Hypertension
Description
- Hypertension is both a cause and a consequence of CKD - a self-reinforcing cycle
- Renovascular and renoparenchymal disease are the commonest secondary causes of hypertension overall
Epidemiology
- HTN present in >80% of CKD stage 4-5
- Prevalence and severity rise with declining eGFR
- Secondary (renal) causes account for the majority of identifiable secondary hypertension
Aetiopathogenesis
- Renoparenchymal HTN - nephron loss -> RAAS activation + Na+/volume retention -> hypertension -> further glomerular injury (hyperfiltration) -> self-perpetuating cycle
- Renovascular HTN
- Atherosclerotic renal artery stenosis - older patients, often with diffuse vascular disease
- Fibromuscular dysplasia - younger women, "string of beads" appearance
- Mechanism: reduced renal perfusion -> renin release -> angiotensin II -> systemic vasoconstriction + aldosterone -> Na+ retention
- Sympathetic overactivity and endothelial dysfunction contribute in advanced CKD
Diagnosis
Suspect renovascular disease if
- Resistant HTN (uncontrolled on >=3 agents including a diuretic)
- Sudden worsening of previously controlled HTN, or HTN onset <30 or >55 years
- Renal function decline >30% after starting ACEi/ARB (suggests bilateral RAS or stenosis to a solitary kidney)
- Recurrent flash pulmonary oedema, abdominal bruit, asymmetric kidney size
Investigations
- Renal artery duplex ultrasound (first-line, operator-dependent) or CT/MR angiography
- Renin/aldosterone if suspecting a mineralocorticoid contribution
- Assess for target-organ damage - LVH, retinopathy, proteinuria
Management
Blood pressure target - KDIGO 2024
- Target office SBP <120 mmHg (standardised measurement) for most adults with CKD and hypertension - lowered from the previous <130 target
- Individualise/relax in frailty, high falls risk, limited life expectancy, or symptomatic orthostasis
Drug choice
- RAAS inhibition (ACEi or ARB) first-line if proteinuric CKD - reduces intraglomerular pressure independent of systemic BP effect
- Expect and tolerate a creatinine rise up to ~30% after initiation - do not stop unless it exceeds this or hyperkalaemia is uncontrollable
- Add diuretic (thiazide-like if eGFR permits; loop diuretic once eGFR <30) for volume control
- Potassium binders (SZC/patiromer) allow RAASi continuation despite hyperkalaemia in CKD
- CCB, beta-blocker as further agents per usual algorithm
- Avoid dual RAAS blockade (ACEi + ARB, or + direct renin inhibitor) - no added benefit, inc AKI/hyperkalaemia risk
Renovascular disease
- Medical therapy is first-line even when stenosis is found - RAAS inhibition + statin + antiplatelet
- Angioplasty/stenting reserved for: failure of medical therapy, recurrent flash pulmonary oedema, or progressive renal function decline attributable to the stenosis (revascularisation trials show no routine mortality/renal benefit over medical therapy alone)
Associations
- Left ventricular hypertrophy, heart failure (esp. HFpEF)
- Accelerated CKD progression, proteinuria
- Stroke, retinopathy
- Hypertensive emergency/malignant hypertension -> thrombotic microangiopathy, AKI
Natural history & complications
- Uncontrolled HTN is the single most modifiable driver of CKD progression alongside proteinuria control
- Renal artery stenosis - progressive luminal narrowing over years; some progress to renal atrophy despite intervention
- Adequate BP control substantially reduces cardiovascular events, the leading cause of death in CKD
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