Kidney role in Acid/base bal Flashcards
How does HCO3- prevent the continuous build up of 60meq of nonvolatile acid in the body?
“the twist”
- You need high [ ]s of HCO3-
- it converts nonvolatile(nongaseous) acid to a gaseous volatile form that can be ELIMINATED from ECF via respiration (CO2)
(it acts more than just a buffer)
Where does most of the recapture of HCO3- take place?
Prox tubule - and is obligatory
Describe the process of how HCO3- is continuous replaced while maintaining electoneutrality?
- H+ is moved to lumen via H+/Na+ antiporter
- H+ binds to HCO3- → H2CO3
- H2CO3 is broken down via CA to H2O + CO2
- CO2 is transported into the cell via highly permeable membrane
- CO2 binds to H20 in the cell via CA→ H2CO3
- H2CO3 is broken down to H+ and HCO3-
- HCO3- is transferred out of the cell into the serosa via Na+/HCO3+ cotransporter
Which cells make HCO3-?
Intercalated cells (secrete H+ and HCO3-) in distal tubule
How do you not piss out acid with all of the H+ being moved to the lumen? (via Na/H+ antiporter and H+ pump?)
2 main buffering mechs:
- titratable acid
- ammonia trapping
titratable acid buffering mech
complexing H+ ion to a filtered anion (HPO42-)
Ammonia trapping buffering mech
- tubular cells break ↓ glutamine → ammonia (NH3)
- ammonia (NH3) readily diffuses through the apical membrane into tubule
- in Lumen, NH3 has very high affinity for H+ → NH4 +
(ammonia is now “trapped” with buffered H+)
- can be up/downregulated depending on H+ secretion
During metabolic acidosis, what happens to ammonia (NH3)?
Glutaminase is upregulated → more NH3 is made to buffer the increased secretion of H+
Is the process of HCO3- reabsorption neutral in terms of acid/base terms? What about Synthesis of HCO3-?
R: is neutral
S: not neutral - results in the elimination of acid in the urine
(note that R is a much larger process than S)
How is HCO3- R and secretion similar?
They both require apical secretion of H+ and basolateral movement of HCO3- into the ECF
Which takes priority, HCO3- reabsorption or Secretion?
reabsorption: its also a much larger process
What competitively inhibits HCO3- synthesis?
When the H+ in the lumen is used to convert HCO3- to CO2 + H2O.
This causes CO2 to go into the cell and ultimately result in H+ and HCO3- forming inside the cell.
This will inhibit the entry of CO2 from the serosa/blood and will compete for secretory and HCO3- extrusion transporters required for synth pathway.
Can synthesis take place with HCO3- in the tubular fluid?
No, only R will take place.
HCO3- synthesis can only occur after all the filtered load has been reabsorbed
- usually only cells in the very distal parts of the tubule will end up synth HCO3-
What is the rate limiting for HCO3- homeostasis? What does this rate depend on?
Apical secretion of H+ and basolateral extrusion of bicarb
- rates depends on ECF pH and CO2 levels (they determine the # of transporters in the apical and basolateral membrane)
During metabolic imbalances, what two organ systems work together to deal with the threat?
Kidney and lungs
In the short term, how do the kidneys respond to respiratory acidosis? Long term?
Kidney responds to respiratory acidosis by increasing their excretion of H+ ions to counteract it.
Eventually . . . compensation is limited by increased filtered load of HCO3- that results
(thus in prolonged resp acidosis, one sees a partial renal compensation with elevated HCO3-)
Hypokalemia will cause in alkalosis or acidosis?
Alkalosis
Hypokalemia induced shift of H+ into tubular cells results in inappropriately increased H+ secretion and urinary excretion → alkalosis
*the opp is also true, alkalosis leads to increased K+ and H+ excretion → hypokalemia
Hyperkalemia will induce acidosis or alkalosis?
acidosis:
hyperkalemia reduces the rate of H+ secretion and subsequent excretion, and H+ is inappropriately retained in ECF
