Oster J R, Hotchkiss J L, Carbon M, Vaamonde C A
J Lab Clin Med. 1975 Jun;85(6):987-1000.
After ingestion of 150 mEq. of calcium chloride (CaCl-2), urinary acidification was studied for 6 hours in 22 normokalemic patients with alcoholic liver disease (L) of varying severity, and in 7 control (C) subjects during 10 studies. The degree of the induced systemic acidosis was similar in all groups. Nine L patients were unable to normally lower urine pH below 5.25 (L-I) and these were compared with the 13 L patients achieving lower pH (L-II) and with control subjects. This defect was consistently reproduced. Titratable acid excretion was less in L-I than in the other groups. The percentage contribution of ammonium to maximal net acid excretion was significantly higher in L-I and L-II than in C. No L-I patient had spontaneous metabolic acidosis, nor was there evidence of encephalopathy or of proximal tubular dysfunction. Sodium excretion was significantly lower in L-I than in either L-II or C. Sodium sulfate and sodium phosphate infused after acid-loading rapidly reduced urine pH into the appropriately acidic range in L-I patients with alcoholic liver disease by means of a simple, safe, and short acid-loading test. Although the mechanism of this renal tubular acidfying defect remains unknown a low distal delivery of sodium by limiting the transtubular potential difference may have been partially responsible.
摄入150毫当量氯化钙（CaCl₂）后，对22例不同严重程度的酒精性肝病（L）正常血钾患者进行了6小时的尿酸化研究，并在10项研究中对7名对照（C）受试者进行了研究。所有组中诱导的全身酸中毒程度相似。9例L组患者无法将尿pH值正常降低至5.25以下（L-I），将这些患者与13例能将pH值降至更低水平的L组患者（L-II）以及对照受试者进行比较。这种缺陷持续存在。L-I组的可滴定酸排泄量低于其他组。L-I组和L-II组中铵对最大净酸排泄的贡献百分比显著高于C组。没有L-I组患者出现自发代谢性酸中毒，也没有脑病或近端肾小管功能障碍的证据。L-I组的钠排泄量显著低于L-II组或C组。通过简单、安全且短暂的酸负荷试验，对酒精性肝病L-I组患者进行酸负荷后输注硫酸钠和磷酸钠可迅速将尿pH值降至适当的酸性范围。尽管这种肾小管酸化缺陷的机制尚不清楚，但通过限制跨管电位差导致的低远端钠输送可能是部分原因。
