High Na & Low K (with high BP): patients are clinically eivolemic;
If Na and K are changing in opposite direction Eg; high Na and low K; the only one mechanism which would explain this, is Renin-Aldosterone excess.
Underlying Concept;
Sympathetic nerves stimulate Beta 1 receptors to produce renin. Renin then converts Angiotensiongen to AI & ACE then converts AI to AII. This is AII which stimulates adrenal glands to produce Aldosterone, which then works on its receptors on the collecting tubules to operate N/K/H channels.
High Renin- High Aldosterone:
Renin secreting cells (JG) are producing more renin due to decreased renal blood flow or CKD or tumour etc.
1): Renal Artery Stenosis
2): Renin secreting tumours (very rare)
3): CKD
4): Hypertension itself can cause
5): Sympathetic overdrive such as Pheochromocytoma can also increase Renin production.
****(Note; High renin and high aldosterone can also be there in dehydration (such as diuretics, polyuria, Diarrhea, vomiting etc) OR volume overload conditions due to low effective intra arterial volume caused by fluid leaking into tissues (such as CCF/Cirrhosis/Low albumin) But it often have low measured Na (due to high ADH or due to Na loss from body) and also doesn’t have high BP and patient is not clinically euvolemic)
Low Renin, High Aldosterone:
Adrenal gland is producing aldosterone independent of renin.
1): Adrenal Adenoma / carcinoma
2): CAH with 17-OH defi ***(Carcinomas rarely produce Aldostetone)
Low Renin, Low Aldostetone
Receptors don’t need aldosterone
1): Liddel Sybdrome (hyperactive Aldosterone receptor associated Na channel which doesn’t need Aldostetone to stimulate it):
2): Exogenous Fludrocortison