Background: Hypokalemia is a common and sometimes serious clinical problem,
whose etiological diagnosis can frequently be based on the patient's histo
ry and the clinical setting. Measurement of urinary indices such as excreto
ry rate of K+, random urine K+ concentrations and blood acid-base parameter
s have been employed in the pathophysiological diagnosis, though with some
pitfalls.
Methods: To investigate the diagnostic usefulness of the transtubular potas
sium concentration gradient (TTKG) and urine ammonium in the differentiatio
n of hypokalemia, we measured serum K+ and osmolality, random urine electro
lytes, osmolality and ammonium, the urinary [Na]/[K] ratio (U-Na/K), plasma
aldosterone and TTKG in 7 patients with diarrhea, 6 with vomiting, 7 with
mineralocorticoid excess, 6 with diuretic usage, and compared them with tho
se of 7 overnight fasted and acid-loaded healthy volunteers.
Results: The urine K+ concentrations did not reflect urinary loss of potass
ium according to the subjects hydration status. U-Na/k in the hypokalemic p
atients with mineralocorticoid excess (1.4 +/- 0.5) was lower than in norma
l subjects (2.3 +/- 0.4) (p < 0,05). TTKG was higher in hypokalemic patient
s with mineralocorticoid excess (13.3 +/- 4.4) and diuretic usage (8.6 +/-
1.3) and lower in those with diarrhea (1.6 +/- 0.3) than in the normal cont
rols (5.0 +/- 0.7) (p < 0.5). TTKG in the patients with vomiting (3.5 +/- 0
.6) was the same as in normal controls. TTKG was stronger correlated with t
he plasma aldosterone levels in the hypokalemic patients due to renal potas
sium loss. Urine ammonium concentrations of the acid-loaded normal subjects
(73.3 +/- 5.0 mEq/L), patients with diarrhea (74.4 +/- 2.0 mEq/L) and pati
ents with mineralocorticoid excess (68.7 +/- 6.9 mEq/L) were higher than in
overnight-fasted normal subjects (31.3 +/- 4.9 mEq/L).
Conclusion: TTKG and random urine ammonium were useful in the pathophysiolo
gical differential diagnosis of hypokalemia.