Sodium balance in CKD

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Happy Sawires
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Sodium balance in CKD

Postby Happy Sawires » Thu Jun 16, 2016 1:09 am

[b]Progressive chronic renal insufficiency is typified by an adaptive increase in the sodium excretion rate per nephron as the total glomerular filtration rate declines. This increase is caused, at least in part, by the effect of atrial natriuretic peptide and other natriuretic peptides, whose release is augmented in the setting of volume expansion and renal failure. However, exogenous administration of natriuretic peptides in clinical chronic and acute renal disease does not consistently increase renal sodium excretion. As the glomerular filtration rate progressively declines towards end-stage renal disease, total renal sodium excretion eventually decreases, and extracellular volume expansion, hypertension, and edema develop.[/b]

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Happy Sawires
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Re: Sodium balance in CKD

Postby 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]

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Re: Sodium balance in CKD

Postby Happy Sawires » Sat Jun 18, 2016 12:49 am

Sodium in Neonate and Pre-term infants

- In the immediate period after birth, neonates manifest a NEGATIVE Na balance associated with increased urinary Na excretion and high FeNa.
- Urinary Na excretion in the early neonatal period is due to effect of ANP released as a result of atrial stretch after birth.ANP is implicated in increase GFR and inhibition of RAS.
- So there is an initial balance between low GFR (decrease Na excretion) and natriuretic effect of ANP resulting in negative Na balance.
- After sometime, maturational change resulting in increase GFR and simultaneous tubular maturation and decrease ANP release >>> positive Na balance to compensate low Na in breast milk.

N.B. Urinary excretion of Na is inversely related to gestational age.... premature < 30 weeks have FeNa near 5% where full-term NB has FeNa 3%.


N.B. initial negative Na balance is needed to eliminate excess ECW and Na.


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