Nephrotic syndrome induced by D-penicillamine therapy

The paper presents a female patient in whom the penicillamine therapy for aggressive hepatitis triggered off the development of nephrotic syndrome. Histological findings revealed membranous glomerulonephritis.After the withdrawal of penicillamine therapy, the laboratory results returned to normal. The authors concluded that penicillamine should only be administered in conditions in which other means of therapy prove inefficient (i.e. Wilson's disease, cystinuria associated with calculi).     

Intraoperative hypernatremia and polyuric syndrome induced by dexmedetomidine

Hypernatremia and polyuria are the main symptoms of diabetes insipidus. Polyuria is characterized by a 24-h urine volume in excess of 40–50 ml/kg in adults. Dexmedetomidine, a highly selective, short-acting intravenous alpha-2 agonist, is used as a component of anesthesia, and has been suspected to induce polyuric syndrome. We report a patient who presented with severe hypernatremia and polyuria after intravenous infusion of dexmedetomidine.     

Hemolytic uremic syndrome induced by lipopolysaccharide and Shiga-like toxin

Induction of experimental hemolytic uremic syndrome (HUS) by simply administering Shiga-like toxin (Stx) to rodents has not yet been successful. Attention has been paid to the role of lipopolysaccharide (LPS) in the pathogenesis of HUS. In this study, we showed successful induction of an experimental HUS in LPS responder mice by administering Stx together with LPS. Intraperitoneal administration of 200 ng of Stx 2 for 2 days, followed by 250 g of LPS on the 2nd day of Stx administration, caused a significant decrease of thrombocytes and deterioration of renal function, with proteinuria and hematuria. Electron microscopy revealed alterations of glomerular endothelial cells. Administration of Stx alone or LPS alone caused neither hematological nor histopathological changes, as were observed with Stx and LPS co-administration. Interestingly, when LPS was administered before Stx, no hematological and histological changes were observed. The results showed that LPS was essential for the induction of HUS, but LPS pretreatment might protect against Stx toxicity. The order of LPS and Stx administration is important for the induction of experimental HUS.     

Myofascial pain syndrome induced by malpositioning during surgery--a case report

It is a real challenge to the anesthesiologists to differentiate brachial plexus injury (BPI) from myofascial pain syndrome (MPS). The possibility of MPS should be suspected in a patient with complaints of pain and dysfunction of the upper arm immediately after surgery. Here we report a case of gallstone with cervical ankylosing spondylitis who sustained myofascial pain syndrome (MPS) immediately after open cholecystectomy. We utilized dry needle stimulation to deactivate the trigger point of the pectoris minor muscle and stretching the muscle to relieve the muscle pain after the diagnosis was made. The patient completely recovered 2 weeks later.     

慢性骨筋膜间隔综合征致下腰痛的临床研究

[目的]探讨慢性骨筋膜间隔综合征所致下腰痛的发病机理。[方法]选取明确诊断为腰骶部慢性骨筋膜间隔综合征且未合并其他腰部疾病的患者30例，分别行腰腹肌肌力测定，竖脊肌内压测定，血常规，血沉，肌酸激酶（CK）及同工酶（CK—MM），乳酸脱氢酶（LDH）及同工酶（LDH，）测定，采用骨筋膜间隔切开减压手术治疗。术中切取竖脊肌标本用于组织病理学观察和透射电镜观察。[结果]各项酶学检验无异常；组织学光镜下观察到竖脊肌纤维部分溶解变性，肌纤维肥大，少量炎性细胞浸润；电镜下观察到肌纤维灶状溶解，核周线粒体聚集，胞内脂滴、溶酶体增多，肌卫星细胞增殖分化。[结论]腰骶部慢性骨筋膜间隔综合征是由于内在压力增加，筋膜间隔内组织代谢障碍，骨骼肌慢性受损，炎症因子释放，最终影响脊神经后支导致的下腰痛。     

Neuroleptic malignant syndrome induced by haloperidol following traumatic brain injury

