Articles
| Open Access |
https://doi.org/10.5281/zenodo.20001850
HYPERTENSIVE CRISIS IN ENDOCRINE AND RENAL DISORDERS: PATHOPHYSIOLOGY, CLINICAL MANIFESTATIONS, AND EVIDENCE-BASED MANAGEMENT
Dr Aman Khandelwal , Assistant Teacher, Samarkand state medical university, Uzbekistan, Fathimath zulaikha , Medical Student, Samarkand state medical university Uzbekistan , Hima nishali , Medical Student , Samarkand state medical university, Uzbekistan Rifna firos MV , Medical Student, Samarkand state medical university, UzbekistanAbstract
Hypertensive crisis represents a critical medical emergency characterized by severe blood pressure elevation (systolic ≥180 mmHg and/or diastolic ≥120 mmHg) with potential for acute target-organ damage. While essential hypertension accounts for approximately 95% of cases, secondary causes—particularly endocrine and renal disorders—contribute significantly to hypertensive emergencies and are potentially curable with timely intervention. Endocrine causes including pheochromocytoma, Cushing's syndrome, and primary aldosteronism account for nearly 3% of secondary hypertension cases, whereas renovascular and renoparenchymal diseases represent major non-endocrine secondary etiologies. This comprehensive narrative review examines the pathophysiological mechanisms linking endocrine and renal disorders to hypertensive crisis, delineates clinical manifestations and diagnostic approaches, and synthesizes current evidence-based management strategies. Understanding the interplay between hormonal dysregulation, renin-angiotensin-aldosterone system activation, and renal dysfunction is essential for clinicians to recognize secondary causes, initiate targeted therapy, and prevent life-threatening complications including stroke, myocardial infarction, and acute renal failure.
Keywords
Hypertensive crisis, endocrine hypertension, renal hypertension, pheochromocytoma, Cushing's syndrome, primary aldosteronism, chronic kidney disease, hypertensive emergency, secondary hypertension, target organ damage, renin-angiotensin-aldosterone system
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