Clinical Case. Renal Physiology
EEOB 410
Williams, J.B.
A 50-year old man with a history of a duodenal ulcer is admitted to the hospital after several days of
intermittent vomiting. On physical examination he is noted to have orthostatic ( when he stands up)
changes in his blood pressure and pulse, no visible jugular venous distension, and marked decrease in his
skin turgor. Laboratory tests reveal the following:
serum [Na+] = 138 mmole/L
serum [K+] = 2.4 mmole/L
serum [Cl- ] = 88 mmole/L
serum [HCO3- ] = 40 mmole/L
arterial pH = 7.52
arterial pCO2 = 50 mm Hg
Urine [Na+] = 38 mmole/L
Urine [K+] = 60 mmole/L
Questions:
1.
2.
What disorder does this man have?
Gastric secretions contain about 10mmole/L potassium. How do you account for the low serum
potassium in this patient?
Solution:
This represents a case of metabolic alkalosis caused by vomiting which causes the
loss of large quantities of H+ ions.
The low serum [K+] reflects in excretion of K+ by the kidneys rather than loss in vomitus.
The increased K+ excretion results from increased secretion by the distal tubule and
collecting duct. Secretion is stimulated by the hormone aldosterone, the levels of which
are elevated because of a decreased extracellular fluid volume (ECV). Symptoms of
decreased ECV are orthostatic changes in blood pressure and pulse, no jugular venous
pressure, and poor skin turgor. The decreased ECV will also prevent the kidneys from
excreting HCO3-, thereby maintaining the alkalosis. HCO3- excretion is impaired in this
case because proximal tubule Na+ reabsorption is stimulated in response to decreased
ECV. This obligates HCO3- reabsorption because Na+ absorption is linked to H+ secretion
via the Na+-H+ antiporter. In addition, H+ secretion by the distal tubule and collecting
duct is stimulated by increased aldosterone.