Department of Nephrology, Pitie-Salpetriere Hospital, Paris, France.
Crit Rev Oncol Hematol. 2010 Mar;73(3):213-9. doi: 10.1016/j.critrevonc.2009.03.012. Epub 2009 Apr 28.
It is now clearly established that anti-vascular endothelial growth factor (VEGF) drug class induces hypertension and proteinuria sometimes related to thrombotic microangiopathy and/or various glomerulopathies, according to capillary and glomerular VEGF and VEGF-receptor expressions. As reported in the literature, anti-epidermal growth factor receptor (EGFR) therapies seem to be less nephrotoxic. Indeed, many reports of anti-EGFR nephrotoxicity are tubular dependent such as acute tubular necrosis, electrolyte disorders (hypophosphatemia, hypomagnesemia, etc.) or both. This is explained by elective tubular expression of renal EGF/EGFR. In this paper, we focus on electrolyte disorders related to anti-EGFR treatment and discuss the tubular involvement of these drugs based on their renal expression.
现在已经明确,抗血管内皮生长因子 (VEGF) 药物类别会导致高血压和蛋白尿,有时与血栓性微血管病和/或各种肾小球病有关,这取决于毛细血管和肾小球中 VEGF 和 VEGF 受体的表达。正如文献中所报道的,抗表皮生长因子受体 (EGFR) 疗法似乎毒性较小。事实上,许多抗 EGFR 肾毒性的报告都与肾小管有关,如急性肾小管坏死、电解质紊乱(低磷血症、低镁血症等)或两者兼有。这是由肾脏 EGF/EGFR 的选择性肾小管表达所解释的。在本文中,我们重点关注与抗 EGFR 治疗相关的电解质紊乱,并根据这些药物在肾脏中的表达讨论其肾小管受累情况。