Conditions · Nephrology and urology
Hypertensive nephrosclerosis !
Long-standing high blood pressure scars the small arteries of the kidneys, slowly reducing kidney function. It is a leading cause of chronic kidney disease.
Updated 2026-11-01
Structures involved
Tap one to see what it is and open it in 3D.
- Kidneys
- Vessels inside the kidney
- Right renal artery
- Left renal artery
- Abdominal aorta
- Right adrenal gland
- Left adrenal gland
- Left ventricle
- Retina
Why it happens
- Intracellular accumulations: cholesterol, proteins, hyaline, glycogen
- Atrophy
- Physiology of hypertension
- Renal blood flow, autoregulation and tubuloglomerular feedback
- Blood vessels: artery, vein and capillary layers
- Kidney: cortex, medulla and the nephron
What it is
Kidney damage caused by chronic hypertension, with thickening and hyalinisation of the small renal arteries and arterioles, ischaemic glomerular scarring and slow loss of function. A rare acute form, malignant nephrosclerosis, occurs with very severe hypertension.
Who gets it
Hypertension is very common in Colombia and Latin America and is, after diabetes, one of the most frequent causes of chronic kidney disease and dialysis. It is more frequent and more aggressive in people of African ancestry, partly linked to APOL1 gene variants, which is relevant to Afro-Colombian populations.
Causes
- Long-standing, poorly controlled essential hypertension (benign nephrosclerosis)
- Severe or malignant hypertension (malignant nephrosclerosis)
- Genetic susceptibility, notably APOL1 risk variants in people of African ancestry
Risk factors
- Uncontrolled hypertension of long duration
- African ancestry
- Older age
- Diabetes, obesity, smoking and dyslipidaemia
- Low birth weight (fewer nephrons) and family history of kidney disease
Pathophysiology
Chronic high pressure causes hyaline arteriolosclerosis (glassy thickening of arteriolar walls) and intimal fibrosis of interlobular arteries. The narrowed vessels reduce glomerular blood flow, producing global glomerulosclerosis, tubular atrophy and interstitial fibrosis; kidneys become small with a finely granular surface. In malignant hypertension, endothelial injury causes fibrinoid necrosis and concentric "onion-skin" hyperplastic arteriolosclerosis with acute ischaemia and possible haemolysis.
Classification
- Benign (chronic) nephrosclerosis: hyaline arteriolosclerosis, slow decline
- Malignant nephrosclerosis: fibrinoid necrosis and hyperplastic (onion-skin) arteriolosclerosis, acute kidney injury
Symptoms and signs
- Usually no symptoms until kidney function is advanced
- Found by a rising creatinine or mild proteinuria on routine tests in a hypertensive patient
- Nocturia from reduced concentrating ability
- Late: fatigue, oedema, nausea and itching of chronic kidney disease
- Other target-organ damage: left ventricular hypertrophy, hypertensive retinopathy
Diagnosis
- Clinical
- Mostly a diagnosis of exclusion: long-standing hypertension preceding kidney disease, other target-organ damage, bland urine sediment and no evidence of another kidney disease.
- Tests
- Creatinine with eGFR, urine albumin-to-creatinine ratio (usually modest proteinuria), urinalysis without active sediment, electrolytes, ECG for left ventricular hypertrophy. Biopsy is reserved for atypical cases (heavy proteinuria, haematuria, rapid decline).
- Imaging
- Kidney ultrasound shows symmetrically small kidneys with thin cortex in advanced disease; renal artery Doppler or CT angiography when renovascular disease is suspected. Echocardiography for left ventricular hypertrophy.
Differential diagnosis
- Diabetic kidney disease
- Renal artery stenosis (renovascular hypertension)
- Chronic glomerulonephritis causing secondary hypertension
- Focal segmental glomerulosclerosis (including APOL1-associated)
- Atheroembolic kidney disease
Goal of treatment
Control blood pressure to target, reduce albuminuria and cardiovascular risk, and slow progression to kidney failure.
Treatment
- Lifestyle
- Lifestyle: salt restriction, weight control, physical activity, limiting alcohol and stopping smoking.
- Medical
- Antihypertensives, preferring ACE inhibitors or ARBs when albuminuria is present; diuretics and calcium-channel blockers are often added to reach target.
- Medical
- Additional kidney and heart protection in CKD: statins, and SGLT2 inhibitors in selected patients.
- Acute
- Hypertensive emergency with malignant nephrosclerosis: controlled lowering of blood pressure with intravenous agents in a monitored setting.
- Follow-up
- Monitoring of home and clinic blood pressure, creatinine, potassium (especially after starting ACE inhibitors or ARBs) and albuminuria; dialysis or transplant planning when kidney failure approaches.
Complications
- Chronic kidney disease progressing to kidney failure and dialysis
- Left ventricular hypertrophy and heart failure
- Coronary disease and stroke
- Hypertensive retinopathy
- Malignant hypertension with acute kidney injury and thrombotic microangiopathy
Prognosis
With good blood pressure control, most patients have slow progression; cardiovascular disease is a bigger threat than kidney failure. Progression is faster in people of African ancestry, with heavy proteinuria or with poor control. Malignant hypertension untreated has a high mortality.
Prevention
- Early detection and sustained control of hypertension
- Screening of hypertensive patients for albuminuria and reduced eGFR
- Healthy diet low in salt and ultra-processed food
Test yourself
Think of the answer, then tap the question to see it.
What is the characteristic vascular lesion of benign hypertensive nephrosclerosis?
Hyaline arteriolosclerosis: homogeneous pink thickening of arteriolar walls.
What arteriolar change is seen in malignant hypertension?
Hyperplastic "onion-skin" arteriolosclerosis with fibrinoid necrosis.
What do the kidneys look like on imaging in advanced hypertensive nephrosclerosis?
Symmetrically small kidneys with thin cortex and a finely granular surface.
Which antihypertensive classes are preferred when albuminuria is present?
ACE inhibitors or angiotensin receptor blockers.
Which genetic variant raises the risk of hypertension-related kidney disease in people of African ancestry?
APOL1 risk variants.
Related conditions
- Arterial hypertension
- Chronic kidney disease
- Hypertensive heart disease
- Hypertensive retinopathy
- Hypertensive emergency and urgency
- Diabetic kidney disease
- Renovascular hypertension (renal artery stenosis)
- Focal segmental glomerulosclerosis
- Ischaemic stroke
Educational information, not medical advice. For any symptom, see a health professional.
Sources: High Blood Pressure & Kidney Disease (NIDDK (National Institutes of Health), 2024).
Spotted a mistake?We are always improving for the community. Tell us what is wrong and our team will review it.Report a mistake
Representative model, for educational purposes only.
