Chapman A B, Johnson A, Gabow P A, Schrier R W
Department of Medicine, University of Colorado School of Medicine, Denver 80262.
N Engl J Med. 1990 Oct 18;323(16):1091-6. doi: 10.1056/NEJM199010183231602.
A high incidence of hypertension (50 to 75 percent) occurs early in the course of autosomal dominant polycystic kidney disease. Cyst enlargement, causing bilateral renal ischemia and subsequent release of renin, is proposed as the cause of this form of hypertension.
To investigate this hypothesis, we measured plasma renin activity and aldosterone concentrations during short-term and long-term converting-enzyme inhibition in 14 patients with hypertension due to polycystic kidney disease, 9 patients with essential hypertension, 11 normotensive patients with polycystic kidney disease, and 13 normal subjects. The groups were comparable with respect to age, sex, body-surface area, degree of hypertension, sodium excretion, and renal function.
During the short-term study, the mean (+/- SE) plasma renin activity was significantly higher in the hypertensive patients with polycystic kidney disease than in the patients with essential hypertension, in the supine (0.36 +/- 0.06 vs. 0.22 +/- 0.06 ng per liter.second, P = 0.05) and upright positions (1.03 +/- 0.14 vs. 0.61 +/- 0.08 ng per liter.second, P less than 0.03) and after converting-enzyme inhibition (1.97 +/- 0.28 vs. 0.67 +/- 0.17 ng per liter.second, P less than 0.0006). The mean arterial pressures measured in the supine and upright positions and the plasma aldosterone concentrations measured in the upright position were significantly higher in the normotensive patients with polycystic kidney disease than in the normal subjects. After six weeks of converting-enzyme inhibition, renal plasma flow increased (P less than 0.005), and both renal vascular resistance (P less than 0.007) and the filtration fraction (P less than 0.02) decreased significantly in the hypertensive patients with polycystic kidney disease but not in the patients with essential hypertension.
The renin-angiotensin-aldosterone system is stimulated significantly more in hypertensive patients with polycystic kidney disease than in comparable patients with essential hypertension. The increased renin release, perhaps due to renal ischemia caused by cyst expansion, probably contributes to the early development of hypertension in polycystic kidney disease.
常染色体显性遗传性多囊肾病病程早期高血压发病率较高（50%至75%）。囊肿增大导致双侧肾脏缺血并随后释放肾素，被认为是这种高血压形式的病因。
为研究这一假说，我们测定了14例多囊肾病所致高血压患者、9例原发性高血压患者、11例血压正常的多囊肾病患者和13例正常受试者在短期和长期服用转换酶抑制剂期间的血浆肾素活性和醛固酮浓度。这些组在年龄、性别、体表面积、高血压程度、钠排泄和肾功能方面具有可比性。
在短期研究中，多囊肾病高血压患者仰卧位（0.36±0.06对0.22±0.06纳克/升·秒，P = 0.05）和立位（1.03±0.14对0.61±0.08纳克/升·秒，P<0.03）以及服用转换酶抑制剂后（1.97±0.28对0.67±0.17纳克/升·秒，P<0.0006）的平均（±标准误）血浆肾素活性显著高于原发性高血压患者。血压正常的多囊肾病患者仰卧位和立位测得的平均动脉压以及立位测得的血浆醛固酮浓度显著高于正常受试者。服用转换酶抑制剂六周后，多囊肾病高血压患者肾血浆流量增加（P<0.005），肾血管阻力（P<0.007）和滤过分数（P<0.02）均显著降低，而原发性高血压患者则无此变化。
多囊肾病高血压患者的肾素 - 血管紧张素 - 醛固酮系统受刺激程度显著高于可比的原发性高血压患者。肾素释放增加可能是由于囊肿扩张导致肾脏缺血，这可能促成了多囊肾病中高血压的早期发展。
