高血壓是慢性腎臟病患者最為常見的共病。但是，腎臟病檢測指標——估算腎小球濾過率（eGFR）和白蛋白尿——與死亡或終末期腎臟病（ESRD）的關聯(lián)是否因高血壓的存在與否而不同，目前尚屬未知。

最近發(fā)表于《TheLancet》的一項薈萃分析顯示，無論有無高血壓，慢性腎臟病均應被視為與死亡和ESRD相關的重要危險因素。

根據(jù)慢性腎臟病預后聯(lián)盟（CKD-PC）的標準選擇研究，進行薈萃分析。數(shù)據(jù)傳輸和分析于2011年3月至2012年6月之間完成。對有或無高血壓的個體，使用 Cox 比例風險模型，評估與eGFR及白蛋白尿相關的死亡和ESRD的風險比（HR）。

研究分析了來自45個隊列入群（25個普通人群，7個高危人群和13個慢性腎臟病人群）1 127 656例受試者的數(shù)據(jù)。結果發(fā)現(xiàn)：其中364 344例患有高血壓。在普通人群和高危人群中，無論是否患有高血壓，低eGFR和高白蛋白尿與死亡相關。eGFR正常的高血壓個體的全因死亡風險為無高血壓個體的1.1～1.2倍。eGFR在45～75 ml/（min.1.73m2）的無高血壓個體與高血壓個體相比相對風險的斜度更陡，因此較低eGFR的個體死亡風險相同。以eGFR 95 ml/（min.1.73m2）作為每組的參照準確評估交互作用，eGFR為45 ml/（min.1.73m2）的無高血壓個體和高血壓個體的校正全因死亡HR分別為1.77（95%CI 1.57～1.99）和1.24（95%CI 1.11～1.39）（總體交互P=0.000 3）。同樣，以白蛋白/肌酐比值（ACR）5 mg/g作為參照，ACR為300 mg/g的無高血壓個體和高血壓個體的全因死亡HR分別為2.30（95%CI 1.98～2.68）和2.08（95%CI 1.84～2.35）（總體交互P=0.019）。對于心血管疾病死亡，得出了同樣的結果。然而，eGFR和白蛋白尿與ESRD的關聯(lián)不因有無高血壓而不同。慢性腎臟病人群的結果與普通人群和高危人群的相似。

Lancet. 2012 Nov 10;380(9854):1648.

Abstract

Hypertension is the most prevalent comorbidity in individuals with chronic kidney disease. However, whether the association of the kidney disease measures, estimated glomerular filtration rate (eGFR) and albuminuria, with mortality or end-stage renal disease (ESRD) differs by hypertensive status is unknown.

We did a meta-analysis of studies selected according to Chronic Kidney Disease Prognosis Consortium criteria. Data transfer and analyses were done between March, 2011, and June, 2012. We used Cox proportional hazards models to estimate the hazard ratios (HR) of mortality and ESRD associated with eGFR and albuminuria in individuals with and without hypertension.

We analysed data for 45 cohorts (25 general population, seven high-risk, and 13 chronic kidney disease) with 1,127,656 participants, 364,344 of whom had hypertension. Low eGFR and high albuminuria were associated with mortality irrespective of hypertensive status in the general population and high-risk cohorts. All-cause mortality risk was 1·1-1·2 times higher in individuals with hypertension than in those without hypertension at preserved eGFR. A steeper relative risk gradient in individuals without hypertension than in those with hypertension at eGFR range 45-75 mL/min per 1·73 m(2) led to much the same mortality risk at lower eGFR. With a reference eGFR of 95 mL/min per 1·73 m(2) in each group to explicitly assess interaction, adjusted HR for all-cause mortality at eGFR 45 mL/min per 1·73 m(2) was 1·77 (95% CI 1·57-1·99) in individuals without hypertension versus 1·24 (1·11-1·39) in those with hypertension (p for overall interaction=0·0003). Similarly, for albumin-creatinine ratio of 300 mg/g (vs 5 mg/g), HR was 2·30 (1·98-2·68) in individuals without hypertension versus 2·08 (1·84-2·35) in those with hypertension (p for overall interaction=0·019). We recorded much the same results for cardiovascular mortality. The associations of eGFR and albuminuria with ESRD, however, did not differ by hypertensive status. Results for chronic kidney disease cohorts were similar to those for general and high-risk population cohorts.

Chronic kidney disease should be regarded as at least an equally relevant risk factor for mortality and ESRD in individuals without hypertension as it is in those with hypertension.