acid-base balance clinical application
TRANSCRIPT
RENAL MODULE
SOLA AOUN BAHOUS
Acid-Base Balance: Clinical Application
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 OH-
required to reach this pH must equal the number of milliequivalents of H+ that were added to the tubular fluid. This value is the titratable acid.
How much new bicarb is contributed by glutamine?
UNH4+ x V
HCO3- loss = negative
contribution
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
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 titratableacidity 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 reabsorbed, calculate:
Net acid excretion in any form
Total H+ secretion
Exercises
3. Is NH4+ excretion included in the measurement of
titratable acidity?
4. A patient with persistent vomiting develops metabolic alkalosis as a result of the loss of HCl in gastric juice. Why isn’t the condition corrected spontaneously by excretion of the excess bicarbonate in the urine?
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?
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
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 urinec. Decreased plasma pH, increased plasma HCO-
3 , acidic urine
d. Decreased plasma pH, decreased plasma HCO-3 , acidic
urinee. 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