Etiology
This condition arises from long-term poorly controlled hypertension. Persistent hypertension over a period of 5 to 10 years can lead to the pathological changes and associated clinical manifestations of benign arteriolar nephrosclerosis.
Pathology
The disease primarily affects the preglomerular arterioles, causing hyaline degeneration of the afferent arterioles and thickening of the muscular intima in interlobular and arcuate arteries. This results in arterial lumen narrowing and reduced blood supply to the kidneys. Consequently, ischemic damage to the renal parenchyma occurs, leading to glomerulosclerosis, tubular atrophy, and interstitial fibrosis.
Clinical Manifestations
Renal tubules are particularly sensitive to ischemia, so the earliest signs include impaired tubular concentration function, such as nocturia, low specific gravity urine, and low osmolality urine. As ischemic damage to the glomeruli progresses, mild abnormalities may appear in urine tests, such as mild proteinuria, occasional red blood cells, and casts. Gradual impairment of glomerular function leads to a decline in glomerular filtration rate, eventually progressing to end-stage renal disease. Alongside kidney damage, hypertension-related complications in the eyes, heart, and brain are often observed.
Prevention and Treatment
The focus should be on prevention by actively managing hypertension. Achieving optimal blood pressure control is critical to preventing kidney damage. For patients with concurrent diabetes or existing kidney damage, most guidelines recommend a target blood pressure below 130/80 mmHg. In terms of medication, ACE inhibitors (ACEI) or angiotensin receptor blockers (ARB) have demonstrated renal protective effects independent of their blood pressure-lowering properties. Once benign arteriolar nephrosclerosis develops, controlling hypertension remains essential for slowing the progression of kidney damage.