Touma T, Muratani H, Iseki K, Kawazoe N, Takishita S, Fukiyama K
Third Department of Internal Medicine, School of Medicine, University of The Ryukyus, Okinawa, Japan.
Am J Nephrol. 1992;12(6):461-5. doi: 10.1159/000168499.
We report a patient with nondiabetic end-stage renal disease on continuous ambulatory peritoneal dialysis (CAPD) associated with chronic hypovolemia. Despite the administration of nilvadipine, the patient showed accelerated hypertension and concomitantly orthostatic hypotension. Plasma renin activity was markedly high, and blockade of angiotensin II action by captopril or an angiotension II antagonist decreased the supine blood pressure. This indicated that the enhanced activity of the renin-angiotensin system was the principal cause of the supine hypertension. The plasma concentration of norepinephrine was also very high. After correction of hypovolemia by blood transfusion, the enhancement of the renin-angiotensin system and high plasma norepinephrine level were reduced, and symptomatic orthostatic hypotension disappeared. The accelerated hypertension was easily controlled by the administration of low-dose captopril and nilvadipine. These findings suggest that chronic hypovolemia related to the intractable supine hypertension as well as orthostatic hypotension. Hypovolemia-induced enhancement of the renin-angiotensin system and sympathetic nerve activity may cause vasoconstrictive hypertension in patients on CAPD.
我们报告一例接受持续性非卧床腹膜透析（CAPD）的非糖尿病终末期肾病患者，该患者伴有慢性血容量不足。尽管使用了尼群地平，但患者仍出现高血压加速，同时伴有体位性低血压。血浆肾素活性明显升高，卡托普利或血管紧张素II拮抗剂阻断血管紧张素II作用可降低仰卧位血压。这表明肾素-血管紧张素系统活性增强是仰卧位高血压的主要原因。去甲肾上腺素的血浆浓度也非常高。通过输血纠正血容量不足后，肾素-血管紧张素系统的增强和高血浆去甲肾上腺素水平降低，症状性体位性低血压消失。低剂量卡托普利和尼群地平给药可轻松控制高血压加速。这些发现表明，慢性血容量不足与难治性仰卧位高血压以及体位性低血压有关。血容量不足引起的肾素-血管紧张素系统增强和交感神经活动可能导致CAPD患者出现血管收缩性高血压。
