Fig. 4

Clinical course of the patients who showed renal dysfunction. The patient had been treated with standard cardioprotective therapy, including ACEI and beta-blocker, but continued to have elevated BNP and enlarged LVDD. Because of nocturnal bradycardia, carvedilol dose escalation was not feasible. When BNP exceeded 400 pg/mL and LVDD became 61 mm, we considered induction of tranilast. Before introducing tranilast, we started eplerenone and increased the dose of torasemide. Then patient's BNP decreased to less than 300 pg/mL at the start of tranilast. After initiation of tranilast, his BNP decreased, and renal indices deteriorated gradually. Firstly, we reduced eplerenone, but the renal function worsened further. Then tranilast was reduced. However, renal function worsened rapidly. In addition, the LVDD was significantly reduced to 47 mm. From these facts, we suspected hypovolemia by diuretics and renal dysfunction due to ACEI. Reduction of ACEI and diuretics resulted in rapid improvement in renal function and an increase in BNP. After re-introducing tranilast, renal indices and BNP became stable. ACEI, angiotensin-converting enzyme inhibitors; BNP, brain natriuretic peptide; LVDD, Left Ventricular Diastolic Dysfunction