IgA ACEI/ARB, ACEI/ARB. IgA ACEI/ARB. IgA. (P = 0.007) (1.5 g/d vs. 0.7 g/d,p = 0.008), 15.1%(95%CI:-18.7%~48.9%),

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1 ACEI/ARB IgA * (ACEI/ARB)IgA 32 3 ACEI/ARB 0.5 g/d IgA 16 (20 mg/d) ACEI/ARB ACEI/ARB %[95% (CI):-71.2%~-16.1%] 15.1%(95%CI:-18.7%~48.9%) (P = 0.007) (1.5 g/d vs. 0.7 g/dp = 0.008) (1.1 g/d vs. 1.1 g/dp = 0.996) 9 (56.3%) 1 (6.3%P = 0.003) 2 ACEI/ARB IgA IgA Clinical observational study on the effectiveness of ACEI/ARB combined with Spironolactone for the treatment of IgA nephropathy ZHANG Qing-xian LI Yue-ting QIN Shao-hua et al (Department of Nephrology the First Hospital Peking University Beijing ) Abstract Objective The purpose of this study was to evaluate the efficacy and safety of combining spironolactone and angiotensin-converting enzyme (ACE) inhibitors or angiotensin receptor blockers (ARBs) in the treatment of IgA nephropathy (IgAN). Methods Thirty-two patients with IgAN who had already been treated with ACE inhibitors or ARBs for at least 3 months and continued to have proteinuria greater than 0.5 g/24 h were enrolled into this open-label randomized non-placebo-controlled study. The patients were randomly allocated to spironolactone (20 mg/day) plus ACE inhibitors/arbs (spironolactone group n=16) or ACE inhibitors/arbs alone (control group n=16)group. The primary end point was a comparison of changes in 24-hour urinary protein excretion level from the baseline to the last measurement during the study period. Results By the end of the ninth month of treatment the mean change in urinary protein excretion was -43.6% (95% CI -71.2% to -16.1%) in the spironolactone group and 15.1% (95%CI -18.7% to 48.9%) in the control group (P = 0.007). There was a significant decrease in proteinuria in the spironolactone-treated group (1.5 to 0.7 g/24 h P = 0.008) but not in the control group (from 1.1 to 1.1 g/24 h P = 0.996). The secondary end point was the achieving of persistent of proteinuria less than 0.5 g/24 h which was attained by one patient our of 16 (6.3%) in the control group and nine out of 16 (56.3%) in the spironolactone group (P = 0.003). Two male patients in the spironolactone group developed gynecomastia during the trial. Conclusions This study suggests that the addition of spironolactone to ACE inhibitors or ARBs can result in a significant decrease in proteinuria in IgAN. Key words IgA nephropathy Proteinuria Spironolactone (ACEI) [1] RAAS CKD (ARB) - (RAAS) (CKD) ( ) *

2 ACEI/ARB ACEI/ARB [23] 24 h (MRB) ACEI ()ARB MRB CKD [1112] CKD IgA 30%~ 40% 10 ~20 (ESRD) [4~6] IgA = / 24 h IgA ; = 24 h - [7] IgA 24 h ACEI ()ARB IgA 0.5 g/d [89] MRB IgA SPSS 16.0 x 軃 ± s ACEI/ARB IgA ~12 IgA :1 18~65 ; 2 3 ACEI/ARB /80 mmhg g/d;3 (egfr) 60 ml/(min 1.73 m 2 ) [10] :1 5.0 mmol/l;2 1 (1)ACEI/ARB ; (3~28) 12(3~29)(P ;4 = 0.6) ACEI ARB DDD (1.5 ± 0.9 vs. 1.6 ± 0.6P = 0.7) ;5 IgA ACEI/ARB (MAP) 1/3 t Kaplan-Meier log rank 6 9 (1.5±0.9) IgA SAS (0.9±0.6) (0.9±0.7) (0.7±0.5)g/d(P = 0.008) (1A) 9 ACEI/ARB -43.6%[95% 20 mg/d ; (CI):-71.2%~-16.1%]+15.1% (95% CI: ACEI/ARB ACEI/ARB -18.7%~+48.9%) ( <130/80 mmhg ACEI/ARB -58.7% 95% CI:-100.2%~-17.3% ;P = 0.007) (DDD) 1B ( g/d 95% CI:-1.42~-0.16 g/d;p = 0.016) 9 (56.3%) (6.3%) (P = 0.003) 32 IgA 3

3 (n=16) (n=16) (y) 34.5± ± (/) 9/7 7/9 0.7 (mmhg) 113.4± ± (mmhg) 74.7± ± (g/d) 1.5± ± (μmol/l) 91.8± ± egfr[ml/(min 1.73 m 2 )] 88.2± ± ( ) 1 M0/M1 7/9 11/5 0.3 E0/E1 7/9 10/6 0.5 S0/S1 2/14 6/ T0/T1/T2 15/1/0 13/2/1 0.5 ACEI/ARB (DDD) 1.5 (0.5~4) 1.6 (0.5~2) 0.7 () 8 5 () 3 2 () 1 2 () 3 7 () 1 0 P 1A 2 IgA ACEI/ARB IgA MAP MAP (P = 0.81) 3A B egfr 3 [88.4 vs ml/(min 1.73m 2 )P = 0.6] 6 egfr [(-0.04±1.0) vs. (-0.3± 0.9)ml/ (min 1.73 m 2 )P = 0.4] 4 1B 2 4 T1 T2

