Role of kidneys in regulation of Acid Base balance.pptx HCO3 reabsorption and Hydrogen ion secretion Acidosis and alkalosis Metabolic acidosis metabolic alkalosis

1. Role of kidneys in regulation of
Acid Base balance
By Dr. Irtaza Rehman
Author of the book “The Extraordinary Life”

3. Learning objectives
• To understand acid base balance by kidneys
• To understand the mechanism of HCO3-
reabsorption and H+ secretion
• To know about compensatory mechanisms in
metabolic acidosis and alkalosis.

6. Acids and Bases
• Acids release H+ ions
• Bases accepts H+ ions

7. Examples
• HCl H+ + Cl-
• H2CO3 H+ + HCO3-
• H2PO4 H+ + HPO4-

8. Normal H+ ion concentration
40 nEq/L

9. Formula of pH
pH = log 1/[H+]
pH = -log [H+]
pH = -log [0.00000004]
pH = 7.4
DEATH!!
IF
<6.8
>8

10. What are Buffers??
• Prevent a change in pH when H+ ions are added to
or removed from a solution.
• 1. Extracellular buffers:
• Major  HCO3
• Minor  Phosphate H2PO4− /HPO4−2
(most important as Urinary Buffer)

11. • 2. Intracellular buffers
• a. Organic phosphates (e.g., AMP, ADP, ATP)
• b. Proteins (e.g., Hemoglobin)
What are Buffers??

12. What are types of Acid produced??
• 1. Volatile acid
• CO2
• produced from the aerobic metabolism of cells.

13. • 2. Nonvolatile acids
• sulfuric acid (a product of protein catabolism)
• phosphoric acid (a product of phospholipid
catabolism)
• In pathologies: Ketoacids, lactic acids, oxalic
acid etc
What are types of Acid produced??

15. How to prevent acidosis or alkalosis??
• 3 Systems
• 1. Buffer system of body fluids (within seconds)
• 2. Respiratory center (within minute)
• 3. Kidneys (hours to days) Slowest but Powerful

16. Renal control of Acid Base balance
• Excreting H+ ions (acidic urine)
• Excreting HCO3- ions (Basic urine)

17. By 3 Physiological changes
• HCO3- reabsorption
• H+ secretion
• New HCO3- production
Renal control of Acid Base balance

18. • Filtered HCO3- reabsorption: Early PCT
Renal control of Acid Base balance

20. Q. Can filtered HCO3-
be reabsorbed
directly?
• Ans. No
WHY??
• Because luminal membrane of tubular cells are impermeable to
HCO3- .
• That’s why it is first produced in tubular cells than reabsorbed
passively. Because the basolateral membrane of tubular cells are
permeable.

21. How to regulate the reabsorption
of filtered HCO3- ??
• 1. Filtered load:
• Increased F.L  Increased Reabsorption
• If plasma level above normal  Inc Excretion

22. • 2. PCO2
• Increased PCO2  Increased HCO3- reabsorption
• *Renal compensation for respiratory acidosis
• Decreased PCO2  Decreased HCO3- reabsorption
• *Renal compensation for respiratory alkalosis
How to regulate the reabsorption of
filtered HCO3- ??

23. • 3. ECF Volume
• ECF expansion  Decreased HCO3- reabsorption
• ECF contraction  Increased HCO3- reabsorption
How to regulate the reabsorption of
filtered HCO3- ??

24. • Angiotensin II
• stimulates Na+–H+ exchange and thus increases
HCO3 − reabsorption
• contraction alkalosis that occurs secondary to
ECF volume contraction.
How to regulate the reabsorption of
filtered HCO3- ??

25. How H+ ions are excreted??
• As titratable acid (H2PO4) and NH4+
• H.w: Why H2PO4 is known as titratable acid??

26. How H+ ions are excreted??
As titratable acid (H2PO4)
This process results in net secretion of H+ and
net reabsorption of newly synthesized HCO3-

27. How H+ ions are excreted??
• As titratable acid (H2PO4)
Depends upon amount of urinary
buffer and the pK of the buffer.

28. How H+ ions are excreted??
as NH4 +

29. How H+ ions are excreted??
as NH4 +
Collecting tubular
depends on amount of NH3 synthesized by
renal cells and the urine pH.

30. How H+ ions are excreted??
as NH4 +
Diffusion Trapping:
Diffusion of NH3 into tubular lumen bcz Collecting ducts are
permeable to NH3
Trapping of NH4 in tubular lumen bcz colllecting ducts are less
permeable to NH4

31. How H+ ions are excreted??
as NH4 +
Chronic acidosis: Increased NH4 Excretion
Increased H+  Increased Renal glutamine
Metabolism  Inc NH4 and Inc HCO3-
Hyperkalemia inhibits NH3 synthesis, which
produces a decrease in H+ excretion as NH4 +

32. Tubular cells – Type A intercalated cells
PCT, Thick Asc. limb, Early DCT Late DCT, Collecting ducts
H+ secreted: 80-90%
Least possible pH: 6.7 (less efficient)
H+ secreted: 5%
Least possible pH: 4.5(more efficient)
Aldosterone

34. Q. Is there any
mechanism for H+ ion
reabsorption?
Ans. NO
If there is decreased H+ ions in
blood, kidneys can only decrease
their excretion to conserve them

35. Acid–base disorders
• Metabolic acidosis
• Overproduction or ingestion of fixed acid
• loss of base (HCO3-)
• Decrease in arterial [HCO3 - ]  Primary disturbance
• Decreased HCO3-  Decreased pH (acidemia)

36. • Metabolic acidosis: How to compensate??
• Respiratory: Decreased pH  Hyperventilation
(Kussmaul breathing)
• Renal: increased excretion of the excess fixed H+
as titratable acid and NH4+
• Increased new HCO3- reabsorption
Acid–base disorders

37. Q. Why HCO3-
filtration is decreased
in acidosis?
• Ans. Bcz more HCO3- will be used up in
buffering the excess H+ ions in the ECF.
• Leads to Increased H+ secretion, bcz of less need
to bind with HCO3- as it is low in filtrate.

38. • Metabolic alkalosis
• Loss of fixed H+ or gain of base
• Increase in arterial [HCO3-]  Primary disturbance
• Increased HCO3−  increase in blood pH (alkalemia)
Acid–base disorders

39. • Metabolic alkalosis: How to compensate??
• Respiratory: Hypoventilation  Inc. CO2
• Renal: Increased HCO3- excretion
Acid–base disorders

40. • Metabolic alkalosis
“If metabolic alkalosis is accompanied by ECF volume
contraction (e.g., vomiting), the reabsorption of HCO3−
increases (secondary to ECF volume contraction and
activation of the renin–angiotensin– aldosterone system),
worsening the metabolic alkalosis
(contraction alkalosis)”
Acid–base disorders

44. Jazakumullahu Khair ♥
(May ALLAH swt reward you with goodness)