How does kidney disease cause hypertension

How does kidney disease cause hypertension?

• Nephron number: A recent pathologic study noted that middle-aged Caucasians with essential hypertension or left ventricular hypertrophy had significantly fewer nephrons than age-matched controls. The fewer nephrons that develop during fetal life mean less kidney mass for sodium and volume homeostasis, and may predispose these patients to hypertension.

• Salt and volume: African Americans, patients who are obese, and elderly patients nearly all have salt-sensitive hypertension. Conversely, primitive societies that ingest little salt have no hypertension. Usually, when salt is consumed, a pressure natriuresis occurs that excretes the excess salt and volume. Patients who are salt sensitive need higher BPs to excrete a sodium load. One reason for sodium sensitivity could result from kidney tubulointerstitial inflammation and ischemia.

• The sympathetic nervous system: The sympathetic nervous system increases renin secretion, decreases urinary sodium excretion, and decreases kidney blood flow. Increased sympathetic activity may be one of the mechanisms that leads to kidney damage and salt-sensitive hypertension. The sympathetic nervous system is overactive in patients with CKD, and kidney denervation, nephrectomy, or angiotensin-converting enzyme inhibition are possible treatment modalities to decrease sympathetic activation. The recently discovered enzyme renalase, which is mostly produced in the kidney, inactivates circulating catecholamines and may be important for BP regulation.

• The renin-angiotensin-aldosterone system: Renin, secreted by the juxtaglomerular cells of afferent arteriole, cleaves angiotensinogen to angiotensin I (ATI). ATI is converted to angiotensin II (ATII) by ACE. ATII increases kidney sodium reabsorption, kidney arteriolar vasoconstriction, and aldosterone secretion. With kidney damage, increased ACE expression may occur and lead to elevated ATII levels. Pathologic levels of ATII can cause kidney damage and salt-sensitive hypertension.

• Oxidative stress: Reactive oxygen species (ROS) are produced in the kidney in the course of oxidative metabolism. An elegant system of enzymes exists in the kidney to neutralize excess ROS. In patients with CKD, this neutralizing system is impaired. Excess ROS can have deleterious consequences. For example, increased ROS can inactivate nitric oxide (NO), a molecule that causes endothelium-dependent vasodilation. Inactivation of NO occurs in oxidative stress (nitrosative stress), and this can lead to hypertension through increased vasoconstriction. Salt-sensitive hypertensives and patients with CKD also have elevated levels of asymmetric dimethylarginine—an inhibitor of NO synthase—which also leads to the reduced production of NO.

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