The use of neuroleptics in the acute management of traumatic brain injury (TBI) is controversial and may be detrimental to recovery. The following case report describes a patient developing neuroleptic malignant syndrome (NMS) secondary to the use of haloperidol given to control the patient's agitation. The patient began to exhibit symptoms consistent with NMS (high fever, dystonia, diaphoresis, tachycardia, and decerebrate posturing) shortly after administration of the haloperidol. Upon transfer to a rehabilitation hospital, the symptoms persisted. When NMS issuspected, the first intervention is to remove the offending agent; thus, the administration of haloperidol was suspended, and the patient was placed on Amantadine and propranolol. Amantadine was used to increase the availability of dopamine to the mid-brain region, and the propranolol was used to control the fever, which was beleived to be central in origin. The patient was able to complete his rehabilitation with no further incidence of fever or agitation. The patient met or exceeded all short-term physical therapy goals and was able to complete most of the neuropsychological tasks presented. The patient returned home 38 days after admission to the rehabilitation hospital and was able to perform most activities of daily living. At the 6-months follow-up visit, the patient was considering entrance into an adult vocational school.     

Complete remission of minimal-change nephrotic syndrome induced by apheresis monotherapy

We report a case of a 17-year-old male with relapse of minimal-change nephrotic syndrome (MCNS), in whom apheresis monotherapy without steroids or immunosuppressants resulted in complete remission. The patient initially developed nephrotic syndrome in February 1998. The first renal biopsy confirmed the diagnosis of MCNS. The patient was also found to be a carrier of hepatitis B virus. Steroid therapy was started with oral prednisolone 60 mg/day. Complete remission was achieved in 3 months, and the steroid treatment was tapered off in May 2001. During the steroid tapering, temporal exacerbation of liver function was noted. In July 2002, the patient was admitted to our hospital again due to relapse of nephrotic syndrome. Second biopsy reconfirmed the diagnosis of MCNS. Since the serum titer of HBV was elevated, apheresis monotherapy was selected to avoid the risk of steroid-induced fulminant hepatitis. Four sessions of low-density lipoprotein apheresis (LDL-A) and 5 sessions of double-filtration plasmapheresis (DFPP) reduced the proteinuria from 9.2 g/day to 0.2 g/day over 38 days without any additional medication. Proteinuria remained suppressed below 0.2 g/day for more than 12 months and no exacerbation of liver function was observed up to the final follow-up in September 2003. The present case suggested the potential of apheresis monotherapy to induce and maintain complete remission of MCNS and an important role of circulating factors in the pathogenesis of MCNS.     

L-Histidinol attenuates Fanconi syndrome induced by ifosfamide in rats.

The effect of L-histidinol (LHL), a structural analogue of the essential amino acid L-histidine, on ifosfamide (IFO) induced nephrotoxicity was investigated in the rat. The aim of this study was to assess whether oral supplementation of LHL could attenuate Fanconi syndrome (FS) induced by IFO. Male Wistar albino rats received daily injections of IFO (50 mg/kg) for 5 days with or without oral supplementation of 0.5% LHL in the drinking water. LHL was supplemented for 3 days before IFO administration and daily thereafter. Control rats were injected with saline with or without oral LHL. The results demonstrated that IFO induces a FS characterized by wasting of glucose, electrolytes, and organic acids, along with elevated serum creatinine and urea levels and decreased creatinine clearance. IFO-induced FS was associated with significant renal nonprotein sulfhydryl depletion and lipid peroxide (malondialdehyde) accumulation. LHL strongly ameliorated the severity of renal dysfunction induced by IFO, with significant decreases in total and fractional excretions of Na(+), K(+), PO(4)(3-), and glucose. Also, LHL significantly decreased the elevated serum creatinine and urea levels and significantly increased the creatinine clearance. Moreover, the beneficial effects of LHL were associated with a significant improvement of IFO-induced nonprotein sufhydry depletion and lipid peroxide accumulation. These results demonstrate that oral supplementation of LHL can partially protect against IFO-induced FS in rats.     

Catheter induced superior vena cava syndrome aggravated by shunt placement

A case is presented of a dialysis catheter induced SVC syndrome aggravated by a recently surgically created AV fistula. Conventional angiography as well as computed tomography showed a catheter induced stenosis in the SVC. Removal of the catheter and treatment with anticoagulants resulted in resolution of the syndrome without the need for invasive endovascular intervention.