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Patients who lack sodium and/or body fluids: In patients with severe sodium and/or body fluid deficiency such as those who receive high doses of diuretics, symptomatic hypotension can rarely occur after starting with Valsartan. Conditions for sodium deficiency and/or body fluids must be treated before starting treatment, for example by reducing the dose of diuretic. If hypotension occurs, the patient must be placed in the supine position and if necessary, given a normal IV saline infusion. Treatment can be continued after the blood pressure has stabilized.
Renal artery stenosis: Short-term administration for 12 patients with secondary renovascular hypertension unilateral renal artery stenosis did not cause significant changes in renal hemodynamics, serum creatinine or BUN. However, because other drugs that affect RAAS can increase blood urea and serum creatinine in patients with bilateral or unilateral renal artery stenosis, safety monitoring is recommended.
Impaired kidney function: Dose adjustment is not required for patients with impaired kidney function. However, in severe cases (creatinine clearance <10 ml/min) data are not available, and therefore care must be taken. Liver disorders. Based on pharmacokinetic data, which shows an increase of about 2-fold plasma concentrations of valsartan in patients with mild to moderate hepatic impairment, doses >80 mg daily should be considered if clinical benefits tend to outweigh the risks that might be associated with increased exposure to valsartan.
Heart failure/post myocardial infarction: Use of Valsartan in patients with heart failure or post myocardial infarction usually causes a decrease in blood pressure, but discontinuation of Valsartan therapy due to symptoms of ongoing hypotension is usually not necessary during administration initial dose followed. Caution must be observed when starting therapy in patients with heart failure or post myocardial infarction (see Dosage & Administration). As an RAAS inhibitor, it can anticipate changes in kidney function in susceptible individuals. In patients with severe heart failure whose renal function depends on RAAS activity, treatment with ACE inhibitors and angiotensin receptor antagonists is associated with oliguria and/or progressive azotemia and (rarely) with acute kidney failure and/or death. Evaluation of patients with heart failure or post myocardial infarction should always include examination of kidney function. In patients with heart failure, attention must be observed with three combinations of ACE inhibitors, beta blockers and (angiotensin II ARBs) receptor blockers).
Effects on the ability to drive or operate machinery: As with other antihypertensives, it is recommended to be careful when driving or operating machinery.
Renal impairment: As predicted for substances whose clearance is only 30% of the total plasma clearance, there is no correlation between kidney function and valsartan exposure in the systemic circulation. Therefore, dosage adjustments are not necessary for patients with impaired kidney function. There was no study in patients undergoing dialysis. However, valsartan is very strongly bound to plasma proteins and cannot be removed during dialysis.
Liver impairment: About 70% of the absorbed dose is secreted in the bile in an unchanging form. Valsartan does not go through an extensive biotransformation process and as suspected valsartan exposure to the systemic canal does not correlate with liver dysfunction. No dose adjustment is needed in patients with insufficiency that are not derived from the bile duct and without cholestasis. The AUC of valsartan has doubled in patients with cirrhosis or bile duct obstruction.
Use in the Elderly: In elderly patients, a higher valsartan systemic exposure was observed compared with younger patients. However, this has not yet shown clinical significance and a lower initial dose is recommended for elderly patients.
