Acid-Base Balance: Clinical

Application
RENAL MODULE
SOLA AOUN BAHOUS

Learning Objectives
Discuss renal contribution to acid-base maintenance

and compensation
Calculate the amount of filtered bicarbonate given
the GFR and plasma concentration
Calculate the amount of secreted H+ given GFR,
plasma bicarbonate concentration, titratable acidity
and urine bicarbonate concentration
Calculate titratable acidity from urinary and plasma
parameters

Outline

Quantitation of renal acid-base compensation

Exercises

Outline

Quantitation of renal acid-base

compensation
Exercises

Relationship between the arterial pH and [H+] in

the physiologic range

pH

[H+], nanomol/L

7.80

16

7.70

20

7.60

26

7.50

32

7.40

40

7.30

50

7.20

63

7.10

80

7.00

100

6.90

125

6.80

160

Quantitation of renal acid-base compensation

How much bicarb is excreted?

How much new bicarb is added to the plasma through

phosphate buffer?

How much new bicarb is contributed by glutamine?

Quantitation of renal acid-base compensation

How much bicarb is excreted? Ubicarb x V

How much new bicarb is added to the plasma through

phosphate? We titrate the urine with NaOH to a pH of 7.4

(plasma pH). The number of milliequivalents of OHrequired to reach this pH must equal the number of
milliequivalents of H+ that were added to the tubular fluid.
this happens in the distal tubule coz
This value is the titratable acid. mainly
bil proximal bikoon we r still returning the
hco3-

How much new bicarb is contributed by glutamine?

UNH4+ x V

HCO3- reabsorption
prevents further loss

H+ secretion and binding

to phosphate yields
titratable acidity
H+ excretion in the form of
ammonium contributes to
correction of acidosis

HCO3- loss = negative

contribution

Quantitation of renal acid-base compensation

Titratable acid excreted + NH4+ excreted HCO-3

excreted = contribution of the kidney to acid-base

regulation

Total = net HCO-3 gain or loss

Negative value loss
Positive value gain

Quantitation of renal acid-base compensation

Quantitation of renal acid-base compensation

The glutamine-NH4+ mechanism for new HCO3-

generation becomes the preeminent renal process for

opposing the acidosis mainly the 1st few days of an
acidosis

Many inputs exist that affect tubular H+ secretion:

PCO2, pH, volume, ionic composition of the plasma,

renal sympathetic nerves and many hormones

Quantitation of renal acid-base compensation

Renal compensation for respiratory acidosis and
alkalosis
Respiratory acidosis CO2 retention and plasma pH
Respiratory alkalosis CO2 loss and plasma pH

Quantitation of renal acid-base compensation

By HCO-3 the acidosis will be compensated

Low pH and high PCO2 stimulate the kidneys to excrete

H+ and NH4+, consequently, blood pH returns toward

normal

In respiratory alkalosis the opposite occurs

Quantitation of renal acid-base compensation

Renal compensation for metabolic acidosis and alkalosis:
Metabolic disturbance acid-base disturbance not

caused by a primary disturbance in PCO2

Metabolic acidosis = addition to the body (by
ingestion, infusion or production) of increased
amounts of any acid other than carbonic acid, or
alternatively, the loss from the body of HCO-3 (as in
diarrhea)
The pH and HCO-3

Quantitation of renal acid-base compensation

The lungs will try to compensate for metabolic acidosis

by hyperventilation to decrease PCO2

The kidneys, to compensate, must reabsorb all the

HCO-3 and add new bicarb to the blood through

increased formation and excretion of NH4+ and
titratable acid

Quantitation of renal acid-base compensation

The kidneys may be a cause of metabolic acidosis or

alkalosis or may fail to compensate for a metabolic

disturbance

Quantitation of renal acid-base compensation

Quantitation of renal acid-base compensation

Factors causing the kidneys to generate or maintain a
metabolic alkalosis:
1- extracellular volume contraction:
EC volume contraction stimulates Na+ reabsorption

