PDF(Pubmed)
Abstract：
OBJECTIVE: Hyperuricemia is associated with the progression of chronic kidney disease (CKD). Whether urate-lowering treatment with allopurinol can delay disease progression remains controversial.
METHODS: Relevant databases were searched. Randomized clinical trials comparing the efficacy and -safety of allopurinol in patients with CKD were selected. The primary outcomes were changes in serum uric acid concentration and estimated glomerular filtration rate (eGFR). Random-effects modeling was used to -calculate the standard mean difference (SMD) with 95% CIs.
RESULTS: Four trials enrolling 698 participants were included. All were 2-arm parallel trials with a mean duration follow-up of 22.5 months. Congenital anomalies of the kidney and urinary tract were the most common cause of CKD in children, whereas diabetes was the leading cause of CKD in adults. Allopurinol significantly increased the eGFR compared with control groups (SMD, 2.04; 95% CI, 0.60-3.49; p = 0.005; I2 = 98.23%). Allopurinol led to a significant decrease in serum uric acid concentration compared with the control group (SMD, -5.16; 95% CI, -8.31 to -2.01; p = 0.001; I2 = 98.80%). No significant difference in adverse effects was identified between treatment and control groups.
CONCLUSIONS: Allopurinol treatment in patients with CKD and hyperuricemia slows the decline in eGFR as compared with placebo, without risk of increased adverse effects.
METHODS: Relevant databases were searched. Randomized clinical trials comparing the efficacy and -safety of allopurinol in patients with CKD were selected. The primary outcomes were changes in serum uric acid concentration and estimated glomerular filtration rate (eGFR). Random-effects modeling was used to -calculate the standard mean difference (SMD) with 95% CIs.
RESULTS: Four trials enrolling 698 participants were included. All were 2-arm parallel trials with a mean duration follow-up of 22.5 months. Congenital anomalies of the kidney and urinary tract were the most common cause of CKD in children, whereas diabetes was the leading cause of CKD in adults. Allopurinol significantly increased the eGFR compared with control groups (SMD, 2.04; 95% CI, 0.60-3.49; p = 0.005; I2 = 98.23%). Allopurinol led to a significant decrease in serum uric acid concentration compared with the control group (SMD, -5.16; 95% CI, -8.31 to -2.01; p = 0.001; I2 = 98.80%). No significant difference in adverse effects was identified between treatment and control groups.
CONCLUSIONS: Allopurinol treatment in patients with CKD and hyperuricemia slows the decline in eGFR as compared with placebo, without risk of increased adverse effects.
摘要：
目的：高尿酸血症与慢性肾脏病（CKD）的进展有关。别嘌呤醇降尿酸治疗是否可以延缓疾病进展仍存在争议。
方法：检索相关数据库。选择比较别嘌呤醇在CKD患者中的疗效和安全性的随机临床试验。主要结果是血清尿酸浓度和估计的肾小球滤过率（eGFR）的变化。随机效应建模用于-以95%CI计算标准平均差(SMD)。
结果：纳入4项纳入698名受试者的试验。所有均为双臂平行试验，平均随访时间为22.5个月。肾脏和泌尿道的先天性异常是儿童CKD的最常见原因，而糖尿病是成人CKD的主要原因。与对照组相比，别嘌呤醇显著增加eGFR(SMD，2.04；95%CI，0.60-3.49；p=0.005；I2=98.23%）。与对照组相比，别嘌醇导致血清尿酸浓度显着降低（SMD，-5.16；95%CI，-8.31至-2.01；p=0.001；I2=98.80%）。在治疗组和对照组之间没有发现明显的不良反应差异。
结论：别嘌醇治疗CKD和高尿酸血症的患者与安慰剂相比，eGFR的下降有所减缓，没有增加不良反应的风险。
方法：检索相关数据库。选择比较别嘌呤醇在CKD患者中的疗效和安全性的随机临床试验。主要结果是血清尿酸浓度和估计的肾小球滤过率（eGFR）的变化。随机效应建模用于-以95%CI计算标准平均差(SMD)。
结果：纳入4项纳入698名受试者的试验。所有均为双臂平行试验，平均随访时间为22.5个月。肾脏和泌尿道的先天性异常是儿童CKD的最常见原因，而糖尿病是成人CKD的主要原因。与对照组相比，别嘌呤醇显著增加eGFR(SMD，2.04；95%CI，0.60-3.49；p=0.005；I2=98.23%）。与对照组相比，别嘌醇导致血清尿酸浓度显着降低（SMD，-5.16；95%CI，-8.31至-2.01；p=0.001；I2=98.80%）。在治疗组和对照组之间没有发现明显的不良反应差异。
结论：别嘌醇治疗CKD和高尿酸血症的患者与安慰剂相比，eGFR的下降有所减缓，没有增加不良反应的风险。
