Congestive nephropathy: a neglected entity? Proposal for diagnostic criteria and future perspectives.
Congestive nephropathy: a neglected entity? Proposal for diagnostic criteria and future perspectives.
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DOI：
10.1002/ehf2.13118
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发表时间：
2021-03
影响因子：
3.8
通讯作者：
Birk HW
中科院分区：
文献类型：
--
作者：
Husain-Syed F;Gröne HJ;Assmus B;Bauer P;Gall H;Seeger W;Ghofrani A;Ronco C;Birk HW
静脉淤血已成为心肾综合征患者肾功能不全的重要原因。然而，在区分这种肾功能不全的血液动力学表型方面仅取得了有限的进展，因为与长期高血压、糖尿病和肾血管疾病引起的既存肾损害有显著重叠。我们建议充血性肾病（CN）作为这种被忽视的临床实体。CN是一种潜在可逆的肾功能不全亚型，与肾静脉流出量下降和肾间质压进行性升高相关。静脉充血可能导致激素激活、腹内压升高、肾小管钠重吸收过度和容量超负荷的恶性循环，从而导致进一步的右心室（RV）应激。最终，可能需要肾脏替代治疗来缓解利尿剂抵抗性充血。有效的缓解充血可以保护或改善肾功能。充血性急性肾损伤可能与细胞损伤无关，肾功能完全恢复可能是确诊标准。相反，持续的低肾灌注压可能会随着时间的推移诱导肾功能不全和组织病理学病变。因此，尿液标记物可能不同。CN主要见于双心室心力衰竭，但也可能继发于肺动脉高压和腹内压升高。中心静脉压升高至>6 mmHg与肾小球滤过率急剧下降相关。然而，可以提供RV和肾功能的最佳平衡的中心静脉压范围仍有待确定。我们提出了识别可能从缓解充血或肺动脉高压特异性治疗中获益的心肾综合征亚组的标准，并提出了未来研究的领域。
Venous congestion has emerged as an important cause of renal dysfunction in patients with cardiorenal syndrome. However, only limited progress has been made in differentiating this haemodynamic phenotype of renal dysfunction, because of a significant overlap with pre‐existing renal impairment due to long‐term hypertension, diabetes, and renovascular disease. We propose congestive nephropathy (CN) as this neglected clinical entity. CN is a potentially reversible subtype of renal dysfunction associated with declining renal venous outflow and progressively increasing renal interstitial pressure. Venous congestion may lead to a vicious cycle of hormonal activation, increased intra‐abdominal pressure, excessive renal tubular sodium reabsorption, and volume overload, leading to further right ventricular (RV) stress. Ultimately, renal replacement therapy may be required to relieve diuretic‐resistant congestion. Effective decongestion could preserve or improve renal function. Congestive acute kidney injury may not be associated with cellular damage, and complete renal function restoration may be a confirmatory diagnostic criterion. In contrast, a persistently low renal perfusion pressure might induce renal dysfunction and histopathological lesions with time. Thus, urinary markers may differ. CN is mostly seen in biventricular heart failure but may also occur secondary to pulmonary arterial hypertension and elevated intra‐abdominal pressure. An increase in central venous pressure to >6 mmHg is associated with a steep decrease in glomerular filtration rate. However, the central venous pressure range that can provide an optimal balance of RV and renal function remains to be determined. We propose criteria to identify cardiorenal syndrome subgroups likely to benefit from decongestive or pulmonary hypertension‐specific therapies and suggest areas for future research.
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