Background/Aims:Immunoglobulin A nephropathy (IgAN) is a generally progressive disease, even in patients with favorable prognostic features. In this study, we aimed to investigate the antiproteinuric effect and tolerability of low-dose valsartan (an angiotensin II receptor blocker) therapy in normotensive IgAN patients with minimal proteinuria of less than 0.5 to 1.0 g/day.Methods:Normotensive IgAN patients, who had persistent proteinuria with a spot urine protein-to-creatinine ratio of 0.3 to 1.0 mg/mg creatinine, were recruited from five hospitals and randomly assigned to either 40 mg of valsartan as the low-dose group or 80 mg of valsartan as the regular-dose group. Clinical and laboratory data were collected at baseline, and at 4, 8, 12, and 24 weeks after valsartan therapy.Results:Forty-three patients (low-dose group, n = 23; regular-dose group, n = 20) were enrolled in the study. Proteinuria decreased significantly not only in the regular-dose group but also in the low-dose group. The change in urine protein-to-creatinine ratio at week 24 was −41.3% ± 26.1% (p < 0.001) in the regular-dose group and −21.1% ± 45.1% (p = 0.005) in the low-dose group. In the low-dose group, blood pressure was constant throughout the study period, and there was no symptomatic hypotension. In the regular-dose group, blood pressure decreased at weeks 8 and 12. No significant change in glomerular filtration rate, serum creatinine level, or serum potassium level was observed during the study period.Conclusions:Our results suggest that low-dose valsartan can significantly reduce proteinuria without causing any intolerability in normotensive IgAN patients with minimal proteinuria.

1816PARK KM et al. Circulation Journal Official Journal of the Japanese Circulation Society http://www. j-circ.or.jpThis suggests that VPD QRSd could be a marker for the severity of underlying substrate abnormality. 12, 13 Based on this, we hypothesized that VPD QRSd depends on ventricular myocardial conduction time and LV dimension might be correlated with VPD QRSd. In our clinical experience, some patients with frequent VPD that initially appear to be idiopathic have irreversible CMP, even after undergoing successful VPD suppression and optimal medical management for heart failure. We postulate that these patients may have pre-existing subclinical occult structural myocardial disease at baseline and this may be one of the mechanisms leading to idiopathic irreversible VPD-induced CMP. In this study, we examined echocardiographic parameters in patients with frequent VPD and LV dysfunction to determine if these parameters predicted irreversibility of LV CMP.diopathic ventricular premature depolarizations (VPD) are usually considered a benign condition, even when they occur frequently. 1,2 Several recent studies, however, reported that a high burden of VPD is associated with left ventricular (LV) cardiomyopathy (CMP) that usually resolves after successful VPD ablation. 3-10 Nevertheless, in some patients, LV function does not return to normal, even after successful VPD ablation. The mechanism(s) underlying the development of VPD-induced CMP are incompletely understood. Previous reports indicated that tachycardia-induced CMP is reversible with medical or procedural interventions, and LV diastolic dimension helps differentiate tachycardia-induced CMP from idiopathic dilated CMP. 11 In patients with LV dysfunction and frequent VPD, VPD QRS duration (QRSd) is the only independent predictor for recovery of LV function after ablation.

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