Can Diovan (valsartan) cause hyponatremia or hypokalemia?

Diovan and Electrolyte Disturbances

Diovan (valsartan) causes hyperkalemia, not hypokalemia, and does not typically cause hyponatremia as a direct effect. 1

Hyperkalemia Risk with Valsartan

Valsartan, like all angiotensin receptor blockers (ARBs), increases potassium levels by blocking aldosterone's effects on renal potassium excretion. 1

• ARBs block angiotensin II binding to AT1 receptors, which reduces aldosterone secretion and subsequently decreases renal tubular potassium excretion 1, 2
• The risk of hyperkalemia with ARB monotherapy is approximately 2% in hypertensive patients without additional risk factors, but increases to 5% with dual RAAS inhibition 1
• Hyperkalemia risk is substantially elevated in patients with chronic kidney disease (up to 73% in advanced CKD), heart failure (up to 40%), diabetes, or advanced age 1
• Monitoring of serum potassium and creatinine is required periodically when using valsartan 1

High-Risk Populations Requiring Vigilant Monitoring

• Patients with estimated glomerular filtration rate (eGFR) <60 mL/min/1.73 m² 1
• Concurrent use of potassium-sparing diuretics, NSAIDs, or potassium supplements 1
• Diabetic patients, particularly those with diabetic nephropathy 1
• Elderly patients (>70 years) 1

Hyponatremia: Not a Direct Effect of Valsartan

Valsartan does not cause hyponatremia as a primary adverse effect. 1

• When hyponatremia occurs in patients taking valsartan, it is typically due to concurrent thiazide or thiazide-like diuretic use, not the ARB itself 1
• Thiazide-type diuretics (hydrochlorothiazide, chlorthalidone, indapamide) are well-documented causes of hyponatremia and require monitoring for this complication 1
• The combination product Diovan-HCT (valsartan/hydrochlorothiazide) carries risk of hyponatremia from the hydrochlorothiazide component 1

Hypokalemia: The Opposite Problem

Valsartan does not cause hypokalemia; it actually opposes potassium loss. 1, 2

• ARBs are frequently combined with hydrochlorothiazide specifically because the ARB component counteracts the hypokalemia induced by the diuretic 1, 2
• In fixed-dose ARB/hydrochlorothiazide combinations, the ARB's potassium-retaining effect balances the diuretic's potassium-wasting effect 2
• If hypokalemia occurs in a patient taking valsartan, investigate other causes such as concurrent diuretic use, gastrointestinal losses, or inadequate dietary intake 1

Clinical Monitoring Recommendations

Routine monitoring for patients on valsartan should focus on blood pressure, renal function, and serum potassium levels. 1, 3

• Check serum potassium and creatinine within 1-2 weeks of initiating therapy 1
• Recheck electrolytes and renal function periodically, particularly after dose adjustments or when adding interacting medications 1
• In heart failure patients with history of hyperkalemia, consider potassium binders (patiromer) to enable continuation of RAAS inhibitor therapy 1
• Document baseline values before initiating therapy to identify changes 1

Common Pitfall to Avoid

Do not discontinue valsartan prematurely for mild hyperkalemia (potassium 5.0-5.5 mEq/L) without first attempting dose reduction, dietary potassium restriction, or addition of a loop diuretic, as the mortality benefits of RAAS inhibition in appropriate patients outweigh mild electrolyte disturbances 1