Cyclosporine-associated microangiopathic hemolytic anemia in a renal transplant recipient

A case of microangiopathic hemolytic anemia (MHA) associated with the immunosuppressive agent, cyclosporine, is reported herein. The patient manifested anemia with red blood cell fragmentation, hypertension, thrombocytopenia, elevation of serum LDH levels and glomerular capillary thromboses within a few days of his transplantation. Extensive treatments with urokinase and heparin proved ineffective and graftectomy was performed 7 days after his transplantation. Immunofluorescent staining failed to show immunoglobulin (IgG or IgM) or complement (C₃) deposition within the glomeruli, which discriminated MHA from acute humoralvascular rejection.     

Atypical mycobacterium infection with dermatological manifestation in a renal transplant recipient

In April 1997, a 58-year-old renal transplant recipient presented with abscess-like nodules in his left calf and on his right foot. Furuncular disease was suspected and the patient was treated with flucloxacillin. However, the lesions increased in size and became ulcerative. In the following 3 months, cultures of punctuated material, blood, and urine remained negative and gram stains did not reveal micro-organisms. In June 1997, acid-fast stains were positive. A diagnosis of a nontuberculous mycobacterium (NTM) infection was made and empirical antimycobacterial therapy was started. The combination of relatively minor symptoms with enlarged purulent lesions, causing severe morbidity, raises the possibility of NTM infection in the immunocompromised patient. Received: 24 March 1998 Received after revision: 28 July 1998 Accepted: 23 September 1998     

Successful treatment of recurrent focal segmental glomerulosclerosis with a low dose rituximab in a kidney transplant recipient

Recurrence of focal segmental glomerulosclerosis (FSGS) is a major therapeutic challenge in kidney transplantation (KT). Although intensive plasmapheresis and high-dose rituximab have been introduced to treat recurrent FSGS, the most effective dosage and regimen of rituximab have not been determined. Herein we reported the first case of successful treatment of recurrent FSGS with a low-dose rituximab. The patient showed marked proteinuria (3.5?g/d) and oliguria 2?d after KT. Two courses of plasmapheresis and immunoglobulin were applied to the patient, however, nephrotic range proteinuria persisted and creatinine level increased to 3.56?mg/dL. Five months post-transplant, the patient received injection with only one dose of rituximab 100?mg, without further plasmapheresis, which resulted in immediate reduction of serum creatinine and full remission of proteinuria during the following 18 months. This case suggested that recurrent FSGS, which frequently relapses after plasmapheresis, could be treated successfully with a low-dose rituximab even without plasmapheresis.     

Prolonged liver dysfunction caused by hemosiderosis in a renal transplant recipient

BACKGROUND: Liver dysfunction is a frequent complication that arises in the period following kidney transplantations, often resulting in death. We reported a case proving hemosiderosis as a cause of prolonged liver dysfunction after cadaveric kidney transplantation. METHODS: A 47-year-old man, who had been undergoing hemodialysis, was referred to our hospital on 2 November 1999. On the same day, cadaveric kidney transplantation was performed, and serum creatinine level reached a normal level within 2 weeks after surgery. However, serum transaminase gradually increased in the postoperative period. Serum ALT rose up to 116 IU/L on day 20 after the operation and 215 IU/L on day 30. Microscopic examination by needle biopsy revealed hemosiderosis of the liver. Recombinant human erythropoietin was administered and phlebotomy was performed. Liver function improved as a result. CONCLUSION: Early histological diagnosis can be a useful marker in predicting the course of chronic liver disease.     

A kidney transplant recipient with renal cell carcinoma derived from a native kidney

A case of renal cell adenocarcinoma which originated from a left native kidney following kidney transplantation, with widespread metastases, including multiple bone and liver metastases, is presented herein. An extensive clinical investigation, including bone marrow biopsy, liver biopsy abdominal computerized tomography, excretory urography and examination of the gastiointestinal tract failed to determine the site of the primary lesion in this patient. Examination at autopsy revealed a small adenocarcinoma of the left native kidney with lobulated nodular capsular invasion and metastases to the bone and liver.     

