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김혜영,한진석,이정상,김현리,김진,이중건,이서진,김근호,진호준,전은실,주권욱,나기영,정우경,오지은,엄재호,궁성수 대한신장학회 2000 Kidney Research and Clinical Practice Vol.19 No.5
The purpose of this study was to elucidate whether the molecular defect of acid-base transporters in renal tubules is related to the functional defect of urinary acidification in distal renal tubular acidosis(RTA). We performed NH₄Cl, furosemide, or bicarbonate loading test to evaluate renal acidification function, and immunohistochemistry using antibodies to H^+ -ATPase, Cl^-/HCO₃^- exchanger(band-3 protein), and Na^+/K^+ -ATPase in kidney tissue in 6 patients with RTA and renal cell carcinoma patients as normal controls. Kidney tissue was obtained either by percutaneous needle biopsy(RTA) or nephrectomy(NC). The results were as follows; 1) In all six RTA patients, proton secretory defect of distal acidification was shown by a failure to lower the urine pH after NHC1 loading or furosemide test or abnormally low urine-blood pCO₂ difference during bicarbonate loading. In two patients with RTA, proximal acidification defect was combined, which was demonstrated by increased fractional excretion of bicarbonate. 2) In mal control, intense H^+ -ATPase and band-3 protein staining was observed in collecting ducts. 3) In distal RTA patients, H6+ -ATPase and band-3 protein staining was not demonstrable or markedly decreased in the intercalated cells of distal nephron. 4) In two patients who had both proximal and distal RTA, H^+ -ATPase staining was markedly decreased in the brush border of proximal tubules as well as the distal nephron. In conclusion, the defect of acid-base transporters in renal tubule was related with the functional defect of urinary acidification in distal RTA.