同胞姐妹同患远端肾小管酸中毒

同胞姐妹同患远端肾小管酸中毒吕祖芳，马志根，张立明（潍坊市人民医院儿科２６１０４１）关键词酸中毒．肾小管性，同胞，肾性佝偻病例１，同胞姐，女，１４岁。８年前开始出现口渴、多饮、多尿、伴厌食、消瘦、体重不增。２年来出现双膝关节疼痛，站立不稳，步行困难。...     

系统性红斑狼疮继发肾小管性酸中毒1例

系统性红斑狼疮 (SL E)引起的狼疮性肾炎临床较为普遍 ,而 SL E继发的肾小管性酸中毒 (RTA)并不多见。现将临床所遇 1例报道如下。患者　女 ,30岁 ,已婚 ,电焊工作 8年。有持续不规则低热、厌食、腹胀、手足小关节疼痛 3月余 ,反复恶心、呕吐 2 0天 ,呕吐为非喷射状 ,吐出胃内容物和胃液。乏力 ,稍稍活动心悸、气促。在持续性便秘中合并有短期腹泻。体检 :神清 ,慢性病容 ,营养不良 ,血压 110 /70 mm Hg,颊面部可见蝶形红斑 ,未见其它皮损。体温在 37℃～ 38.5℃之间波动。心率 90次 /分。心尖部可闻 级收缩期杂音 ,两肺呼吸音清晰 ,腹…     

肾小管性酸中毒2例

肾小管性酸中毒是一种有多系统表现的少见病,易误诊误治。现将收治的2例报告如下。例1 女,29岁,农民。因烦渴、多饮、多尿2年,伴四肢瘫痪2天急症入院。2年来每日尿量5000～6000ml,反复查血糖、尿糖无异常。查体:皮肤干燥无弹性,双眼窝下陷明显,舌面干裂。心肺     

4例肾小管性酸中毒误诊分析

<正> 肾小管性酸中毒(RTA)系由各种疾病所致的肾调节酸碱平衡失常与尿酸化机能降低的症群。由于临床表现复杂,易误诊或漏诊。现将笔者近8年来收治的4例肾小管性酸中毒曾误诊为其他疾病报告如下: 临床资料 1、一般资料:男2例、女2例。发病年龄4月～8岁。远端RTA(Ⅰ型)3例,近端RTA(Ⅰ型)1例,原发型RTA3例,继发于肾盂肾炎1例。 2、临床表现:烦渴、多饮多尿3例;厌食、消瘦、生长发育迟缓3例,其中1例Ⅱ度营养不良;2例身高较同龄正常儿童矮小;体重均有减轻;肌无力3例;呕吐、抽搐1例。     

远端肾小管酸中毒误诊 3 例

远端肾小管酸中毒误诊３例张学才１孙建平１张乐１赵培森２于苏华２例１，男，２７岁。因烦渴、多饮、多尿及夜尿增多２３年，尿痛和腰痛６年入院。曾在当地医院诊断为低钾血症、周期性麻痹及肾结石。查体：ＢＰ２０／１２ｋＰａ，体形矮小，心肺无异常，腹软，肝脾肾未触...     

肾小管性酸中毒误诊2例分析

肾小管性酸中毒误诊较为常见,有时会引起严重并发症,现报告2例,并结合文献复习就误诊原因及并发症的抢救问题加以探讨。 1 病例介绍 例1.女,28岁,工人。因进行性四肢乏力1天,呼吸困难3小时于1991年4月21日入院,在当地医院诊断为“格林—巴利综合征”。既往因烦渴、多饮、多尿10余年被诊断为“尿崩症”。入院查体:青年女性,急性病容,神志清,口唇轻度紫绀,双肺呼吸音粗。心率86次/分,律齐。四肢软瘫,浅、深感觉存在,腱反射迟钝,以同样诊断给予吸氧、输液加抗生素、激素治疗。呼吸困难进行性加重,2小时后出现呼吸浅快,口唇紫绀加重,自诉呼吸无力,考虑有呼吸肌麻痹,急给予气管插管并用呼吸机辅助呼吸,憋气明显减轻。急查血钾2.1mmol/L,二氧化碳结合力17mmol/L,尿pH7。追问病史,患者曾长期食用棉籽油。最后诊断:肾小管性酸中毒。给予补钾、纠正酸中毒、口服枸橼酸合剂等治疗,10天后痊愈出院。     

肾小管性酸中毒1例

患者,女,29岁,待业.因反复发作性四肢无力4年,再发12 h入院.于4年前出现尿量及夜尿多,继而出现四肢无力,不能行走,发作时在当地医院查血钾低,给予口服及静脉应用氯化钾治疗,症状可缓解,并长期口服氯化钾预防发作,但于疲劳后常有类似发作,12 h前在干家务活时再次发作,出现四肢瘫痪,不能行走,平卧时不能自己翻身,在当地医院查血K 1.62 mmol/L,心电图出现U波,静脉及口服补钾6 g,症状无改善转到我科治疗.入院查体:BP 123/86 mmHg,神清,言语清晰,对答切题,颅神经(-),四肢肌张力正常,双上肢肌力近端1级,远端2级,双下肢肌力近端0级,远端1级,腱反射略活跃,深浅感觉正常,无病理征,心肺(-).     

