Etiology
Malignant arteriolar nephrosclerosis is a form of renal damage caused by malignant hypertension. It represents the renal manifestation of a hypertensive emergency and is often accompanied by damage to other target organs, such as retinal hemorrhage and hypertensive encephalopathy. Malignant hypertension frequently occurs in patients with poorly controlled or irregular antihypertensive medication use, as well as in those with excessive sympathetic stimulation due to the abuse of substances such as cocaine or amphetamines.
Pathology
This condition primarily affects the preglomerular arterioles. However, the nature and severity of the lesions differ from those seen in benign arteriolar nephrosclerosis. Pathological features include fibrinoid necrosis of afferent arterioles, interlobular arteries, and arcuate arteries, along with glomerular collapse. In interlobular and arcuate arteries, there is cellular proliferation within the arterial wall, deposition of extracellular matrix, and thickened, multilayered intima, giving the appearance of "onion-skin" lesions. The arterial lumen is severely narrowed or even occluded, and perivascular inflammatory cell infiltration can be seen. The progression of renal parenchymal damage is rapid, leading to glomerular sclerosis, tubular atrophy, and interstitial fibrosis within a short timeframe.
Clinical Manifestations
Clinical features may include hematuria (macroscopic or microscopic) and proteinuria, consistent with manifestations of nephritic syndrome. Renal function deteriorates progressively, often resulting in oliguria and progression to end-stage renal disease within weeks to months. Fundoscopic examination may reveal papilledema. Neurological symptoms such as headache, seizures, or even coma, as well as cardiac complications such as congestive heart failure, may also occur. In some cases, microangiopathic hemolytic anemia develops.
Prevention and Management
Malignant hypertension constitutes a medical emergency. It is essential to manage severely elevated blood pressure to prevent life-threatening complications affecting the heart, brain, and kidneys, while avoiding the risks associated with overly rapid or excessive blood pressure reduction. The recommended approach involves intravenous antihypertensive therapy aimed at reducing blood pressure gradually. During the first hour, the reduction in blood pressure should not exceed 20%–25% of baseline levels. Over the next 2–6 hours, the blood pressure reduction should remain around 25% of the initial level, or diastolic pressure should be maintained between 100–110 mmHg (whichever threshold is higher). Systolic blood pressure is typically lowered to approximately 160 mmHg in the first hour, followed by a gradual reduction to around 140 mmHg over the subsequent 24 hours. Within the next 24–48 hours, based on the patient’s tolerance to antihypertensive therapy, blood pressure is controlled to below 140/90 mmHg.
If malignant arteriolar nephrosclerosis has already developed and renal failure ensues, timely initiation of dialysis is required. In some patients, renal vascular damage may partially improve following blood pressure control, potentially avoiding the need for maintenance dialysis.