Angiotensin II type 1a receptor-deficient mice with hypotension and
hyperreninemia. J Biol Chem.
Bartter syndrome is a hereditary salt-losing renal tubular disorder characterized by hypokalemic metabolic alkalosis, hypercalciuria, nephrocalcinosis, polyuria, and
hyperreninemia with normal arterial blood pressure.
According to clinical presentations, the major symptoms include the following: (1) Hypokalemia (2) hyperkaluria (3) metabolic alkalosis (4)
hyperreninemia (5) hyperaldosteronemia (6) exogenous vasopressin insensitivity (7) juxtaglomerular hyperplasia (8) hypochloremia (9) normal blood pressure, and (10) clear family history.
Indeed, further investigations revealed that VDR knockout mice developed
hyperreninemia, hypertension, cardiac hypertrophy, and polyuria, and these abnormalities were independent of vitamin D's actions on calcium and skeletal homeostasis.
In the kidneys, injury to the medium-sized arteries can precipitate scleroderma renal crisis (SRC) with malignant hypertension and
hyperreninemia, microangiopathic hemolytic anemia, and rapidly progressive renal failure.