High urine volume and low urine osmolality are risk factors for faster progression of renal disease

High urine volume and low urine osmolality are risk factors for faster progression of renal disease
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DOI:
10.1016/s0272-6386(03)00193-8
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发表时间:
2003-05-01
影响因子:
13.2
通讯作者:
Klahr, S
Klahr, S
中科院分区:
医学1区
文献类型:
--
作者:
Hebert, LA;Greene, T;Klahr, S

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背景:在动物模型中,增加液体摄入量可减缓肾脏疾病的进展。尽管经常建议慢性肾功能不全患者增加液体摄入量,但这些发现与人类肾脏疾病的相关性尚不清楚。本研究检验了以下假设:尿量、尿渗透压 (Uosm) 或两者均与慢性肾功能不全患者的肾小球滤过率 (GFR) 下降显着相关。方法:这是对肾病饮食调整 (MDRD) 研究 A 的患者 (N = 139) 和非多囊肾病 (PKD;N = 442) 患者的回顾性分析。主要结果指标是研究 A 随访期间(平均 2.3 年)期间与平均 24 小时尿量和 Uosm 相关的 GFR 斜率。结果.,GFR 斜率对平均随访 24 小时尿量的回归(根据体表面积和 MDRD 饮食和血压组进行调整)表明,尿量越大,患有和不患有 PKD 的患者的 GFR 下降越快。例如,对于那些平均随访 24 小时尿量为 2.4 L 和 1.4 L 的患者,GFR 斜率差异为 -1.01 mL/min/y(置信区间,-0.27 至 -1.75)(无 PKD 患者)和 -1.20 mL/min/y(置信区间,-0.06 至 -2.34)(置信区间,-0.06 至 -2.34)。在有 PKD 的患者 (P = 0.01) 和无 PKD 的患者 (P = 0.001) 中,GFR 下降和平均 24 小时 Uosm 之间显示出类似但反向的关系。在调整 13 个相关基线和后续协变量后,这些关联仍然显着。结论:持续高尿量和低Uosm是慢性肾功能不全患者GFR下降较快的独立危险因素。因此,高液体摄入量似乎并不能减缓人类肾脏疾病的进展。我们建议,在获得更好的证据之前,慢性肾功能不全患者通常应该通过口渴来引导液体摄入。避免“推液”的建议对于 PKD 患者可能尤其重要。
Background: Increased fluid intake slows renal disease progression in animal models. The relevance of these findings to human renal disease is not clear, although increased fluid intake often is recommended to patients with chronic renal insufficiency. This study tested the hypothesis that urine volume, urine osmolality (Uosm), or both are significantly associated with glomerular filtration rate (GFR) decline in patients with chronic renal insufficiency. Methods: This is a retrospective analysis of Modification of Diet in Renal Disease (MDRD) study A patients with (N = 139) and without polycystic kidney disease (PKD; N = 442). The key outcome measure was GFR slope in relation to mean 24-hour urine volume and Uosm during follow-up in study A (mean, 2.3 years). Results.,The regression of GFR slope on mean follow-up 24-hour urine volume (adjusted for body surface area and MDRD diet and blood pressure group) showed that the greater the urine volume, the faster the GFR decline in patients both with and without PKD. For example, the difference in GFR slope for those with a mean follow-up 24-hour urine volume of 2.4 versus 1.4 L was -1.01 mL/min/y (confidence interval, -0.27 to -1.75) for patients without PKD and -1.20 mL/min/y (confidence interval, -0.06 to -2.34) for those with PKD. A similar but inverse relationship was shown between GFR decline and mean 24-hour Uosm in patients with (P = 0.01) and without PKD (P = 0.001). These associations remained significant after adjustment for 13 relevant baseline and follow-up covariates. Conclusion: Sustained high urine volume and low Uosm are independent risk factors for faster GFR decline in patients with chronic renal insufficiency. Thus, high fluid intake does not appear to slow renal disease progression in humans. We suggest that until better evidence becomes available, patients with chronic renal insufficiency should generally let their thirst guide fluid intake. The advice to avoid "pushing fluids" might be particularly important for patients with PKD.