Bench-to-bedside review: lactate and the kidney.
Bench-to-bedside review: lactate and the kidney.
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DOI：
10.1186/cc1518
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发表时间：
2002-08
期刊：
影响因子：
--
通讯作者：
Bellomo R
中科院分区：
文献类型：
--
作者：
Bellomo R
天然肾脏在乳酸代谢中起着重要作用。肾皮质似乎是人体内仅次于肝脏的主要乳酸消耗器官。在外源性高乳酸血症的情况下，肾脏负责清除25%-30%的输注乳酸。大多数这种排泄是通过乳酸代谢而不是排泄，尽管在明显的高乳酸血症条件下，这种排泄可以占肾脏乳酸处置的大约10%-12%。事实上，肾切除术导致外源性乳酸清除减少了约30%。然而，与肝脏不同的是，重要的是，肾脏清除乳酸的能力因酸中毒而增强。虽然酸中毒抑制了肝脏的乳酸代谢，但它通过刺激磷酸烯醇式丙酮酸羧酸激酶的活性，通过糖异生增加了乳酸的摄取和利用。即使在内毒素休克期间，肾脏仍然是一个有效的乳酸清除器官。人工肾对乳酸平衡也有深远的影响。如果在需要持续血液滤过的患者中使用乳酸缓冲液，并且患者有预处理的高乳酸血症，则血清乳酸水平可能会显著升高。在某些情况下，这种增加可能会导致代谢性酸中毒的恶化。如果使用碳酸氢盐缓冲的置换液，也可以显著纠正酸中毒或酸血症。临床医生需要了解这些肾脏对乳酸水平的影响，以了解危重患者高乳酸血症的发病机制，并避免误解和不必要或不适当的诊断或治疗活动。
The native kidney has a major role in lactate metabolism. The renal cortex appears to be the major lactate-consuming organ in the body after the liver. Under conditions of exogenous hyperlactatemia, the kidney is responsible for the removal of 25–30% of all infused lactate. Most of such removal is through lactate metabolism rather than excretion, although under conditions of marked hyperlactatemia such excretion can account for approximately 10–12% of renal lactate disposal. Indeed, nephrectomy results in an approximately 30% decrease in exogenous lactate removal. Importantly and differently from the liver, however, the kidney's ability to remove lactate is increased by acidosis. While acidosis inhibits hepatic lactate metabolism, it increases lactate uptake and utilization via gluconeogenesis by stimulating the activity of phospho-enolpyruvate carboxykinase. The kidney remains an effective lactate-removing organ even during endotoxemic shock. The artificial kidney also has a profound effect on lactate balance. If lactate-buffered fluids are used in patients who require continuous hemofiltration and who have pretreatment hyperlactatemia, the serum lactate levels can significantly increase. In some cases, this increase can result in an exacerbation of metabolic acidosis. If bicarbonate-buffered replacement fluids are used, a significant correction of the acidosis or acidemia can also be achieved. The clinician needs to be aware of these renal effects on lactate levels to understand the pathogenesis of hyperlactatemia in critically ill patients, and to avoid misinterpretations and unnecessary or inappropriate diagnostic or therapeutic activities.