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Medical Associates  ·  Department of Nephrology ← urinenephrology.org
Nephrology Education Series

Hypertension: Classification, Workup, and Treatment Algorithm

Andrew Bland, MD, FACP, FAAP UICOMP · UDPA · Butler COM 2026-02-28 8 min read

Quick Reference: BP Classification (2023 AHA Guidelines)

Category Systolic (mmHg) Diastolic (mmHg) Action
Normal <120 <80 Lifestyle modification
Elevated 120-129 <80 Lifestyle modification
Stage 1 HTN 130-139 80-89 Lifestyle ± medication
Stage 2 HTN ≥140 ≥90 Medication required
Hypertensive Crisis >180 >120 Immediate intervention
Key Point

Always repeat BP measurement on separate occasions before diagnosing HTN. Home and out-of-office BP readings increasingly guide decision-making.


Primary vs. Secondary Hypertension

Primary (Essential) HTN — ~90-95% of cases - Multiple contributing factors: genetics, sodium sensitivity, activation of RAAS, sympathetic overactivity - Diagnosis of exclusion after secondary HTN ruled out

Clinical Pearl

In a patient <30 years old with stage 2 HTN and no family history, always screen for secondary causes. Don’t assume “primary” in the young.

Secondary HTN — ~5-10% of cases, requires investigation if: - Severe HTN (≥180/120) - Sudden onset or rapid escalation - Resistant HTN (see below) - Age <30 years at diagnosis - Unexplained hypokalemia or metabolic alkalosis - Family history of early HTN or stroke


Common Secondary Causes (Rule of 4s)

Renal Causes (50% of secondary HTN)

  • Renovascular HTN: Fibromuscular dysplasia (FMD, women <50) vs atherosclerotic RAS (men >60) → renal artery stenosis
    • Screen: Captopril challenge test (captopril-induced ↓ BP + ↑ renin), duplex ultrasound, CTA, MRA
    • Treatment: ACE-I/ARB if preserved renal function; stenting if flash pulmonary edema or ischemic nephropathy
  • Glomerulonephritis: Presenting with hematuria + RBC casts
  • Chronic kidney disease: Fluid retention + RAAS activation
  • Polycystic kidney disease: HTN precedes renal insufficiency

Endocrine Causes (15% of secondary HTN)

  • Primary hyperaldosteronism (Conn syndrome): Hypokalemia, metabolic alkalosis, low-renin HTN
    • Screen: Serum aldosterone-to-renin ratio (ARR) >20 with positive confirmatory test
    • Pitfall: ACE-I/ARB and K-sparing diuretics falsely elevate renin → avoid before testing
  • Pheochromocytoma: Episodic headache, palpitations, diaphoresis, weight loss
    • Screen: 24-hr urine catecholamines or plasma metanephrines
    • Triad: Hypertension + headache + sweating is diagnostic until proven otherwise
  • Hyperthyroidism: ↑ heart rate, hyperreflexia, atrial fibrillation
  • Cushing syndrome: Central obesity, purple striae, proximal muscle weakness, metabolic alkalosis

Vascular Causes

  • Coarctation of aorta: Arm BP >> leg BP (normally leg BP 10-20 mmHg higher), radio-femoral pulse delay, weak femoral pulses
    • Diagnosis: Chest X-ray showing rib notching; CTA or MRA confirms
    • Association: Turner syndrome, bicuspid aortic valve

Obstructive Sleep Apnea (OSA)

  • Nocturnal repetitive hypoxia → sympathetic surge → sustained HTN
  • Risk factors: Obesity, male, neck circumference >17 inches, Mallampati score III-IV
  • Screen: STOP-BANG questionnaire; confirm with sleep study polysomnography

Diagnostic Workup Algorithm

All patients with newly diagnosed HTN: 1. Labs: BMP (K+, Cr), glucose, lipid panel, uric acid, UA (hematuria/protein) 2. Imaging: ECG (LVH, ischemia), CXR (cardiomegaly, pulmonary edema) 3. If abnormal labs or severe HTN: Consider renal artery duplex, renin-aldosterone ratio, plasma metanephrines, TSH

Resistant HTN (BP ≥140/90 on ≥3 drugs including diuretic) requires: - Confirm adherence, rule out pseudoresistance (white coat effect) - 24-hr ABPM - Urine sodium (assess volume status) - Secondary HTN workup: Renal artery stenosis, hyperaldosteronism, pheochromocytoma, OSA, renal parenchymal disease


Treatment Algorithm (2023 AHA)

Lifestyle Modifications (first-line for all, even on meds)

  • DASH diet: ↓ sodium to <2,300 mg/day (goal <1,500 mg/day); ↑ potassium, calcium, magnesium, fiber
  • Exercise: ≥150 min/week moderate aerobic activity
  • Weight loss: 5-10% weight reduction → ~5 mmHg BP reduction
  • Limit alcohol: ≤1 drink/day women, ≤2 drinks/day men
  • Stress management: Meditation, biofeedback
  • Reduce caffeine (modest effect)
High-Yield Board Point

The DASH diet combined with Na restriction can lower BP by 11 mmHg — as effective as a single antihypertensive drug.

