Renin is an endoprotease (hormone-like enzyme) produced in the kidney, more specifically in the juxtaglomerular apparatus. It represents an important link in the renin-angiotensin-aldosterone system (RAAS), which helps regulate blood pressure and salt balance. Increased renin is produced when a lack of sodium in the blood or hypovolemia (decreased blood volume) is determined by the receptors. Renin in turn stimulates the activation of angiotensinogen to angiotensin I, which is then converted to angiotensin II by other hormones. Angiotensin II leads to vasoconstriction (narrowing of blood vessels) and thus to an increase in blood pressure. In addition, it leads to a release of aldosterone, which results in sodium and water reabsorption.
The procedure
Material needed
- EDTA plasma, frozen (note: do not store in refrigerator due to risk of cryoactivation).
Preparation of the patient
- Potassium levels should be normalized before any measurement.
- The patient should be encouraged to follow a balanced diet regarding his salt intake.
- Blood sampling should be done in the morning, approximately 2 hours after getting up, in a sitting position after 5 to 15 minutes of rest.
Interfering factors
- Four weeks prior to testing, spironolactone, eplerenone, drospirenone-containing contraceptives (contraceptives), amiloride, and triamterene must be discontinued, as these have a lasting effect on the aldosterone-renin quotient (ARQ).
- Refrain from eating licorice and chewing tobacco.
Normal values adults
| Body position | Normal values in ng/l |
| Lying down | 6-65 |
| Standing | 6-30 |
Normal values children
| Age | Normal values in ng/l |
| Newborn | 24-850 |
| 1 month – 1 year | 5-308 |
| < 5 years | 5-112 |
| 5-16 years | 5-143 |
Indications
- Suspected renal cause of hypertension (high blood pressure).
- Diagnosis and course assessment
- Primary hyperaldosteronism (Conn’s disease)-disease resulting in elevated serum aldosterone levels and decreased serum renin levels; often due to adenomas (benign tumors).
- Isolated mineralocorticoid deficiency
- Aldosterone dysfunction
Interpretation
Interpretation of increased values
- Adrenogenital syndrome (AGS) – autosomal recessive inherited metabolic disorder characterized by disorders of hormone synthesis in the adrenal cortex. These disorders lead to a deficiency of aldosterone and cortisol. as well as an increase in renin
- Aldosterone depletion disorder: liver dysfunction, such as cirrhosis (irreversible (non-reversible) damage to the liver and pronounced remodeling of liver tissue).
- Aldosterone-secreting tumor
- Renin-secreting tumors: Renal cell carcinoma (kidney cancer), bronchial carcinoma (lung cancer), Bartter syndrome (very rare genetic metabolic disorder with autosomal dominant or autosomal recessive or X-linked inheritance; Defect of tubular transport proteins; hyperaldosteronism (disease states associated with increased secretion of aldosterone), hypokalemia (potassium deficiency), and hypotension (low blood pressure)).
- Secondary hyperaldosteronism
- Stimulation of the renin-angiotensin-aldosterone system:
- Renin ↑, aldosterone ↑.
- Manifest arterial hypertension (high blood pressure).
- Renal artery stenosis – narrowing of the vessels supplying the kidneys.
- Licorice – leads to an increase in aldosterone in a daily intake of > 500 g.
- Medications
- Carbenoxolone (anti-inflammatory) → aldosterone ↑
- Diuretics (diuretic drugs) → aldosterone ↑
- Glucocorticoids → renin ↑
- Pregnancy – physiological increase
Interpretation of decreased values
- Primary hyperaldosteronism (Conn’s disease) – disease resulting in elevated serum aldosterone levels and decreased serum renin levels; often due to adenomas (benign tumor).
- Idiopathic hyperaldosteronism – usually caused bilateral hyperplasia (bilateral enlargement) of the adrenal cortex.
- Primary macronodular hyperplasia of the adrenal cortex.
Further notes
- When hyperaldosteronism is suspected, the ratio of aldosterone to renin, the aldosterone-renin quotient (ARQ), should be determined initially in the blood.
