Plasma renin is an enzyme released by kidney juxtaglomerular cells that initiates the renin–angiotensin system. It cleaves angiotensinogen to angiotensin I, leading to angiotensin II formation, which raises blood pressure and conserves sodium and fluid. Renin secretion rises with low renal perfusion, low sodium, or sympathetic activation. Measuring plasma renin helps evaluate hypertension and aldosterone-related disorders.

High plasma renin activity indicates renin-driven (secondary) hypertension or volume depletion. Causes include renal artery stenosis, renin-secreting tumors, diuretics, heart failure, cirrhosis or dehydration. Next steps are clinical review, medication reconciliation, measuring aldosterone and the aldosterone-to-renin ratio, and renal artery imaging when indicated. Treatment targets the underlying cause (revascularization for stenosis, stopping offending drugs, surgery for rare tumors) under physician guidance.

Renin is an enzyme released by kidney juxtaglomerular cells that initiates the renin–angiotensin–aldosterone system. It cleaves circulating angiotensinogen into angiotensin I, which is converted to angiotensin II, a potent vasoconstrictor that stimulates aldosterone release. Through these actions renin regulates blood pressure, vascular tone, sodium and water balance, and overall fluid–electrolyte homeostasis.

Low renin reduces activation of the renin–angiotensin–aldosterone system, which can cause low aldosterone leading to low blood pressure, salt wasting, hyponatremia, hyperkalemia and metabolic acidosis. Alternatively, low renin can reflect volume expansion or autonomous aldosterone production (low‑renin hypertension), causing fluid retention, high blood pressure and low potassium. Symptoms include dizziness, weakness, fatigue, and palpitations.

Plasma renin activity (PRA) normal values vary by posture and assay. Typical PRA is about 0.2–2.8 ng/mL/hr when supine and generally higher when upright, roughly 1–5 ng/mL/hr. Reference intervals differ between labs, assays and with medications, so clinicians interpret results against the lab’s specific range and the patient’s posture/medication status. If measured as direct renin concentration, ranges will be lab-specific.

Treatment depends on the cause. Manage reversible causes by stopping offending drugs and correcting volume status. For primary hyperaldosteronism: unilateral adrenalectomy if adenoma, or mineralocorticoid receptor antagonists (spironolactone, eplerenone). For Liddle syndrome use amiloride; congenital adrenal enzyme defects require specific hormone therapy. Salt restriction, blood-pressure control, and monitoring of electrolytes and renal function are essential; refer to an endocrinologist.