Case 6: Maria Rossi

Renal Artery Stenosis (RAS)

Narrowing of renal arteries or branches = Impair blood flow to kidneys

RAS: Epidemiology

Cause 1-10% of HTN cases

Risk Factors:

• Depend on underlying cause

• Smoking

RAS: Etiology

Atherosclerosis

Renal artery fibromuscular dysplasia

RAS: Atherosclerosis

90%

Mostly men > 50 years

Aterionephrosclerosis: Atherosclerotic plaques in renal arteries

RAS: Renal Artery Fibromuscular Dysplasia

Renal artery stenosis from connective tissue and muscle fibre proliferation

• 10%

• Mostly women < 50 years

RAS: Pathophysiology

1. Cause dependent:

• Arterionephrosclerosis: Sustained high BP = Endothelial injury = Hyaline deposition in arterial walls

• Fibromuscular Dysplasia: Connective tissue and muscle tissue hyperplasia = Obstruct renal artery

2. Renal artery lumen narrowing = Decrease blood flow to kidneys = Ischemia

• Prolonged ischemia = Renal injury + atrophy

3. Renal hypoperfusion = JG cells release renin = Activate RAAS = Increase aldosterone = Increase Na+ retention and vasoconstriction

• JG hyperplasia

4. Secondary HTN

RAS: Clinical Presentation

Severe/early-onset HTN

Abdominal bruit

Pulmonary edema

Atherosclerosis symptoms

• CAD

• Carotid stenosis

RAS: Investigations

Imaging

Lab studies

RAS: Imaging

Diagnostic

First-Line:

• Duplex ultrasonography

• MR angiography

• CT angiography

Second-Line: Catheter angiography

RAS Imaging: Duplex Ultrasonography

Ultrasound image + Doppler

Determine occlusion site + severity

RAS Imaging: MR Angiography

MRI for blood vessels

No contrast (kidney injury)

RAS Imaging: CT Angiography

Fibromuscular dysplasia

RAS Imaging: Catheter Angiography

Gold standard

Catheter + dye to visualize arteries

RAS: Lab Studies

Supportive

BMP:

• Renal insufficiency

• Hypokalemia (rare)

Urinalysis:

• Proteinuria

RAS: Complications

CVD

Kidney disease

• Progress to end-stage

• Renal injury + atrophy

Renal artery dissection

Secondary HTN

Elevated BP (≥ 140/90 mmHg) caused by underlying condition

Secondary HTN: Etiology

RAS

Hyperaldosteronism

Thyroid dysfunction

Renal parenchymal disease

Secondary HTN: Pathogenesis

Depend on underlying cause

Vasoconstriction + Na+/water retention = Increase ECF (intravascular) = Increase BP

Secondary HTN: Clinical Presentation

Usually asymptomatic

Nonspecific symptoms

• Same as primary HTN

Severe symptoms

• Treatment-resistant HTN

• Organ damage disproportionate to HTN degree

Unusual onset

• Abrupt

• < 30 years

Hypokalemia

Secondary HTN: Investigations

Same as primary HTN

• BP measurements

• Lab studies

• ECG

• Physical exam

Secondary HTN: Lab Studies

Blood test

• Fasting glucose or Hb A1c

• CBC

• Lipid profile

• Serum creatinine

• Electrolytes

• TSH

Urinalysis

• Albumin:Creatinine

Secondary HTN: ECG

Abnormal → Echo

Secondary HTN: Treatment/Management

Same as primary HTN

• Treat underlying cause

• Pharmacotherapy (ACE inhibitors, ARBs)

Secondary HTN Pharm Adverse Effects: ACE Inhibitors

Increased bradykinin (inflammatory mediator) = Vasodilation + bronchoconstriction

• C: Dry Cough

• A: Angioedema (deep skin swelling)

P: Pemphigus vulgaris (autoimmune skin blistering)

T: Teratogenicity

O: HypOtension

P: Hyperkalemia (Potassium)

R: Renal failure (proteinuira)

I: Increased creatinine

L: Low GFR → AKI

Switch to ARBs

Secondary HTN Pharm Adverse Effects: ARBs

Angioedema

Hyperkalemia

Teratogenicity

Low GFR + High creatinine → AKI

Secondary HTN Pharm: Pregnant and Breastfeeding

NO ACE inhibitors, ARBs, direct renin inhibitors, and atenolol (beta blocker)

Labetolol: Beta blocker

Nifedipine: Dihydropyridine CCB (extended release)

Methyldopal: Alpha-2 agonist

Secondary HTN: Complications

HTN crises

HTN Crisis

Acute severe HTN

• Systolic BP ≥ 180 mmHg

• Diastolic BP ≥ 120 mmHg

Hypertensive Urgency

Hypertensive Emergency

Hypertensive Urgency

Hypertensive crisis without symptoms or with nonspecific symptoms

• No signs of acute organ damage

• BP > 180/120 mmHg

Hypertensive Emergency

Hypertensive crisis with signs of acute end-organ damage

• BP > 180/120 mmHg

End-Organ Damage:

• Cardiovascular

  • HF

  • Pulmonary edema

  • MI

  • Aortic dissection

• CNS

  • Cerebral edema

  • Stroke

  • Seizures

  • Altered mental status

• Renal: Acute hypertensive nephrosclerosis (AKI)

• Ophthalmic: Acute hypertensive retinopathy

  • Blurry vision

  • Retinal hemorrhages

HTN and Hypokalemia

Excess mineralocorticoids = Stimulate mineralocorticoid receptors = Increase Na+/water reabsorption + K+ excretion = HTN + Hypokalemia

• Hyperaldosteronism

• Cushing’s syndrome

Hyperaldosteronism

Increased aldosterone (mineralocorticoid) secretion from adrenal cortex = Stimulate ENaC in DCT

Cushing’s Syndrome

Increased cortisol (mineralocorticoid) secretion = Stimulate mineralocorticoid receptors