Hypertension in this case is caused by retained sodium and water with increase in circulation system or excessive release of hormones in renal organs that lead to general and local narrowed arteries. According to professional literature, renovascular hypertension and hypertension caused by kidney disease are not the same things. The first one is caused by ischemic nephropathy in renin-angiotensin activation that is set up by renal artery stenosis or its vein’s. Angiotensin II increases pressure in several ways. It acts directly in a vasoconstrictive way, simulates aldosterone synthesis (that retains sodium) and makes sympathetic tone rise. Plasma renin activity absolute values exceed the upper limit of normal only in 50% of patients with renovascular hypertension, but with regard to sodium level it happens more frequently. There is a plenty of evidences of excessive arterial tension in kidney disease caused by inflammation and sclerosis in minute vessels of renal parenchyma and renin-angiotensin system activation.
It is considered that, high blood pressure in kidney disease might be caused by the facts that some kidneys:
- 1. Produce an unknown vasoconstrictive agent
- 2. Do not produce vasodilatators (prostaglandins and bradykinin)
- 3. Do not break vasoconstrictors
- 4. Are bad at getting the sodium out
These listed pathogenesis mechanisms including renin-angiotensin system activation are mostly reliable, but the most authentic hypothesis is about sodium retention. This is also proved by the fact, that hypertension is abnormal in patients with multicystic kidney disease and chronic pyelonephritis, who suffer from excessive sodium excretion and the fact, that removal of liquid and electrolytes with the help of hemodialysis or diuretics provides normal hypertension level to patients. Rare causes of hypertension are renin-secreting tumors and Wilms tumor. The last one reminds of hyperaldosteronism: with observable elevation in blood pressure level, hypokalemia, aldosterone hypersecretion. Renin overactivity helps to distinguish renin-secreting tumors from true hyperaldosteronism and from secondary hyperaldosteronism – normal kidney function and renin overactivity in one of the renal veins in absence of arterial stenosis.