Bianchi Stefano, Bigazzi Roberto, Caiazza Alberto, Campese Vito M
Unitá Operativa Nefrologia, Spedali Riuniti di Livorno, Livorno, Italy.
Am J Kidney Dis. 2003 Mar;41(3):565-70. doi: 10.1053/ajkd.2003.50140.
Chronic kidney diseases, particularly if presenting with significant proteinuria, are commonly associated with substantial alteration of serum lipid levels. Experimental evidence suggests that lipid abnormalities may contribute to the progression of kidney disease. However, studies in humans on the subject are scarce.
In a prospective, controlled open-label study, the authors have evaluated the effects of one-year treatment with atorvastatin, a 3-hydroxy-3-methyglutaryl coenzyme A (HMG-CoA) reductase inhibitor, versus no treatment on proteinuria and progression of kidney disease in 56 patients with chronic kidney disease. Before randomization, all patients had already been treated for one year with angiotensin-converting enzyme (ACE) inhibitors or angiotensin AT1 receptor antagonists (ARBs) and other antihypertensive drugs.
By the end of one-year treatment, urine protein excretion decreased from 2.2 +/- 0.1 to 1.2 +/- 1.0 g every 24 hours (P < 0.01) in patients treated with atorvastatin in addition to ACE inhibitor and ARBs. By contrast, urinary protein excretion decreased only from 2.0 +/- 0.1 to 1.8 +/- 0.1 g every 24 hours (P value not significant) in patients who did not receive atorvastatin in addition to ACE inhibitor or ARBs. During this time, creatinine clearance decreased only slightly and not significantly (from 51 +/- 1.8 to 49.8 +/- 1.7) in patients treated with atorvastatin. By contrast, during the same period of observation, creatinine clearance decreased from 50 +/- 1.9 to 44.2 +/- 1.6 mL/min (P < 0.01) in patients who did not receive atorvastatin.
This study has shown that treatment with atorvastatin in addition to a regimen with ACE inhibitors or ARBs may reduce proteinuria and the rate of progression of kidney disease in patients with chronic kidney disease, proteinuria, and hypercholesterolemia. The benefits appear to occur in addition to those of treatment with ACE inhibitor and ARBs.
慢性肾脏病,尤其是出现大量蛋白尿时,通常与血清脂质水平的显著改变相关。实验证据表明脂质异常可能促使肾脏疾病进展。然而,关于该主题的人体研究很少。
在一项前瞻性、对照开放标签研究中,作者评估了阿托伐他汀(一种3-羟基-3-甲基戊二酰辅酶A(HMG-CoA)还原酶抑制剂)治疗一年与未治疗对56例慢性肾脏病患者蛋白尿及肾脏疾病进展的影响。在随机分组前,所有患者均已接受血管紧张素转换酶(ACE)抑制剂或血管紧张素AT1受体拮抗剂(ARB)及其他降压药物治疗一年。
在接受阿托伐他汀联合ACE抑制剂和ARB治疗的患者中,经过一年治疗后,尿蛋白排泄量从每24小时2.2±0.1克降至1.2±1.0克(P<0.01)。相比之下,在仅接受ACE抑制剂或ARB而未接受阿托伐他汀治疗的患者中,尿蛋白排泄量仅从每24小时2.0±0.1克降至1.8±0.1克(P值无统计学意义)。在此期间,接受阿托伐他汀治疗的患者肌酐清除率仅略有下降且无统计学意义(从51±1.8降至49.8±1.7)。相比之下,在相同观察期内,未接受阿托伐他汀治疗的患者肌酐清除率从50±1.9降至44.2±1.6毫升/分钟(P<0.01)。
本研究表明,在使用ACE抑制剂或ARB治疗方案的基础上加用阿托伐他汀治疗,可能降低慢性肾脏病、蛋白尿和高胆固醇血症患者的蛋白尿及肾脏疾病进展速度。这些益处似乎是在ACE抑制剂和ARB治疗的基础上额外获得的。