肾小管酸中毒是由肾小管泌氢与碳酸氢钠代谢障碍所引起的一组临床症群,常以低钾性麻痹首现,容易造成误诊误治。现将我院近1年收治的确诊为Ⅰ型肾小管酸中毒的两例病人报告如下。 1 病例报告 例1 女,58岁,因四肢瘫痪1天,呼吸困难4小时于1998年1月22日收入院。既往有多发肾盂结石病史。查体:神清,半卧位。颅神经检查未见异常。颈软,双肺呼吸音粗,未闻及干湿啰音。心率130次份,律齐。腹部无异常发现。四肢肌张力减低,腱反射(+),肌力0级,病理征未引出。入院后查血电解质:K~+1.87mmol/L,Na~+136mmol/L,Cl~-111.9mmol/L。血沉89mm/1h,血BUN9mmol/L。尿常规:pH6.5,比重1.015,蛋白(+),镜检(-)。血气分析未查。心电图示窦速,房早,阵发性室上性心动过速,偶发室 Tubular acidosis is caused by the tubular hydrogen production and sodium bicarbonate metabolism disorders caused by a group of clinical syndromes, often with hypokalemic paralysis of the first appearance, easily lead to misdiagnosis and mistreatment. Now in our hospital admitted to nearly 1 year confirmed type Ⅰ renal tubular acidosis in two patients reported as follows. 1 Case Report 1 female, 58 years old, paralyzed for one day due to limbs, difficulty breathing four hours on January 22, 1998 income hospital. Past history of multiple pelvic stones. Examination: God clear, semi-recumbent position. No abnormal cranial nerve examination. Neck soft, breath sounds thick lungs, no smell and wet and dry rales. 130 times the heart rate, law Qi. Abdominal abnormalities found. Limb muscle tension decreased, tendon reflex (+), muscle strength 0, the pathological signs did not lead. Check blood electrolytes after admission: K ~ + 1.87mmol / L, Na ~ + 136mmol / L, Cl ~ -111.9mmol / L. ESR 89mm / 1h, blood BUN9mmol / L. Urine routine: pH6.5, specific gravity 1.015, protein (+), microscopic examination (-). Blood gas analysis was not checked. ECG shows sinus speed, morning room, paroxysmal supraventricular tachycardia, sporadic room