Collagenofibrotic glomerulopathy in a kidney transplant recipient: A first report

Collagenofibrotic glomerulopathy (CG) is a rare disease characterized by the deposition of collagen type 3 fibrils in the glomeruli. Patients may have proteinuria, hematuria, and/or renal dysfunction. CG is considered a progressive disease with variable rates of progression. The definitive diagnosis is made by electron microscopy with the presence of characteristic subendothelial and mesangial curved, comma-like, banded collagen type 3 fibers of 40–65 nm periodicity. We are reporting the first case of CG in a kidney transplant recipient with kidney disease of unknown cause.     

Rare cause of weight loss in a kidney transplant recipient: iron overload

Various reasons such as malignancies and chronic infections may cause weight loss in kidney transplant patients. In this report, iron overload as a rare cause of weight loss in a kidney transplant patient is presented. Forty-seven-year-old male patient who transplanted from a deceased donor 5 years ago was hospitalized because of 20?kg of weight loss. In medical history, he had history of hemodialysis for 89 months and received 100–300?mg of intravenous iron therapy per week before transplantation and transfused eight units of blood. In physical examination, weight and height were 45?kg and 185?cm, respectively. Respiratory and cardiac auscultation was normal. Laboratory results revealed as follow: glucose 76?mg/dL, urea 60?mg/dL, creatinine 1.35?mg/dL, aspartate aminotransferase 74?U/L, alanine aminotransferase 77?U/L, C-reactive protein 2.59?mg/dL, albumin 3.3?g/dL, globulin 3.4?g/dL, white blood cells 3200/mm³, hemoglobin 13.1?g/dL and platelets 190,000/mm³. Chest and abdominal tomography didn’t reveal any pathology. Portal Doppler ultrasound showed signs of early cirrhosis. Viral and autoimmune hepatitis markers were negative. Ferritin was 5300?ng/mL and transferrin saturation was 82%. In liver biopsy, hemosiderosis was diagnosed and heterozygous H63D gene mutation was detected. Totally, 19 units of phlebotomy were performed. Liver function tests and serum ferritin decreased gradually. At outpatient follow-up in 6 months, he returned to former weight. In conclusion, there can be several causes of weight loss in kidney transplant patients. Iron overload can come across as a rare cause of weight loss. In these patients, ferritin levels should be checked and diagnosis should be clarified by liver biopsy and gene mutation analysis.     

Acute drug toxicity related to drinking herbal tea in a kidney transplant recipient

Calcineurin and mTOR inhibitors are commonly used immunosuppressive agents with narrow therapeutic range. As the drugs are mainly metabolized by the P450 cytochrome system, the interaction between food and herbs are also commonly seen and affect the drug levels. We present a case of a kidney transplant recipient with toxic therapeutic levels of cyclosporine A and sirolimus due to interaction between the immunosuppressive agents and Chinese herbal tea. Ingredients within the herbal tea were reported to have inhibitory effect on cytochrome CYP3A4 in-vitro studies. Transplant recipients should be alert that there may be potent interaction between the immunosuppressive drugs and herbs resulting in adverse effect on allograft function.     

Nocardia niigatensis infection in a kidney transplant recipient

This is the first reported case of Nocardia niigatensis infection in an adult kidney transplant recipient. A 57-year-old Asian woman presented with multiple cutaneous abscesses and rapidly growing fungating mass on the left pretibial area for 2 months. She received a cadaveric kidney transplant 4 years previously and was undergoing immunosuppression with prednisolone, cyclosporine and mycophenolate sodium. The microbiological diagnosis was established by isolation of Nocardia from the purulent material expressed from a granule. The strain was identified to the species level by 16S rRNA gene-targeted PCR. The closest match was with N. niigatensis . Antibiotic treatment (trimethotrim–sulfamethoxazole) was continued for 6 months and the skin lesions improved.     

Multiple vascular anomalies in a paediatric kidney transplant recipient.

