Olbricht C J, Wanner C, Thiery J, Basten A
Klinik für Nieren- und Hochdruckkrankheiten, Katharinenhospital, Stuttgart, Germany.
Kidney Int Suppl. 1999 Jul;71:S113-6. doi: 10.1046/j.1523-1755.1999.07128.x.
Hyperlipidemia of the nephrotic syndrome is a risk factor for the development of systemic atherosclerosis, but it also may aggravate glomerulosclerosis and enhance the progression of glomerular disease. HMG-CoA reductase inhibitors are effective in reducing cardiovascular morbidity and mortality. Whether they may influence the progression of glomerular disease is not clear. The Simvastatin in Nephrotic Syndrome Study addressed the question of whether or not cholesterol lowering by the HMG-CoA reductase inhibitor simvastatin was superior to placebo treatment in limiting the decline of GFR and reducing proteinuria in nephrotic patients with primary glomerulonephritis.
This was a prospective, two-year, double-blind trial that included 56 patients with primary glomerulonephritis, hypercholesterolemia due to the nephrotic syndrome (proteinuria > 3 g/24 hr), and a creatinine clearance > 40 ml/min/1.73 m2. They were randomly assigned to treatment with simvastatin or placebo targeted to achieve low density lipoprotein (LDL) cholesterol levels below 120 mg/dl. The objectives were to determine the efficacy and safety of simvastatin, the rate of GFR decline as measured by inulin clearance, and the change in proteinuria over a two-year treatment period.
Simvastatin produced a mean change in cholesterol, LDL cholesterol, high density lipoprotein (HDL) cholesterol and triglycerides of -39% -47%, +1%, and -30%, respectively. Serum lipoprotein(a) [Lp(a)] was not affected. No major simvastatin related events occurred. Minor events included elevations in serum creatine kinase without clinical symptoms. The course of renal function and of proteinuria during the study are still under evaluation and are not given here.
Long-term treatment with simvastatin in nephrotic patients with hypercholesterolemia is effective and safe.
肾病综合征高脂血症是全身性动脉粥样硬化发生的危险因素，但它也可能加重肾小球硬化并加速肾小球疾病的进展。HMG-CoA还原酶抑制剂可有效降低心血管疾病的发病率和死亡率。它们是否会影响肾小球疾病的进展尚不清楚。肾病综合征辛伐他汀研究探讨了HMG-CoA还原酶抑制剂辛伐他汀降低胆固醇在限制原发性肾小球肾炎肾病患者肾小球滤过率（GFR）下降和减少蛋白尿方面是否优于安慰剂治疗。
这是一项为期两年的前瞻性双盲试验，纳入了56例原发性肾小球肾炎、因肾病综合征导致高胆固醇血症（蛋白尿>3g/24小时）且肌酐清除率>40ml/min/1.73m²的患者。他们被随机分配接受辛伐他汀或安慰剂治疗，目标是使低密度脂蛋白（LDL）胆固醇水平低于120mg/dl。目的是确定辛伐他汀的疗效和安全性、通过菊粉清除率测量的GFR下降率以及两年治疗期内蛋白尿的变化。
辛伐他汀使胆固醇、LDL胆固醇、高密度脂蛋白（HDL）胆固醇和甘油三酯的平均变化分别为-39%、-47%、+1%和-30%。血清脂蛋白(a) [Lp(a)]未受影响。未发生与辛伐他汀相关的重大事件。轻微事件包括血清肌酸激酶升高但无临床症状。研究期间的肾功能和蛋白尿进程仍在评估中，此处未给出。
高胆固醇血症的肾病患者长期使用辛伐他汀治疗有效且安全。