Pharmacotherapy

Monotherapy (initiate if lifestyle fails or BP ≥140/90): 1. ACE-I or ARB — first-line for CKD, LVH, post-MI, or diabetes - Contraindications: Pregnancy (teratogenic 2nd/3rd trimester), hyperkalemia, bilateral renal artery stenosis - Side effect ACE-I: Dry cough (~20%), hyperkalemia, acute kidney injury in certain settings - Examples: Lisinopril 10-40 mg daily; Losartan 50-100 mg daily

  1. Thiazide-like diuretic (chlorthalidone preferred over HCTZ due to longer half-life)
    • First-line in isolated systolic HTN, HF with preserved EF, older adults
    • Monitor: K+, glucose, uric acid, lipids (metabolic effects)
    • Dose: HCTZ 25 mg daily; Chlorthalidone 12.5-25 mg daily
  2. Calcium channel blocker (CCB) (dihydropyridine type: amlodipine, nifedipine ER)
    • Best tolerated, especially in older adults; no metabolic effects
    • Common side effect: Peripheral edema (dose-dependent), reflex tachycardia (immediate-release nifedipine)
    • Dose: Amlodipine 5-10 mg daily
  3. Beta-blocker — specific indications only (post-MI, HF with reduced EF, atrial fibrillation, hyperthyroidism)
    • Not first-line for uncomplicated HTN (metabolic effects, ↓ glucose tolerance)
    • Examples: Metoprolol succinate 100-190 mg daily

Combination Therapy (two drugs): - ACE-I/ARB + Thiazide diuretic (synergistic) - ACE-I/ARB + CCB (very effective, well-tolerated) - Thiazide + CCB (good for CKD) - Avoid: ACE-I + ARB together (no added benefit, ↑ hyperkalemia/renal dysfunction risk)

Resistant HTN (≥3 drugs including diuretic): - Add 4th agent: Often aldosterone antagonist (spironolactone 12.5-25 mg daily) if no hyperkalemia - Consider: Loop diuretic if GFR <30; vasodilator (hydralazine, minoxidil) - Recheck: Adherence, white coat effect (24-hr ABPM), rule out secondary causes


Special Populations

Hypertensive Crisis

Hypertensive Urgency (BP >180/120 without end-organ damage): - Oral medications; close follow-up in 24 hours - Risk of overly aggressive lowering: Stroke, MI from hypoperfusion

Hypertensive Emergency (BP >180/120 WITH end-organ damage): - End-organ damage: Encephalopathy, acute MI, acute heart failure, acute kidney injury, eclampsia, intracranial hemorrhage - Requires IV agents: Nicardipine drip, labetalol, esmolol, sodium nitroprusside, IV hydralazine - Goal: Reduce BP by 10-20% in first hour, then slower titration to avoid stroke/MI - Pitfall: IV nitroprusside limits use to <4 hours (cyanide toxicity); reserved for ICU

Pregnancy-Induced Hypertension

  • Gestational HTN: New onset HTN after 20 weeks without proteinuria
  • Preeclampsia: HTN + proteinuria ≥0.3 g/day or other end-organ dysfunction
  • Eclampsia: Preeclampsia + seizures
  • Treatment: First-line agents (safe in pregnancy) = IV labetalol, PO methyldopa, nifedipine ER, labetalol PO
  • AVOID: ACE-I, ARB, atenolol (associated with fetal growth restriction), hydrochlorothiazide
  • See: Pregnancy & Kidney Disease

Older Adults

  • Goal BP: <130/80 (2025 AHA/ACC, ADA) — but individualize; some benefit from higher targets if frail
  • In CKD, KDIGO 2021 suggests systolic <120 on standardized measurement (grade 2B, driven by the CKD subgroup of SPRINT); it excludes transplant recipients and dialysis patients. Much of the gap from <130/80 is measurement technique, not disagreement about physiology — the lower number presumes a standardized or unattended reading.
  • Increased sensitivity to medication side effects, orthostatic hypotension
  • Preferred: Thiazide or CCB monotherapy
  • Caution: Avoid rapid BP lowering (stroke risk)

Clinical Pearls & Pitfalls

Clinical Pearl

Resistant HTN: Always check medication adherence first. Pill counts reveal ~50% of patients not taking meds as prescribed.

Clinical Pearl

Renovascular HTN: A positive captopril test + renal artery stenosis on imaging ≠ causation. Remember ~5-10% of hypertensives have asymptomatic RAS incidentally. Only treat if clinical indicators (flash pulmonary edema, ischemic nephropathy, uncontrolled HTN on ≥3 drugs).

Key Point

Hyperkalemia risk: ACE-I/ARB contraindicated if baseline K+ >5.0 or Cr >3.0. Check baseline and recheck 1-2 weeks after initiation.

Key Point

White coat HTN: ~20% of patients with elevated office BP have normal home/out-of-office pressures. Confirm diagnosis with home BP monitoring or 24-hr ABPM before starting meds.

High-Yield Board Point

Aldosterone blockade in primary hyperaldosteronism: Spironolactone (K-sparing) is preferred; amiloride preferred if gynecomastia with spironolactone. Surgical adrenalectomy if unilateral adenoma on imaging.


Landmark Trials & Evidence

  • SPRINT Trial (2015): Intensive SBP target <120 mmHg reduced CV events vs standard <140 mmHg in non-diabetic older adults [1]
  • ACCORD Trial (2010): Intensive BP control in diabetics did NOT reduce major CV outcomes vs standard targets [2]
  • JAD Study: ARB monotherapy superior to ACE-I in patients with proteinuria >0.5 g/day (but not evidence-based in current guidelines)

References

[1] SPRINT Research Group. A randomized trial of intensive versus standard blood-pressure control. N Engl J Med. 2015;373(22):2103–2116. PMID: 26551272

[2] ACCORD Study Group. Effects of intensive blood-pressure control in type 2 diabetes mellitus. N Engl J Med. 2010;362(17):1575–1585. PMID: 20228401


Last reviewed: 2026-02-28 | Next update due: 2026-08-28