原发性远端肾小管性酸中毒2例误诊分析

原发性远端肾小管性酸中毒（dRTA）在临床上不多见，常有漏诊或误诊发生。本篇选择较典型的2例误诊分析如下：病例1：患者女性，23岁，住院号92670，因复心悸、四肢乏力1年多，加重1天于90年9月25日入院。患者于89年6月以来先后在两家医院诊断为“甲亢伴周期性麻痹”，间断予抗甲状腺药。入院时查，无凸眼，甲状腺不大，甲状腺区无震颤及血流杂音，双手无震颤，心肺无特殊发现，肝脾助下未们及，双下肢浅感觉正常，双下肢肌张力减低，肌力Ⅲ级，膝反射对称性减弱，未引出病理神经反射。入院后检查：血T3、T4、TSH、TG、FT3、TMRT3查2…     

肾小管性酸中毒148例临床分析

目的探讨肾小管性酸中毒(RTA)的病因、分型、临床特点,以助早期诊断及治疗,减少严重并发症的发生。方法回顾性分析148例RTA患者的临床资料。结果病因原发性RTA占34.5%、继发性RTA占65.5%;临床分型Ⅰ型占77.0%、Ⅱ型占9.5%、Ⅲ型占11.5%,Ⅳ型占2.0%。女性RTA病因以原发性干燥综合征多见(27.5%);成人RTA最常见的临床表现为肌无力(75.5%),儿童以生长发育落后多见(57.1%)。结论 RTA临床表现多样,多种疾病可以继发RTA,临床医生要提高对RTA的认识;RTA伴生长发育落后的儿童使用生长激素追赶生长治疗值得重视。     

Primary hyperparathyroidism and proximal renal tubular acidosis: Report of two cases

Two cases of primary hyperparathyroidism due to single parathyroid adenomas presented with the additional feature of hyperchloremic acidosis. The defect in urinary acidification responsible was not of the distal or gradient-limited type since both patients could lower urine pH adequately. However, there was a defect of bicarbonate reabsorption, an abnormality referred to as the proximal or rate-limited type of renal tubular acidosis. It is suggested that this defect represents an exaggeration of the physiological effect of parathormone on bicarbonate reabsorption and may be responsible for the frequent finding of hyperchloremia in association with primary hyperparathyroidism as well as for the urinary bicarbonate-wasting associated with a variety of causes of secondary hyperparathyroidism.     

干燥综合征合并肾小管性酸中毒

目的：结合实验检测及肾脏病理，了解干燥综合征中肾小管性酸中毒的发生情况。方法：对我科１９８８年１月～１９９７年１月收治的４０例干燥综合征（ＳＳ）肾脏损害患者进行常规、免疫学、肾小管功能及肾活检等检查。结果：２８／４０为远端肾小管性酸中毒（ｄＲＴＡ），１３／２８合并其他自身免疫性疾病，１８／２８合并低钾性麻痹，３／２８合并肾性尿崩症。６７．９％患者为高免疫球蛋白Ｇ血症，５７．１％和５０％患者抗ＳＳ－Ａ、抗ＳＳ－Ｂ抗体阳性。１１／２８行肾活检，发现肾小管间质中有大量淋巴细胞和浆细胞浸润，部分小管萎缩，间质纤维化。２０／２８例患者用激素治疗，４／２８例合并用环磷酰胺治疗。结论：ＳＳ合并ｄＲＴＡ常见，长期中、小剂量激素治疗可减少肾小管及间质损害，改善肾功能     

Incomplete distal renal tubular acidosis with nephrocalcinosis

We report the case of a female patient with incomplete distal renal tubular acidosis with nephrocalcinosis. She was admitted to the hospital because of acute pyelonephritis. Imaging studies showed dual medullary nephrocalcinosis. Subsequent evaluations revealed hypokalemia, hypocalcemia, hypercalciuria, and hypocitraturia with normal acid-base status. A modified tubular acidification test with NH4Cl confirmed a defect of urine acidification, which is compatible with incomplete distal tubular acidosis. We treated our patient with potassium citrate, which corrects hypokalemia and prevents further deposition of calcium salts.     

Life-threatening hypokalaemia associated with ibuprofen-induced renal tubular acidosis

Renal tubular acidosis is an underreported complication of ibuprofen misuse, and can result in life-threatening hypokalaemia. We describe four patients who presented with profound hypokalaemia and muscle weakness associated with excessive ibuprofen ingestion. Ibuprofen cessation and supportive management resulted in complete biochemical resolution within a few days. These cases remind practitioners about potential complications of unmonitored use of over-the-counter analgesics, including those with potential for misuse due to their codeine content.     

Rhabdomyolysis associated with hypokalaemic periodic paralysis of renal tubular acidosis

Two cases of hypokalaemia with serum potassium levels of 1.4 mmol/L and 1.9 mmol/L causing severe periodic paralysis since childhood are presented. There were associated with muscular aches and markedly raised muscle enzymes suggesting massive rhabdomyolysis. These abnormalities were due to renal tubular acidosis with markedly acidic arterial pH. The hypokalaemia and rhabdomyolysis responded to potassium and bicarbonate replacement. We postulate these patients had sporadic distal type of renal tubular acidosis and that the hypokalaemia and acidosis had caused the rhabdomyolysis.