Risk Factors of Arterial Hypertension

Risk factors are classically divided into modifiable and non-modifiable categories.

Non-Modifiable Risk Factors

Factor	Details
Age	BP rises progressively with age; isolated systolic hypertension is common in the elderly due to arterial stiffness
Family history / Genetics	~30–50% heritability; polygenic trait with multiple susceptibility loci
Race/Ethnicity	Higher prevalence and earlier onset in Black populations, with more severe end-organ damage
Sex	Men have higher rates before age ~55; women catch up post-menopause
Obstetric history	Women with a history of preeclampsia or gestational hypertension carry increased long-term cardiovascular risk

Modifiable Risk Factors

Lifestyle

High sodium diet — sodium retention expands plasma volume and raises BP; particularly impactful in "salt-sensitive" individuals
Excess alcohol intake — dose-dependent pressor effect; chronic heavy use is a major reversible cause
Obesity / overweight — increased cardiac output, insulin resistance, RAAS activation, and sympathetic nervous system upregulation all contribute
Physical inactivity — sedentary lifestyle independently raises risk
Smoking — acute vasopressor effect; chronic use accelerates atherosclerosis and arterial stiffness
Dietary patterns — low potassium, low calcium, and low magnesium intake worsen BP control
Psychosocial stress — chronic stress activates the sympathoadrenal axis

Medications and Substances

NSAIDs — impair renal prostaglandin synthesis, causing sodium retention
Oral contraceptives (estrogen-containing) — renin-angiotensin activation
Decongestants (e.g., pseudoephedrine) — sympathomimetic vasoconstriction
Stimulants (e.g., amphetamines, cocaine) — adrenergic hypertension
Corticosteroids / mineralocorticoids — sodium and water retention
Calcineurin inhibitors (cyclosporine, tacrolimus) — renal vasoconstriction
Certain dietary supplements (e.g., licorice root, ephedra)

Metabolic/Clinical Conditions

Obesity and metabolic syndrome — hyperinsulinemia activates the RAAS and SNS
Diabetes mellitus — endothelial dysfunction, nephropathy-related volume retention
Chronic kidney disease — reduced nephron mass, impaired sodium excretion, secondary RAAS activation
Obstructive sleep apnea — intermittent hypoxia triggers sympathetic surges, raising nocturnal and daytime BP

Secondary Hypertension — Identifiable Causes

When a specific underlying cause is found, hypertension is termed "secondary" (~5–10% of cases):

Cause	Mechanism
Primary hyperaldosteronism	Excess aldosterone → sodium retention, volume expansion
Renal artery stenosis (renovascular HTN)	Reduced renal perfusion → RAAS activation
Chronic kidney disease / Parenchymal renal disease	Reduced GFR, fluid retention
Pheochromocytoma	Catecholamine excess
Cushing's syndrome	Glucocorticoid excess → mineralocorticoid effects
Hypothyroidism / Hyperthyroidism	Altered cardiac output and vascular resistance
Coarctation of the aorta	Mechanical obstruction, RAAS activation
Obstructive sleep apnea	Sympathetic activation

Summary

The vast majority (~90–95%) of hypertension is primary (essential), with no single identifiable cause — reflecting the cumulative effect of genetic predisposition interacting with environmental and lifestyle risk factors. Targeting modifiable factors (sodium restriction, exercise, weight loss, smoking cessation, alcohol reduction) forms the cornerstone of both prevention and non-pharmacological management. (Living Kidney Donors Guidelines, p. 59)

This is a shared conversation. Sign in to Orris to start your own chat.