Post by Happy Sawires » Thu Jun 16, 2016 1:19 am
Pathomechanisms underlying salt-induced kidney damage
1. Renal damage may be induced by high salt intake as a result of its interaction with aldosterone. high sodium could amplify the risk of progressive renal function loss by non-blood pressure-dependent direct, e.g. pro-fibrotic, effects of aldosterone.
2. High sodium intake can activate the local RAAS in vessels as well as the kidney. High sodium intake abrogates the effects of ACE inhibition on the conversion from angiotensin I to angiotensin II in vascular tissues.
3. High sodium intake induces hyperfiltration, where it was also associated with albuminuria in otherwise healthy individuals. Hyperfiltration in turn can cause renal damage.
4.Potential mediators of salt-induced kidney damage in chronic renal failure are the Na/K-ATPase inhibitors marinobufagenin and endogenous ouabain. These substances are implicated in sodium regulation and also exert pro-fibrotic effects.
Ref. Salt intake in kidney disease—a missed therapeutic opportunity? [Nephrol Dial Transplant (2012) 27: 3435–3442]
[b][color=#BF0000]Pathomechanisms underlying salt-induced kidney damage[/color][/b]
1. Renal damage may be induced by high salt intake as a result of [u]its interaction with aldosterone[/u]. high sodium could amplify the risk of progressive renal function loss by non-blood pressure-dependent direct, e.g. pro-fibrotic, effects of aldosterone.
2. High sodium intake can [u]activate the local RAAS[/u] in vessels as well as the kidney. High sodium intake abrogates the effects of ACE inhibition on the conversion from angiotensin I to angiotensin II in vascular tissues.
3. High sodium intake induces [u]hyperfiltration[/u], where it was also associated with albuminuria in otherwise healthy individuals. Hyperfiltration in turn can cause renal damage.
4.Potential mediators of salt-induced kidney damage in chronic renal failure are the [u]Na/K-ATPase inhibitors marinobufagenin and endogenous ouabain[/u]. These substances are implicated in sodium regulation and also exert pro-fibrotic effects.
[i]Ref. Salt intake in kidney disease—a missed therapeutic opportunity? [Nephrol Dial Transplant (2012) 27: 3435–3442][/i]