:Normal range
Errect: 1.310-3.950 ng/mL/hr; Supine: 0.150-2.330 ng/mL/hr
Comment: Renin, secreted by the juxtaglomerular cells adjacent to renal afferent arterioles, converts angiotensinogen to angiotensin I. the latter is, in turn, converted to angiotensin II, a biologically active peptide, which both 1) stimulates adrenocortical secretion of aldosterone, and 2) has direct vasopressor activity. Clinical interest in measuring plasma renin centers on patients who have aldosterone excess. There are two types of aldosterone excess: 1) primary hyperaldosteronism (Conn syndrome) in which the aldosterone excess is autonomously produced by an adrenal adenoma or hyperplasia, 2) secondary hyperaldosteronism in which the increased aldosterone is a physiological response to a disease process such as cardiac failure, cirrhosis, renovascular hypertension, a renin secreting tumor (Bartter syndrome), diuretic medication, or protracted vomiting. In primary hyperaldosteronism PR is characteristically low, while in secondary hyperaldosteronism PR is characteristically high. Interpretation of a PR result is difficult because 1) some assays are indirect and therefore nonspecific, many preanalytic variables affect renin production (sodium balance, posture, medications) and 3) the circadian variation in renin production (maximum in early morning, minimum in late afternoon). Renin secretion is stimulated by upright posture, low sodium intake, and diuretic medication. Renin and aldosterone concentrations with other studies, including especially serum / plasma potassium, are needed to evaluate the renin- angiotensin aldosterone system
Sample: EDTA plasma 1 m, state erect or supine
