Secondary Hypertension 

1. When Should You Suspect Secondary Hypertension? 

  • Onset <30 years (without obesity/family history)
  • Onset >55 years with sudden worsening
  • Resistant hypertension (≥3 drugs including diuretic)
  • Malignant/accelerated hypertension
  • Sudden deterioration in renal function after ACEi/ARB
  • Unexplained hypokalaemia
  • Episodic headache, palpitations, sweating
  • Discrepant arm-leg BP
  • Recurrent flash pulmonary oedema

 

2. Causes of Secondary Hypertension

A. Renal Causes (Most Common)

1️⃣ Renal Parenchymal Disease

Most common cause overall.

Pathophysiology

  • Nephron mass sodium retention
  • RAAS activation
  • Volume expansion
  • Sympathetic activation

Causes

  • Chronic glomerulonephritis
  • Diabetic nephropathy
  • Reflux nephropathy
  • Polycystic kidney disease
  • Obstructive uropathy

Clues

  • Abnormal urinalysis
  • Elevated creatinine
  • Small kidneys on ultrasound (except PKD)

Investigation

  • Urine protein
  • eGFR
  • Renal ultrasound

 

2️⃣ Renovascular Hypertension

Causes

  • Atherosclerosis (elderly males)
  • Fibromuscular dysplasia (young females)

Pathophysiology

Renal hypoperfusion RAAS activation Angiotensin II vasoconstriction + aldosterone

Clues

  • Resistant HTN
  • Flash pulmonary oedema
  • Renal bruit
  • Rise in creatinine after ACEi

Investigation

  • Doppler US
  • CT angiography
  • MR angiography

Management

  • ACEi (caution bilateral)
  • Revascularisation (selected cases)

 

B. Endocrine Causes

1️⃣ Primary Hyperaldosteronism (Conn’s Syndrome)

Pathophysiology

Aldosterone sodium retention + potassium loss

Clues

  • Resistant HTN
  • Hypokalaemia
  • Metabolic alkalosis

Screening Test

Aldosterone-renin ratio (ARR)

High aldosterone + suppressed renin = diagnostic clue

Confirmatory tests

  • Saline suppression test
  • Adrenal vein sampling

Management

  • Unilateral adenoma surgery
  • Bilateral hyperplasia spironolactone

Hypertension + hypokalaemia = Think primary aldosteronism

 

2️⃣ Phaeochromocytoma

Tumour of chromaffin cells.

Classic Triad

  • Headache
  • Sweating
  • Palpitations

Pathophysiology

Catecholamines α1 vasoconstriction

Diagnosis

  • Plasma free metanephrines
  • 24-hour urinary metanephrines
  • MRI abdomen

Associations

  • MEN2
  • NF1
  • VHL

Management

  1. Alpha-blockade (phenoxybenzamine)
  2. Then beta-blocker
  3. Surgery

Never give beta-blocker before alpha-blockade.

 

3️⃣ Cushing’s Syndrome

Mechanism

Cortisol has mineralocorticoid activity sodium retention.

Clues

  • Central obesity
  • Striae
  • Diabetes
  • Osteoporosis

Screening

  • Overnight dexamethasone suppression test

 

4️⃣ Thyroid Disorders

Hyperthyroidism

  • Systolic BP
  • Wide pulse pressure

Hypothyroidism

  • Diastolic BP

 

C. Vascular Causes

Coarctation of Aorta

Congenital narrowing of aorta.

Clues

  • Young patient
  • Radio-femoral delay
  • Rib notching
  • Upper limb HTN, lower limb hypotension

 

D. Obstructive Sleep Apnoea (OSA)

Very common cause.

Mechanism

  • Intermittent hypoxia
  • Sympathetic activation
  • RAAS activation

Clues

  • Snoring
  • Daytime sleepiness
  • Resistant HTN

 

E. Drug-Induced Hypertension

  • NSAIDs
  • Steroids
  • OCP
  • Cyclosporine
  • Tacrolimus
  • Erythropoietin
  • Cocaine
  • Decongestants

Always take drug history.

 

3. Investigation Strategy 

Step 1: Basic Screening

  • U&E
  • Creatinine
  • Urine ACR
  • TSH
  • Fasting glucose
  • Lipid profile

Step 2: If Suspicion Based on Clues

Clue

Test

Hypokalaemia

Aldosterone-renin ratio

Episodic symptoms

Plasma metanephrines

Renal bruit

Renal artery imaging

Young + radiofemoral delay

Echo / MRI

Snoring + obesity

Sleep study