Renal hypertension, also called renovascular hypertension, is a type of high blood pressure caused by an identifiable underlying issue originating in the kidneys or their blood supply. This condition is classified as secondary hypertension, meaning it results from a specific medical problem, unlike primary hypertension, which has no known single cause. High blood pressure due to kidney issues indicates dysfunction in the organs responsible for regulating long-term blood pressure. Understanding these specific mechanisms is important for appropriate diagnosis and treatment.
The Renin-Angiotensin-Aldosterone System and Blood Pressure Control
The body maintains blood pressure stability through the hormonal pathway known as the Renin-Angiotensin-Aldosterone System (RAAS). This system activates when specialized juxtaglomerular cells in the kidney detect a reduction in blood flow or pressure within the renal artery. In response to this perceived low pressure, the kidney releases the enzyme renin into the bloodstream.
Renin initiates a cascade by converting a liver-produced protein, angiotensinogen, into angiotensin I. Angiotensin I is then converted by the Angiotensin-Converting Enzyme (ACE) in the lungs and kidneys into the highly active hormone, angiotensin II. Angiotensin II is a potent vasoconstrictor, causing the muscular walls of small arteries throughout the body to tighten and narrow. This immediate constriction increases systemic blood pressure.
Beyond its direct constricting effect, angiotensin II also stimulates the adrenal glands to release a hormone called aldosterone. Aldosterone acts on the kidney tubules, signaling them to increase the reabsorption of sodium and water back into the bloodstream. This retention of salt and fluid increases the total volume of blood circulating in the body. The combination of widespread blood vessel constriction and increased blood volume leads to the sustained elevation in blood pressure characteristic of renal hypertension.
Atherosclerosis and Renal Artery Narrowing
The most frequent cause of renovascular hypertension is the narrowing of the renal artery due to atherosclerosis. This condition involves the progressive buildup of plaque—a sticky mixture of fat, cholesterol, and calcium—within the artery walls. Over time, this plaque hardens and restricts the space through which blood flows to the kidney tissue.
This restriction triggers the RAAS mechanism because the kidney senses the reduced blood flow as low blood pressure. Atherosclerotic renal artery stenosis accounts for approximately 90% of all renovascular hypertension cases. The resulting hypertension is often difficult to manage with standard medications because the underlying hormonal driver remains constantly active.
The risk factors for this form of renal hypertension are the same ones that promote atherosclerosis elsewhere in the body. These include advancing age, high cholesterol levels, diabetes, and a history of tobacco use. Atherosclerotic plaques typically form closer to the opening of the renal artery where it branches off the aorta.
Fibromuscular Dysplasia
Fibromuscular Dysplasia (FMD) is the second major cause of renovascular hypertension, though it is much less common than atherosclerosis. FMD is characterized by the abnormal growth of cells within the walls of the renal artery. This irregular tissue growth causes the artery to develop alternating sections of narrowing and widening.
This uneven structure gives the artery an appearance described as a “string of beads” on imaging tests. Unlike atherosclerosis, FMD is not caused by plaque buildup or driven by inflammation. It most frequently affects younger individuals, particularly women, often causing high blood pressure that begins suddenly or at an unusually young age.
The resulting high blood pressure is directly caused by the narrowed segments of the renal artery. These constrictions impede the normal flow of blood to the kidney, which interprets the reduced delivery as low blood pressure. This false signal leads to the inappropriate activation of the RAAS cascade, raising systemic pressure.
Renal Parenchymal Disease
Renal hypertension can also stem from damage to the functional tissue of the kidney itself, known as the parenchyma, rather than just the supplying arteries. This is the most frequent cause of secondary hypertension overall, accounting for 2.5% to 5% of all hypertension cases. Conditions in this category include chronic kidney disease (CKD), glomerulonephritis, and polycystic kidney disease.
One primary mechanism involves the kidney’s impaired ability to manage fluid and electrolytes. As functioning nephrons are destroyed by disease, the remaining tissue struggles to excrete enough sodium and water. This inability to properly handle salt and fluid leads to an expansion of the body’s blood volume, which directly raises blood pressure.
Tissue damage in the kidney can also lead to the inappropriate activation of the RAAS and other hormonal systems. Scarred or poorly perfused kidney tissue can release renin, even without a major blockage in the main renal artery. Damaged kidneys may also fail to produce sufficient amounts of substances that normally help blood vessels relax, such as nitric oxide. Conversely, they may increase the production of substances that cause vasoconstriction, such as endothelin.