4 IgA [(3.8±0.4) vs. (4.1±0.3)mmol/LP = 0.03] >5.5 mmol/l g/d; 1 (0.19~0.67 g/d) ACEI ARB g/d (0.04~0.25 g/d) 9 egfr 3 egfr [13~17] IgA IgA ACEI/ARB IgA ACEI/ARB [17] [14] ACEI/ARB 3A 3B MAP MAP egfrde [18] Bianchi [16] 165 CKD GFR Chrysostomou [19] ACEI ACEI/ARB [16] CKD Meta 11 ACEI ARB [17]

5 on long-term ramipril: REIN follow-up trial. Gruppo Italiano di Studi Epidemiologici in Nefrologia (GISEN). Ramipril Efficacy in Nephropathy. Lancet : /16 (12.5%) [9] Maschio G Alberti D Janin G et al. Effect of the angiotensin-converting-enzyme inhibitor benazepril on the progres- [ ] IgA sion of chronic renal insufficiency. The Angiotensin -Converting-Enzyme Inhibition in Progressive Renal Insufficiency Study Group. N Engl J Med : [10] Ma YC Zuo L Chen JH et al. Modified glomerular filtration rate estimating equation for Chinese patients with chronic kidney disease. J Am Soc Nephrol200617: IgA [11] Cattran DC Coppo R Cook HT et al. The Oxford classification of IgA nephropathy: rationale clinicopathological correlations and ACEI ARB classification. Kidney Int200976: [12] Roberts IS Cook HT Troyanov S et al. The Oxford classification IgA of IgA nephropathy: pathology definitions correlations and reproducibility. Kidney Int200976: [13] Furumatsu Y Nagasawa Y Tomida K et al. Effect of renin-angiotensin-aldosterone system triple blockade on non-diabetic renal disease: addition of an aldosterone blocker spironolactone to combination treatment with an angiotensin-converting enzyme in- [1] Jafar TH Stark PC Schmid CH et al. Progression of chronic kidney disease: the role of blood pressure control proteinuria and angiotensin -converting enzyme inhibition: a patient level meta-analysis. Ann Intern Med : [2] Sato A Saruta T. Aldosterone escape during angiotensin-converting enzyme inhibitor therapy in essential hypertensive patients with left ventricular hypertrophy. J Int Med Res200129: [3] Struthers AD. Aldosterone escape during angiotensin -converting enzyme inhibitor therapy in chronic heart failure. J Card Fail 19962: [4] Lv J Zhang H Zhou Y et al. Natural history of immunoglobulin A nephropathy and predictive factors of prognosis: a long -term follow up of 204 cases in China. Nephrology (Carlton) : [5] Barratt J Feehally J. IgA nephropathy. J Am Soc Nephrol200516: [6] D'Amico G. Natural history of idiopathic IgA nephropathy and factors predictive of disease outcome. Semin Nephrol200424: [7] Reich HN Troyanov S Scholey JW et al. Remission of proteinuria improves prognosis in IgA nephropathy. J Am Soc Nephrol200718: [8] Ruggenenti P Perna A Gherardi G et al. Renal function and requirement for dialysis in chronic nephropathy patients hibitor and angiotensin II receptor blocker. Hypertens Res200831: [14] Schjoedt KJ Rossing K Juhl TR et al. Beneficial impact of spironolactone on nephrotic range albuminuria in diabetic nephropathy. Kidney Int200670: [15] Schjoedt KJ Rossing K Juhl TR et al. Beneficial impact of spironolactone in diabetic nephropathy. Kidney Int : [16] Bianchi S Bigazzi R Campese VM. Long-term effects of spironolactone on proteinuria and kidney function in patients with chronic kidney disease. Kidney Int200670: [17] Navaneethan SD Nigwekar SU Sehgal AR et al. Aldosterone antagonists for preventing the progression of chronic kidney disease: a systematic review and meta -analysis. Clin J Am Soc Nephrol20094: [18] Epstein M Williams GH Weinberger M et al. Selective aldosterone blockade with eplerenone reduces albuminuria in patients with type 2 diabetes. Clin J Am Soc Nephrol20061: [19] Chrysostomou A Pedagogos E Macgregor L et al. Double-blind placebo-controlled study on the effect of the aldosterone receptor antagonist spironolactone in patients who have persistent proteinuria and are on long -term angiotensin -converting enzyme inhibitor therapy with or without an angiotensin receptor blocker. Clin J Am Soc Nephrol20061: [20] Mubarak M. IgA nephropathy: an update on pathogenesis and classification. J Coll Physicians Surg Pak201121: ( : )

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