and H+ secretion by stimulating aldosterone secretion,

Ang II formation and SNS activity

Quantitation of renal acid-base compensation

Aldosterone stimulates luminal H+-ATPase

Renal nerves and Ang II stimulate Na+/H+ antiporter

in the proximal tubule

Net result = all the filtered bicarb is reabsorbed and

not excreted

Quantitation of renal acid-base compensation

Quantitation of renal acid-base compensation

2- Chloride depletion:
Chloride depletion stimulates H+ secretion and/or

inhibits HCO-3 secretion

Quantitation of renal acid-base compensation

3- Aldosterone excess and K+ depletion:

Excessive diuretic use
ECV contraction
aldosterone secretion
K+ depletion
Creation or maintenance of metabolic alkalosis

Outline

Quantitation of renal acid-base compensation

Exercises

Exercise 1
1.

The daily H+ load is excreted in the urine as titratable

acidity and NH4+. Would H+ retention leading to
metabolic acidosis occur if there were:
a. A marked reduction in titratable acid excretion, as
a result of a decrease in the plasma phosphate
concentration?
b. A marked reduction in NH4+ formation?

Exercise 2
2. Two patients with a normal GFR of 180 L/day are
studied, one with normal acid-base balance and one
with metabolic acidosis. The following laboratory data
were obtained:
Parameter

Patient 1

Patient 2

Plasma [HCO3-]

24 meq/L

6 meq/L

Titratable acidity

30 meq/day

75 meq/day

NH4+ excretion

50 meq/day

140 meq/day

Urine pH

5.5

5.0

Exercise 2
Assuming that all the filtered bicarbonate is
30+50 la patient A
reabsorbed, calculate:
Net acid excretion in any form
Total H+ secretion
24*gfr + titratable
acid only

Exercises
3. Is NH4+ excretion included in the measurement of
titratable acidity?
no bas l hpo4
4. A patient with persistent vomiting develops metabolic
alkalosis as a result of the loss of HCl in gastric juice.
Why isnt the condition corrected spontaneously by
excretion of the excess bicarbonate in the urine?
volume is low so
we have
reabsorbtion of na
secretion of h
secretion of k
reabsorbtion of
bicarb

Exercises 5 and 6
5. The following results were obtained on a patient under
normal physiological conditions: plasma HCO-3 = 22
mmol/L, GFR = 7.5 L/hour, urinary HCO-3 = 8 mmol/d,
titratable acid = 24 mmol/d.

What is the amount of HCO-3 filtered?

3960
a.24 mmol/d
b.180 mmol/d
c.3960 mmol/d
d.4328 mmol/d
e.4340 mmol/d

Exercises 5 and 6
6. What is the total amount of hydrogen ion secreted?
a. 8 mmol/d
b. 24 mmol/d
gfr thingy - excereted + l titratable
c. 3312 mmol/d
d. 3976 mmol/d
e. 4339 mmol/d

Exercise 7
7. Hypoventilation is associated with which acid-base
disturbance?
a. Increased plasma pH, increased plasma HCO-3 ,
alkaline urine
b. Increased plasma pH, decreased plasma HCO-3 ,
alkaline urine
c. Decreased plasma pH, increased plasma HCO-3 , acidic
urine
d. Decreased plasma pH, decreased plasma HCO-3 , acidic
urine
e. Decreased plasma pH, decreased plasma HCO-3 ,
alkaline urine

Exercise 8
8. Choose the correct statement describing the
reabsorption or the addition of new bicarbonate to the
blood.
a. When secreted H+ binds to HCO-3 in the tubular
lumen, addition of new HCO-3 occurs
b. When secreted H+ binds to non HCO-3 buffers in the
tubular lumen, addition of new HCO-3 occurs
c. When NH4+ is produced and excreted, reabsorption of
filtered HCO-3 occurs
d. When H+ binds to phosphate in the tubular lumen,
reabsorption of HCO-3 occurs