Key result
Adding candesartan /day to ramipril reduced 24-hour urinary protein excretion in IgA nephropathy, but not in diabetic nephropathy.
Why the study?
Does adding candesartan to ramipril reduce 24-hour urinary protein excretion differentially in patients with IgA nephropathy versus type 2 diabetic nephropathy when blood pressure is controlled?
RCT (n=41)
Placebo-controlled
Crossover
Does adding candesartan to ramipril reduce 24-hour urinary protein excretion differentially in patients with IgA nephropathy versus type 2 diabetic nephropathy when blood pressure is controlled?
Short-term dual RAS blockade with candesartan and ramipril provides an additive, blood pressure-independent antiproteinuric effect in IgA nephropathy, but not in type 2 diabetic nephropathy.
Answers are grounded in this paper and cite their sources.
Supports dual RAS blockade for proteinuria in IgA nephropathy but not diabetic nephropathy; extends randomized evidence for etiology-specific antiproteinuric responses.
In previous studies, the synergistic antiproteinuric effect of the combination therapy of ACE inhibitors and angiotensin II receptor antagonists (ATRAs) has been inconsistent in relation to underlying renal diseases. The influence from the blood pressure (BP) - reducing effect in some studies might also contribute to this inconclusiveness. To examine the possibility of the benefit being different according to underlying renal diseases, we undertook a crossover therapeutic trial of the combination therapy in two selected homogenous groups of patients with diabetic and non-diabetic renal diseases. The BP-reducing effect was excluded during the study. Nineteen biopsy-proven IgA nephropathy, as examples of non-diabetic renal diseases, and 24 type 2 diabetic nephropathy patients were selected as the study subjects. The subjects had to meet the follow criteria: a creatinine clearance (Ccr) between 25 - 90 ml/min/1.73 m2, 24-hr urinary protein excretion rate over 1.0 g/day and a BP maintained at less than 130/80 mmHg, with more than six-month therapy of ramipril, (5.7 +/- 0.4 mg/day, 13 +/- 2 month). The baseline data between the two groups showed no significantly differences. After a 12-week stabilization period (control period), 4 mg, once daily, dose of candesartan (combination period) followed by a placebo (placebo period), or vice versa, were administered in addition to the ramipril, for 12 weeks. The combination, with candesartan, did not change the Ccr, BP, serum and urinary electrolytes or the urea. The 24 hour urinary protein excretion rate was significantly reduced by the combination therapy in the patients with IgA nephropathy (3.1 +/- 0.3 g/day in combination, 4.2 +/- 0.3 in control, and 4.3 +/- 0.2 in placebo; p < 0.05). However, the patients with diabetic nephropathy showed no reduction in their proteinuria with the combination therapy (3.8 +/- 0.2 g/day in combination, 3.9 +/- 0.3 in control, and 4.1 +/- 0.3 in placebo; p=NS). The changes in proteinuria showed no relationship with the changes in the BP in IgA nephropathy. In conclusions, the benefit of combination therapy of its antiproteinuric effect was different between IgA and diabetic nephropathy over the 12-week trial. The difference in the pathophysiological role, and the importance of the renin- angiotensin system, between the two diseases might contribute to the discrepancy in the result. We suggest the discrimination of the underlying renal diseases in the study subjects is an important prerequisite for future studies on this issue.
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Kim et al. (2003) conducted an RCT in IgA nephropathy and type 2 diabetic nephropathy (n=41). Candesartan added to ramipril vs. Placebo added to ramipril (5.7 +/- 0.4 mg/day) was evaluated on 24-hour urinary protein excretion rate (g/day) (p=<0.05). Adding candesartan /day to ramipril reduced 24-hour urinary protein excretion in IgA nephropathy, but not in diabetic nephropathy.
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