Vallo A, Rodríguez-Soriano J
Miner Electrolyte Metab. 1984;10(6):387-90.
Neutral phosphate infusion results in an elevated urinary minus blood PCO2 gradient (U-B PCO2), providing that the urinary pH is close to the pK (6.8) of the phosphate buffer system. The present investigation was designed to evaluate whether an oral phosphate load could achieve similar results in children. 18 normal children, aged 3-13 years, were studied. Following the oral phosphate load, the urinary phosphate concentration increased to 44.8 +/- 4.7 mmol/l (mean +/- SEM), and U-B PCO2 reached 68.8 +/- 7.0 mm Hg, with a urinary pH of 6.87 +/- 0.07. With a urinary phosphate concentration above 20 mmol/l, all children reached a U-B PCO2 above 40 mm Hg. 4 children with primary distal renal tubular acidosis were also studied. All exhibited a U-B PCO2 below 20 mm Hg despite values of urinary phosphate concentration at or above 20 mmol/l, indicating the presence of a true secretory defect in distal hydrogen ion secretion. The present study demonstrates that an oral phosphate load is as effective as a phosphate infusion in elevating the urinary PCO2 and, therefore, could have a wide application in the pathophysiologic evaluation of renal tubular acidosis.
中性磷酸盐输注会导致尿与血二氧化碳分压梯度（U-B PCO2）升高，前提是尿液pH值接近磷酸盐缓冲系统的pK值（6.8）。本研究旨在评估口服磷酸盐负荷是否能在儿童中取得类似结果。对18名3至13岁的正常儿童进行了研究。口服磷酸盐负荷后，尿磷酸盐浓度升至44.8±4.7 mmol/l（均值±标准误），U-B PCO2达到68.8±7.0 mmHg，尿液pH值为6.87±0.07。当尿磷酸盐浓度高于20 mmol/l时，所有儿童的U-B PCO2均超过40 mmHg。还对4名原发性远端肾小管酸中毒患儿进行了研究。尽管尿磷酸盐浓度等于或高于20 mmol/l，但所有患儿的U-B PCO2均低于20 mmHg，表明存在远端氢离子分泌的真正分泌缺陷。本研究表明，口服磷酸盐负荷在升高尿PCO2方面与磷酸盐输注同样有效，因此在肾小管酸中毒的病理生理评估中可能有广泛应用。
