, patients with mild to moderate hepatic impairment or biliary obstruction generally do not require a dosage adjustment. The manufacturer recommends administering valsartan therapy with caution in patients with impaired renal and/or liver function, particularly if these conditions are severe.

Changes in renal function including acute renal failure can be caused by drugs that inhibit the renin-angiotensin system and by diuretics. Patients whose renal function may depend in part on the activity of the renin-angiotensin system (e.g., patients with renal artery stenosis, chronic kidney disease, severe congestive heart failure, or volume depletion) may be at particular risk of developing acute renal failure with these agents. Monitor renal function periodically in these patients. Consider withholding or discontinuing therapy in patients who develop a clinically significant decrease in renal function with these agents.