Medical Service, VA Connecticut Healthcare System, West Haven, CT, USA.
Curr Hypertens Rep. 2013 Apr;15(2):89-94. doi: 10.1007/s11906-013-0327-6.
Hypertension complicates most cases of chronic kidney disease. While the prevalence and severity of hypertension increase as glomerular filtration rate falls, hypertension is often observed in patients with structural kidney disease while renal function is normal, in particular those with polycystic kidney disease or proteinuric glomerular diseases. On the other hand, even severe reductions in renal function may not result in hypertension, especially if there is effective control of extracellular fluid volume. Recent clinical and experimental data indicate that proteinuria may mediate sodium retention and hypertension via plasmin-mediated activation of the epithelial sodium channel. Current evidence supports the notion that chronic kidney disease is a cause of chronic hypertension, even in the absence of detectable changes in glomerular filtration rate.
高血压是大多数慢性肾脏病患者的并发症。虽然随着肾小球滤过率的下降,高血压的患病率和严重程度增加,但在肾功能正常的情况下,特别是在患有多囊肾病或蛋白尿性肾小球疾病的患者中,常观察到结构性肾病患者伴有高血压。另一方面,即使肾功能严重下降也可能不会导致高血压,尤其是如果能有效控制细胞外液量的话。最近的临床和实验数据表明,蛋白尿可能通过纤溶酶介导的上皮钠通道激活来介导钠潴留和高血压。目前的证据支持这样一种观点,即慢性肾脏病是慢性高血压的一个原因,即使在肾小球滤过率没有检测到变化的情况下也是如此。