Key result
Spironolactone (25 mg) added to ACEI/ARB therapy for six months significantly reduced proteinuria (p=0.003) and urinary TGF-beta1 excretion (p=0.041) in non-diabetic CKD patients.
Why the study?
Does spironolactone reduce proteinuria and urinary TGF-beta1 excretion in non-diabetic CKD patients treated with ACEIs/ARBs?
Cohort (n=30)
Does spironolactone reduce proteinuria and urinary TGF-beta1 excretion in non-diabetic CKD patients treated with ACEIs/ARBs?
The addition of spironolactone to ACEI/ARB therapy significantly reduces proteinuria and urinary TGF-beta1 excretion in non-diabetic CKD patients, suggesting a potential role in preventing renal fibrosis.
May support adjunctive spironolactone in non-diabetic CKD on ACEI/ARB; leaves open randomized confirmation for hard renal endpoints.
AIMS: Proteinuria and transforming growth factor beta (TGF-beta) are parameters that can lead to glomerulosclerosis and tubulointerstitial fibrosis. All components of the renin-angiotensin-aldosterone system (RAAS) activate the TGF-beta. Aldosterone may not be inhibited with angiotensin-converting enzyme inhibitors (ACEIs) and/or angiotensin receptor blockers (ARBs) due to aldosterone escape. We aimed to evaluate the effect of spironolactone on parameters leading to fibrosis. METHODS: This prospective study included 30 non-diabetic chronic kidney disease (CKD) patients treated with ACEIs and/or ARBs. The patients were divided into two groups that are similar in terms of demographic parameters. 25 mg of spironolactone was added to group 1 (n = 15) for six months, though it was not administered to group 2 (n = 15). Creatinine (U-Cr), protein (U-Prot), and TGF-beta1 (U- TGF-beta1) were measured in spot urine sample in the beginning of study and six months later. RESULTS: Twenty-four patients completed the study. There were no significant changes in mean blood pressure, glomerular filtration rate, creatinine, albumin, and plasma aldosterone concentrations during the observation period in either group. U-Prot/U-Cr (mg/mg Cr) was reduced from 2.43 +/- 4.85 at baseline to 1.66 +/- 3.51 at sixth month (p = 0.003) in group 1. In addition, U-TGF-beta1/U-Cr (ng/mg Cr) was also reduced from 22.50 +/- 6.65 at baseline to 17.78 +/- 10.94 at sixth month (p = 0.041) in the same group. U-TGF-beta1/U-Cr and U-Prot/U-Cr ratios after the sixth month were not found significant compared with baseline values in group 2. CONCLUSION: Spironolactone reduced both proteinuria and urinary TGF-beta1 excretion in CKD patients. We consider that spironolactone would be beneficial to prevent progression of renal fibrosis in CKD.
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Güney et al. (2009) conducted a cohort in Chronic Kidney Disease (n=30). Spironolactone vs. No spironolactone was evaluated on Urinary protein/creatinine ratio and urinary TGF-beta1/creatinine ratio (p=0.003). Spironolactone (25 mg) added to ACEI/ARB therapy for six months significantly reduced proteinuria (p=0.003) and urinary TGF-beta1 excretion (p=0.041) in non-diabetic CKD patients.
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