Valdivielso P, et al Nephrology (Carlton) 2003;8:61–4 (Level 4

Valdivielso P, et al. Nephrology (Carlton). 2003;8:61–4. (Level 4)   4. Gazarin S, et al. J Nephrol. 2002;15:690–5. (Level 4)   5. Matzkies FK, et al. Am J Nephrol. 1999;19:492–4. (Level 4)   6. Olbricht CJ, et APR-246 in vitro al. Kidney Int 1999;71 (Suppl):S113–6. (Level 2)   7. Brown CD, et al. Am J Kidney Dis. 1995;26:170–7. (Level 3)   8. Thomas ME, et al. Kidney Int. 1993;44:1124–9. (Level 2)  

9. Shibasaki T, et al. Nihon Jinzo Gakkai Shi. 1993;35:1243–8. (Level 4)   10. Dogra GK, et al. Kidney Int. 2002;62:550–7. (Level 4)   11. Resh M, et al. Thromb Res. 2011;127:395–9. (Level 4)   Are RAS inhibitors recommended for patients with idiopathic membranous nephropathy and hypertension? Hypertension often occurs as a complication of membranous nephropathy and is a risk factor for the progression of CKD. To treat such hypertension, restriction of sodium intake and administration of anti-hypertensive agents have been recommended. The anti-proteinuric effect of RAS inhibitors on diabetic

and non-diabetic nephropathies is well known. Polanco et al. reported that treatment with RAS inhibitors was associated with a significantly increased probability of spontaneous remission of membranous nephropathy. RAS inhibitors are preferred as the first-line antihypertensive therapy and are expected to reduce urine protein and HKI-272 slow the progression of membranous nephropathy. Bibliography 1. Polanco N, et al. J Am Soc Nephrol. 2010;21:697–704. (Level 4)   2. Kosmadakis G, et al. Scand J Urol Nephrol. 2010;44:251–6. (Level RAS p21 protein activator 1 2)   3. Iimura O, et al. Nihon Jinzo Gakkai Shi. 2003;45:439–44. (Level 4)   4. Prasher PK, et al. J Assoc Physicians India. 1999;47:180–2. (Level 4)   5. Ruggenenti P, et al. Am J Kidney Dis. 2000;35:381–91. (Level 4)

  6. Praga M, et al. Nephrol Dial Transplant. 1997;12:2576–9. (Level 4)   7. Rostoker G, et al. Nephrol Dial Transplant. 1995;10:25–9. (Level 4)   8. Gansevoort RT, et al. Nephrol Dial Transplant. 1992;7(Suppl1):91–6. (Level 3)   9. Thomas DM, et al. Am J Kidney Dis. 1991;18:38–43. (Level 4)   10. Kincaid-Smith P, et al. Nephrol Dial Transplant. 2002;17:597–601. (Level 2)   Is treatment with high-dose corticosteroid alone recommended for inducing remission in FSGS? An important prognostic indicator of FSGS is the initial response to therapy. Aggressive immunosuppressive therapy aimed at inducing remission is recommended because sustained nephrotic range proteinuria is a risk factor for progression to ESKD, and, conversely, responders to initial therapy have better long-term outcomes. There are no RCTs comparing corticosteroid or other agents to placebo as the first-line therapy for idiopathic FSGS. Observational studies have shown that high-dose corticosteroid could learn more efficiently induce remission. Therefore, as the first-line therapy, steroid therapy aimed at inducing remission is recommended for patients with FSGS.

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