Introduction:
Hypertensive arteriolar nephrosclerosis is a condition that causes progressive renal damage due to uncontrolled hypertension. Uncontrolled hypertension constricts and narrows the blood vessels and damages them throughout the body, including organs like kidneys. Uncontrolled hypertension is the second main cause of renal failure. Hypertensive arteriolar nephrosclerosis is also referred to as hypertensive nephrosclerosis, hypertensive nephropathy, nephroangiosclerosis, and hypertensive kidney disease.
What Is Hypertensive Arteriolar Nephrosclerosis?
Hypertensive arteriolar nephrosclerosis is a term that refers to the hardening or stiffening of the renal components that are caused by uncontrolled hypertension. Hypertensive arteriolar nephrosclerosis is a clinical syndrome that is characterized by chronic hypertension, left ventricular hypertrophy (thickening of the walls of the heart chambers), minimal proteinuria (presence of proteins in the urine), hypertensive retinopathy (retinal vascular damage due to hypertension), and progressive kidney failure. The pathological changes in the kidneys are due to the effects of uncontrolled hypertension. Chronic hypertension damages the tissues, blood vessels, glomeruli, interstitial tissues, and renal tubules in the kidneys, resulting in chronic kidney disease. Hypertensive arteriolar nephrosclerosis is one of the causes of end-stage kidney diseases. It progresses to end-stage kidney disease in a small percentage of individuals.
How Does Hypertensive Arteriolar Nephrosclerosis Occur?
Benign arterial hypertension causes the accumulation of amorphous homogenous material called hyaline in the walls of small arteries and arterioles. This accumulation results in the thickening and narrowing of the arterial openings by a process called arteriolosclerosis. This process reduces the blood flow to the kidneys and causes interstitial fibrosis, tubular atrophy, glomerular alterations, and scarring around the glomeruli. These pathological changes progress to cause renal failure. It is also associated with complications like protein and blood in the urine due to glomerular damage.
Chronic hypertension is the main factor that is responsible for the development of end-stage renal disease. Two pathological mechanisms contributing to the development of hypertensive arteriolar nephrosclerosis describe how the glomerulus and the network of dense capillaries that carry out the filtration process are affected.
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Glomerular Ischemia: Glomerular ischemia is the main pathological mechanism that contributes to hypertensive nephrosclerosis. High blood pressure that is persistent for long-term damages the lining of the blood vessel called the endothelium. This causes plaque accumulation and deposition in the renal arteries, causing stenosis and ischemic kidney disease. As a result, the narrowed renal artery supplies inadequate blood to the kidneys. This causes a decrease in the size of the kidneys. Arterial stiffening involves the breakdown of elastic fibers and the thickening of the innermost layer of the blood vessel.
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Glomerular Hypertension and Glomerular Hyperfiltration : Another mechanism that causes hypertensive nephropathy is prolonged glomerular hypertension, which results in glomerular hyperfiltration. The mechanism behind this is hypertension causes sclerosis of the glomeruli and reduces kidney function. The unaffected nephrons compensate by vasodilating to increase the blood flow. As a compensatory mechanism, this increases renal perfusion and glomerular filtration across unaffected glomeruli.
What Causes Hypertensive Arteriolar Nephrosclerosis?
Chronic blood pressure damages the kidney tissues, including the glomeruli, small blood vessels, kidney tubules, and interstitial tissues. Hardening of the tissues and narrowing of the blood vessels is observed. The narrowed arteries supply less oxygen to the tissues resulting in ischemia (tissue death). The risk factors include poorly controlled blood pressure, other kidney disorders, and older age.
What Are the Signs and Symptoms Associated With Hypertensive Arteriolar Nephrosclerosis?
Hypertensive arteriolar nephrosclerosis is the second most common cause of end-stage kidney disease, the first being diabetes. The signs and symptoms of hypertensive nephrosclerosis include itching, sleepiness or confusion, nausea, vomiting, loss of appetite, and an unpleasant taste in the mouth. Malignant nephrosclerosis occurs if malignant hypertension is present. Malignant hypertension occurs if the diastolic blood pressure is greater than 130 mmHg. The blood vessels present with fibrinoid necrosis, intimal thickening, thrombosis, red blood cell fragmentation, and extravasation.
How Is Hypertensive Arteriolar Nephrosclerosis Diagnosed?
The diagnosis of arteriolar nephrosclerosis is based on the clinical history and biochemical investigations. This includes the following tests:
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Histopathological Examination: A definitive diagnosis can be made with a biopsy and histological examination. Histological examination shows the presence of large renal arteries with medial hypertrophy, intimal thickening, and duplication of the elastic layer. Hyaline deposition in small arterioles, glomerular collapse, and solidification is seen. Scarring of the tissues can also be observed.
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Urine Test: Chronic kidney diseases damage the glomeruli and allow the filtration of proteins that are too large to enter the nephron. This causes an elevation in the albumin concentration in urine, called albuminuria. Protein in the urine is called proteinuria. Proteinuria is a common finding in individuals with nephrosclerosis. Proteinuria is observed in the range of 0.001 to 0.01 pound per 24-hour urine. Hematuria can occur if glomerular damage is present.
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Other Tests: Other laboratory tests like hematocrit, creatinine, serum potassium, serum calcium, and blood glucose tests are also performed.
The definitive diagnosis is based on morphological examination. This procedure is usually preceded by a provisional diagnosis based on laboratory investigations. Increasing the access and use of genome profiling may help to identify ApoL1 gene variants on chromosome 22 and provide an opportunity for diagnosis.
How Is Hypertensive Arteriolar Nephrosclerosis Treated?
Hypertensive arteriolar nephrosclerosis management is based on strategies to slow down the progression of the disease by controlling blood pressure and reducing albumin levels. According to current guidelines, the ideal blood pressure should be less than 16/11 kPa for individuals with hypertensive nephropathy. Blood pressure higher than this can increase cardiovascular risk.
Drugs like ACE (angiotensin-converting enzyme) inhibitors, direct renin inhibitors, angiotensin receptor blockers, and aldosterone antagonists are prescribed to lower blood pressure and reduce neuropathy and proteinuria. Lifestyle changes, weight reduction, exercise, and reduced salt intake can help manage hypertensive nephropathy. Hemodialysis is done for patients with end-stage kidney disease.
Conclusion:
Hypertensive arteriolar nephrosclerosis is a progressive disease caused by chronic hypertension. It causes stiffening and hardening of the renal components and reduces the blood flow. It progresses to end-stage kidney disease. Uncontrolled hypertension is the main reason for hypertensive arteriolar nephrosclerosis. The treatment aims to reduce blood pressure, nephropathy, proteinuria, and albumin. Lifestyle modifications are also essential to treat hypertensive nephropathy. Early detection and treatment can prevent the progression of the disease.
