Abstract
The important renal endocrine aspect implicated in gym nephropathy is the activation of the renin-angiotensin-aldosterone system (RAAS). Intense exercise can lead to increased sympathetic nervous system activity, resulting in the release of renin from the juxtaglomerular cells in the kidneys. Renin acts on angiotensinogen, leading to the generation of angiotensin II, a potent vasoconstrictor. Angiotensin II stimulates the secretion of aldosterone from the adrenal glands, which promotes sodium reabsorption and potassium excretion in the kidneys. The persistent activation of the RAAS in gym nephropathy may contribute to renal damage by causing vasoconstriction and promoting renal inflammation.
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