RESUMO
In our previous nephrolithiasis studies in the northeast region of Thailand, hypokaliurea and hypocitraturia were the 2 most commonly encountered metabolic abnormalities. This led us to believe that people prone to forming renal-stones in this area were in a state of potassium depletion, a condition which probably caused the low urinary excretion of citrate. Further studies on some aspects of citrate metabolism in these subjects were carried out. Two groups of adult male subjects were included in the study protocol. Group 1 consisted of 20 urban dwellers who were used as normal controls, and group 2 was comprised of 36 renal-stone patients residing in rural villages outside the municipal area. Fasting clotted venous blood and one 24-hour urine specimens were collected and analyzed for creatinine, citrate, calcium, phosphate, magnesium, sodium, potassium, chloride, bicarbonate and uric acid. Values for: creatinine and citrate clearances, the filtered load of citrate and the tubular reabsorption of citrate were then calculated. The results showed that, for both groups, the concentrations of most of the above parameters were within the normal ranges both serum and urine. An exception to this was that the levels of serum potassium and of urinary excretions of sodium, potassium and citrate in people in group 2 were significantly less than those in group 1 (p < 0.005, p < 0.001, p < 0.001 and p < 0.0001, respectively). With respect to citrate metabolism, while the serum citrate levels and the filtered load of citrate were not different between the 2 groups, the average percentage of renal tubular reabsorption of group 2 (95 +/- 1.1%) increased significantly (P < 0.0001)in comparison to group 1 (85 +/- 1.6%). Moreover when results from both groups were combined, a significant negative correlation between the renal tubular reabsorption of citrate and the urinary excretion of potassium was clearly seen (r = 0.4001, p < 0.007). Our data suggests that potassium depletion may affect the renal tubular cells in some manner which, consequently, causes an increase in renal tubular reabsorption of citrate. The final outcome of these changes in these renal stone subjects was hypocitraturia.