心-腎悪液質症候群

心-腎悪液質症候群に関する論文を紹介します。

Mariantonietta Cicoira, Stefan D. Anker and Claudio Ronco: Cardio-renal cachexia syndromes (CRCS): pathophysiological foundations of a vicious pathological circle. Journal of Cachexia, Sarcopenia and Muscle DOI: 10.1007/s13539-011-0038-2

下記のHPで全文PDFで見ることができます。

http://www.springerlink.com/content/31353607661k7ll0/fulltext.pdf

心臓と腎臓の相関に関しては、Cardio-renal syndromesやcardio―renal anemia syndromeといった概念があります。

心-腎症候群はどちらかの臓器に急性もしくは慢性的な障害が生じると、もう1つの臓器にも障害が生じるということです。心臓と肺の相関はよく理解されていますが、心臓と腎臓の相関はまだ十分理解されていないかもしれません。

心-腎症候群には5つのタイプがあり、タイプ2は慢性心-腎症候群、タイプ4は慢性腎-心症候群になります。これらの悪化、相関には悪液質が関与しているので、心-腎悪液質症候群であると提唱されています。心-腎悪液質症候群は難治性で致死率の高い病態ですので、病態の解明と理解が重要です。

Abstract
Cardio-renal syndromes (CRS) are defined as disorders of the heart and kidney whereby acute or chronic dysfunction in one organ may induce acute or chronic dysfunction of the other. CRS have been classified into five categories, where types 2 and 4 represent respectively chronic cardio-renal and chronic reno-cardiac syndromes. In these conditions, the chronic disorder of either the heart or kidney has been shown to induce some degree of cachexia. At the same time, cachexia has been proposed as a possible mechanism contributing to the worsening of such pathological organ cross talk. Common pathogenetic mechanisms underlie body wasting in cachectic states of different chronic heart and kidney diseases. In these circumstances, a vicious circle could arise, in which cachexia associated with either heart failure or chronic kidney disease may contribute to further damage of the other organ. In chronic CRS, activation of the immune and neuroendocrine systems contributes to the genesis of cachexia, which in turn can negatively affect the heart and kidney function. In patients with cardiac sustained activation of the immune and neuroendocrine systems and oxidative stress, renal vascular resistance can increase and therefore impair renal perfusion, leading to worsening kidney function. Similarly, in renal cachexia, increased levels of pro-inflammatory cytokines can cause progressive left ventricular systolic dysfunction, myocardial cell death, endothelial dysfunction and increased myocardial fibrosis, with consequent impairment of the chronic reno-cardiac syndrome type 4. Thus, we speculate that the occurrence of different types of chronic CRS could represent a fundamental step in the genesis of cachexia, being renal and cardiac dysfunction closely related to the occurrence of systemic disorders leading to a final common pathway. Therefore, the heart and kidney and cachexia represent a triad causing a vicious circle that increases mortality and morbidity: In such circumstances, we may plausibly talk about cardio-renal cachexia syndrome. Complex interrelations may explain the transition from CRS to cachexia and from cachexia to CRS. Identification of the exact mechanisms occurring in these conditions could potentially help in preventing and treating this deadly combination.