Angeli P, Gatta A, Caregaro L, Luisetto G, Menon F, Merkel C, Bolognesi M, Ruol A
Istituto di Medicina Clinica, Università di Padova, Italy.
Gastroenterology. 1991 Feb;100(2):502-12. doi: 10.1016/0016-5085(91)90223-8.
The study was designed to evaluate (a) the role of reduced renal phosphate reabsorptive capacity assessed as the ratio of maximum capacity for renal phosphate reabsorption (TmPO4) to glomerular filtration rate (GFR) in the pathogenesis of hypophosphatemia in alcoholics, (b) possible mechanisms leading to reduced TmPO4/GFR, and (c) the effect of liver function impairment on TmPO4/GFR. The TmPO4/GFR, its major extrarenal determinants, ratios of urinary excretion gamma-glutamyl transpeptidase and of alpha-glucosidase to GFR (uGGT/GFR and uAGL/GFR), indices of structural damage of renal tubular cells, and fractional clearance of lysozyme, an index of proximal renal function, were evaluated in 31 alcoholics with alcohol-related liver disease, 24 alcoholics without alcohol-related liver disease, 14 patients with non-alcohol-related liver disease, and 25 control subjects. Hypophosphatemia was found in 35% of alcoholics with alcohol-related liver disease, 29% of alcoholics without alcohol-related liver disease, and no patients with non-alcohol-related liver disease. A reduced TmPO4/GFR was the major determinant of hypophosphatemia in both groups of alcoholics. No difference in extrarenal determinants of TmPO4/GFR was found between alcoholics with and without hypophosphatemia. Alcoholics with and without alcohol-related liver disease had increased uGGT/GFR and normal uAGL/GFR regardless of serum phosphate level. Fractional clearance of lysozyme, instead, was increased only in hypophosphatemic alcoholics with and without alcohol-related liver disease. The TmPO4/GFR correlated inversely with the fractional clearance of lysozyme in both groups of alcoholics (P less than 0.01). The TmPO4/GFR and urinary enzymes were normal in patients with non-alcohol-related liver disease. It was concluded that a reduced TmPO4/GFR is involved in the pathogenesis of hypophosphatemia in alcoholics. A proximal tubular dysfunction seems to be responsible for the reduced TmPO4/GFR. Liver function impairment is not required for the expression of this tubular dysfunction.
(a) 以肾磷酸盐重吸收最大能力（TmPO4）与肾小球滤过率（GFR）之比评估的肾磷酸盐重吸收能力降低在酒精性低磷血症发病机制中的作用；(b) 导致TmPO4/GFR降低的可能机制；(c) 肝功能损害对TmPO4/GFR的影响。对31例患有酒精相关性肝病的酗酒者、24例无酒精相关性肝病的酗酒者、14例非酒精相关性肝病患者和25名对照者进行了评估，测定指标包括TmPO4/GFR、其主要肾外决定因素、尿排泄γ-谷氨酰转肽酶和α-葡萄糖苷酶与GFR之比（uGGT/GFR和uAGL/GFR）、肾小管细胞结构损伤指标以及近端肾功能指标溶菌酶分数清除率。在患有酒精相关性肝病的酗酒者中，35%存在低磷血症；在无酒精相关性肝病的酗酒者中，29%存在低磷血症；非酒精相关性肝病患者中无低磷血症病例。两组酗酒者中，TmPO4/GFR降低是低磷血症的主要决定因素。有低磷血症和无低磷血症的酗酒者在TmPO4/GFR的肾外决定因素方面未发现差异。无论血清磷酸盐水平如何，有和无酒精相关性肝病的酗酒者uGGT/GFR均升高，uAGL/GFR正常。相反，仅在有和无酒精相关性肝病的低磷血症酗酒者中溶菌酶分数清除率升高。两组酗酒者中，TmPO4/GFR与溶菌酶分数清除率呈负相关（P<0.01）。非酒精相关性肝病患者的TmPO4/GFR和尿酶正常。研究得出结论，TmPO4/GFR降低参与了酗酒者低磷血症的发病机制。近端肾小管功能障碍似乎是TmPO4/GFR降低的原因。这种肾小管功能障碍的表现不需要肝功能损害。
