Summary

Hypertensive Nephropathy (also called Benign Nephrosclerosis) is chronic kidney disease (CKD) caused by long-standing systemic hypertension. The sustained elevated blood pressure damages the intrarenal vasculature (afferent arterioles), leading to glomerular ischaemia, scarring (glomerulosclerosis), and progressive loss of renal function. It is the second most common cause of End-Stage Renal Disease (ESRD) worldwide, after Diabetic Kidney Disease, and is particularly prevalent in Afro-Caribbean populations (linked to APOL1 gene variants). The relationship between hypertension and CKD is bidirectional: hypertension causes CKD, and CKD exacerbates hypertension. Treatment focuses on strict blood pressure control, primarily with ACE inhibitors or ARBs, which are renoprotective. [1,2]

Clinical Pearls

Diagnosis of Exclusion: Hypertensive nephropathy is often a presumptive diagnosis. There is no specific diagnostic test. You assume it when a patient with long-standing HTN has mild proteinuria (less than 1g/day), small kidneys, and other end-organ HTN damage (LVH, Retinopathy), and other causes (Diabetes, Glomerulonephritis) are excluded.

Proteinuria is a Key Clue: Hypertensive nephropathy causes MILD proteinuria (typically less than 1g/day). If the patient has HEAVY (Nephrotic range >3g/day) proteinuria, think of a primary glomerular disease (FSGS, Membranous), NOT hypertensive nephrosclerosis.

Ethnicity Matters: Afro-Caribbean individuals are at 3-4x higher risk of developing hypertensive ESRD compared to Caucasians, even with similar BP levels. This is linked to APOL1 gene high-risk variants.

ACE-inhibitors May Cause Initial Creatinine Rise: A rise in creatinine of up to 25-30% after starting ACEi/ARB is acceptable and expected (reduced intraglomerular pressure). A rise >30% suggests Renal Artery Stenosis.

• Slow Progression: With good BP control, CKD can remain stable for years or decades.
• Progression to ESRD: ~5-10% of hypertensive nephropathy patients progress to ESRD.
• Major Determinant of Mortality: Cardiovascular Disease, NOT ESRD.
• Ethnicity: Afro-Caribbean individuals have faster progression.
• Prognostic Factors: Baseline eGFR, Proteinuria level, BP control.

Key Guidelines

Landmark Evidence

1. SPRINT Trial (NEJM 2015)

• Intensive BP control (Target less than 120 Systolic) vs Standard (less than 140) in high-risk non-diabetics.
• Result: Intensive control significantly reduced CV events and mortality.
• Impact: Shifted BP targets lower in CKD (though more AKI in intensive arm).

2. ONTARGET Trial (NEJM 2008)

• Combination ACEi + ARB vs either alone.
• Result: Combination did NOT improve outcomes and INCREASED adverse events (Hypotension, Hyperkalaemia, AKI).
• Impact: Do NOT combine ACEi and ARB.

How did my blood pressure hurt my kidneys?

"Think of your kidneys like a very fine coffee filter. If you blast water through it at high pressure for years, the filter itself thickens and scars up to protect itself. This scarring eventually clogs the filter and stops it working."

Can we fix the damage?

"We cannot reverse the scarring that has already happened. But by lowering your blood pressure carefully with tablets, we can stop any further damage and keep your kidneys working well for a long time. Most people with this condition never need dialysis if their blood pressure is controlled."

Why are you checking if I have heart problems?

"People with kidney problems caused by high blood pressure are much more likely to have problems with their heart – like heart attacks or heart failure. So we check your heart health regularly and give you tablets (like statins) to protect it."

Common Exam Questions

1. Diagnosis: "How do you diagnose hypertensive nephropathy?"
   • Answer: Diagnosis of exclusion. Long-standing HTN + CKD + Mild Proteinuria + Bilateral small kidneys + Other end-organ HTN damage + Exclusion of DM and GN.
2. Histology: "Pathognomonic feature on biopsy?"
   • Answer: Hyaline Arteriolosclerosis.
3. Proteinuria: "Heavy proteinuria in a hypertensive patient with CKD?"
   • Answer: This is NOT typical of hypertensive nephropathy. Consider primary glomerulonephritis (FSGS, Membranous, IgAN).
4. Drug: "Why ACEi first-line?"
   • Answer: Reduces intraglomerular pressure (Efferent arteriole dilation), reduces proteinuria, slows CKD progression (Renoprotection beyond BP lowering).

Viva Points

• Afro-Caribbean Risk: Explain the APOL1 gene risk variants (G1, G2).
• Creatinine Rise on ACEi: Explain why up to 25-30% rise is acceptable (Reduced intraglomerular pressure); >30% suggests Renal Artery Stenosis.

Medical Disclaimer: MedVellum content is for educational purposes and clinical reference. Clinical decisions should account for individual patient circumstances. Always consult appropriate specialists.