Primary Aldosteronism: Clinical findings
Note: This condition is also known as “Primary Hyper-Aldosteronism” or “Conn’s Syndrome”
Authors: Samin Dolatabadi Reviewers: Amanda Henderson, Hannah Yaphe, Yan Yu*, Hanan Bassyouni* Juliya Hemmett* * MD at time of publication
↑ Expression of Cl-/HCO3- exchanger in the basolateral membrane of intercalated cell of cortical collecting duct
↑ HCO3- reabsorption into bloodstream
↑ Autonomous aldosterone secretion from zona glomerulosa of adrenal cortex (e.g. aldosterone producing adenoma)
↑ Serum aldosterone level
↑ Circulating aldosterone activates mineralocorticoid receptors on cardiac myocytes
↑ Transcription of proinflammatory and profibrotic genes in cardiac myocytes
Cardiac fibrosis and hypertrophy
In the rest of the body, K+ moves from intracellular to extracellular environment (down it’s concentration gradient) to compensate for decreased serum K+
Loss of positively charged K+ànegative intracellular chargeàcells take up H+ to remain electrostatically neutral
↑ Expression of epithelial sodium channels in
principal cells of cortical collecting duct
↑ Na+ reabsorption from cortical collecting duct into blood vessels
+ Water follows Na
into the blood vessels to balance the osmotic pressure between the blood and the renal tubules
↑ blood volume within the volume-
constrained space of blood vessels
↑ Activation of Na+/K+ ATPase in principle cells of cortical collecting duct
Removal of positively charged Na+ from tubular lumenà lumen becomes electronegative versus the interstitial space & inside tubular epithelial cells
Positively charged K+ follows the electrical gradient and is secreted into tubular lumen
↓ Serum K+ concentration
↑ Expression of H+ ATPase in the apical (luminal)
membrane of intercalated cell of cortical collecting duct
H+ is secreted into cortical collecting duct → renal loss of H+ from the body
Metabolic Alkalosis
(blood becomes more basic; ↑ serum pH)
Hypertension
Muscle weakness, fatigue, polyuria
↓ pH in intercalated cell
↓ pH in cells of proximal convoluted tubule
↑ loss of H+ through kidneys
H+ secretion into cortical collecting duct
↑ H+ ATPase activity in intercalated cell
Activation of glutaminase in proximal convoluted tubule
HCO3- pumped into blood
↑ production of HCO3- (product of glutamine breakdown)
↑ breakdown of glutamine
Hypokalemia
(See Hypokalemia: Clinical Findings slide)
Legend:
Pathophysiology
Mechanism
Sign/Symptom/Lab Finding
Complications
Published January 16, 2020 on www.thecalgaryguide.com