Effects of pitavastatin add-on therapy on chronic kidney disease with albuminuria and dyslipidemia.
Effects of pitavastatin add-on therapy on chronic kidney disease with albuminuria and dyslipidemia.
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DOI：
10.1186/s12944-015-0164-5
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发表时间：
2015-12-09
影响因子：
4.5
通讯作者：
Umemura S
中科院分区：
文献类型：
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作者：
Ohsawa M;Tamura K;Wakui H;Kanaoka T;Azushima K;Uneda K;Haku S;Kobayashi R;Ohki K;Haruhara K;Kinguchi S;Toya Y;Umemura S
在非透析慢性肾脏病(CKD)合并血脂异常的患者中，他汀类药物被推荐用于预防心血管并发症。血脂异常也被证明是慢性肾脏病进展的独立危险因素。然而，目前尚不清楚他汀类药物治疗是否对合并血脂异常的慢性肾脏病患者的肾脏恶化有抑制作用。本研究的目的是观察他汀类药物对CKD合并血脂异常患者肾功能的可能疗效，以及脂和糖代谢、动脉僵硬和氧化应激等参数的变化，并与饮食治疗进行比较。这项研究是一项随机开放的平行分组试验，包括为期12个月的非透析CKD患者的白蛋白尿和血脂异常的治疗。28名患者被随机分配到单独接受饮食咨询(饮食治疗组)或饮食咨询加他汀类药物(饮食加他汀类药物治疗组)，以实现低密度脂蛋白-胆固醇(LDL-C)目标<；100 mg/dl。所有患者对他汀类药物的耐受性良好，无明显不良反应，治疗后平均剂量为1 ± 0 mg。治疗12个月后，饮食加他汀组的低密度脂蛋白胆固醇明显低于饮食加他汀组(饮食与饮食加他汀组：低密度脂蛋白：12 6 ± 5 vs 83 ± 4 mg/dL，P <； 0.001)。饮食加他汀类药物治疗与饮食治疗相比，并未明显减少蛋白尿或延缓EGFR的下降，低密度脂蛋白-C的变化与EGFR或蛋白尿的变化无相关性。饮食治疗与饮食加他汀类药物治疗对戊二醛水平的降低作用相似(饮食治疗组，基线vs12个月：40 ± 4vs24 ± 3 ng/mL，P = 0.001；饮食加他汀类药物治疗，46 ± 7vs34 ± 6 ng/mLP = 0.008)。多因素回归分析结果显示，戊糖苷的变化对表皮生长因子受体的变化有显著影响(β = −0.536，P = 0.011)。尽管他汀类药物加用治疗未显示出明显的肾脏保护作用，但饮食治疗和饮食加他汀类药物治疗可降低伴有蛋白尿和血脂异常的CKD患者的血浆戊二醛水平。
In non-dialysis chronic kidney disease (CKD) patients with dyslipidemia, statin therapy is recommended to prevent cardiovascular complications. Dyslipidemia has been also shown to be an independent risk factor for the progression of CKD. However, it is still unclear whether statin therapy exerts an inhibitory effect on renal deterioration in CKD patients with dyslipidemia. The purpose of the present study was to examine possible therapeutic effects of statin add-on therapy on renal function as well as parameters of lipid and glucose metabolism, arterial stiffness and oxidative stress, in comparison to diet therapy, in CKD patients with dyslipidemia. This study was a randomized, open-label, and parallel-group trial consisted of a 12-months treatment period in non-dialysis CKD patients with alubuminuria and dyslipidemia. Twenty eight patients were randomly assigned either to receive diet counseling alone (diet therapy group) or diet counseling plus pitavastatin (diet-plus-statin therapy group), to achieve the LDL-cholesterol (LDL-C) target of <100 mg/dl. The statin treatment by pitavastatin was well tolerated in all of the patients without any significant adverse events and the average dose of pitavastatin was 1.0 ± 0.0 mg daily after treatment. After the 12-months treatment period, LDL-C was significantly lower in the diet-plus-statin therapy group compared with the diet therapy group (diet vs diet-plus-statin: LDL-C, 126 ± 5 vs 83 ± 4 mg/dL, P < 0.001). On the other hand, the diet-plus-statin therapy did not significantly reduce albuminuria or delay the decline in eGFR compared with the diet therapy, and there was no relationship between the change in LDL-C and the change in eGFR or albuminuria. However, diet therapy as well as diet-plus-statin therapy exerted similar lowering effects on the pentosidine levels (diet therapy group, baseline vs 12 months: 40 ± 4 vs 24 ± 3 ng/mL, P = 0.001; diet-plus-statin therapy, 46 ± 7 vs 34 ± 6 ng/mL, P = 0.008). Furthermore, the results of multivariate regression analysis indicated that the change in pentosidine was a significant contributor to the change in eGFR (β = −0.536, P = 0.011). Although statin add-on therapy did not show additive renal protective effects, the diet therapy as well as the diet-plus-statin therapy could contribute to the reduction in plasma pentosidine in CKD patients with albuminuria and dyslipidemia.