A 9-year-old girl with end-stage kidney disease secondary toright renal agenesis, and left hydronephrosis due to severevesicoureteral reflux complicated by recurrent urinary tractinfections, was referred to our hospital, to be considered forrenal transplantation. Significant past surgical history includedsurgical     

Pulmonary Rhizopus infection in a diabetic renal transplant recipient

Infectious complications after renal transplantation remain a major cause of morbidity and mortality. Mucormycosis is a rare infection in renal transplant recipients; however, mortality is exceedingly high. Risk factors predisposing to this disease include prolonged neutropenia, diabetes, and patients who are immunosuppressed (Singh N, Gayowski T, Singh J, Yu LV. Invasive gastrointestinal zygomycosis in a liver transplant recipient: case report and review of zygomycosis in solid-organ transplant recipients, Clin Infect Dis 1995: 20: 617). Life-threatening infections can occur, as this fungus has the propensity to invade blood vessel endothelium, resulting in hematological dissemination. We report a case of cavitary Rhizopus lung infection, 2 months after renal transplantation, where the patient was treated successfully with Amphotericin B and surgical resection of the lesions with preservation of his allograft function. In this era of intensified immunosuppression, we may see an increased incidence of mucormycosis in transplant population. Invasive diagnostic work-up is mandatory in case of suspicion; Amphotericin B and, in selected cases, surgical resection are the mainstays of therapy.     

BK virus-associated nephropathy in a kidney transplant recipient successfully treated with cidofovir, the first case in Japan

Abstract:   A 51-year-old female received a kidney transplant, donated by her husband. The patient was induced with tacrolimus, mycophenolate mofetil and prednisolone. After methyl predonisolone pulse therapy without biopsy, allograft biopsy on POD 160 showed severe tubulo-interstitial nephritis with intranuclear inclusions. Urine cytology also showed decoy cells. Blood PCR detected an increase of BK virus DNA. She was diagnosed as having BK virus-associated nephropathy . Reduction of tacrolimus and switching of mycophenolate mofetil to mizoribine were done. Serum Creatinin (sCr) still rose to 3.0 mg/dl with persistent viremia and viruria. From on POD 268, 0.25 mg/kg of cidofovir was administered intravenously every two weeks over about four months. Biopsy on POD 387 revealed the disappearance of tubulitis with intranuclear inclusions, and decoy cells also disappeared from urine cytology. BK virus DNA in the blood decreased under the threshold level. sCr was stable and remained about 2.2 mg/dl for three months after the final treatment of cidofovir.     

Azathioprine hypersensitivity in a renal transplant recipient

Hypersensitive reactions to azathioprine have been reported infrequently, and always in nontransplanted patients. Here, a renal transplant recipient with a severe hypersensitive reaction to azathioprine is described. We suggest that, until recently, hypersensitivity to azathioprine was suppressed in transplant recipients by the association of high doses of corticosteroids. Since the introduction of cyclosporin, azathioprine therapy is usually associated with corticosteroids in a much lower dose, so an increasing occurrence of azathioprine hypersensitivity in transplanted patients might be expected.     

Soluble interleukin 2 receptor (Tac chain) is not a reliable marker in kidney transplant recipient monitoring

T lymphocyte expansion is triggered through interaction of interleukin 2 (IL-2) with its high-affinity receptor (IL-2R). This molecule is a heterodimer comprising an antigen-inducible component, the Tac chain (P55). Activation of T lymphocytes also generates a soluble form of this P55 called S-IL-2R. S-IL-2R is elevated in many T-cell-related pathologies (leukaemia, autoimmunity, etc.). In graft recipients, rejection is a result of T-cell activation by graft antigens and therefore might induce a release of S-IL-2R in the circulation; this parameter is now said to be a good indicator of rejection. We have performed a study in renal graft recipients in order to assess the usefulness of circulating S-IL-2R particularly to discriminate the origin of renal failure in cases of rejection or of cyclosporin-A (CsA)-induced nephrotoxicity. We demonstrated that there are no differences between isolated values in the clinical groups at the time of diagnosis. Variations in S-IL-2R are increased compared to steady-state periods during rejection and cytomegalovirus infections, although not in CsA toxicity episodes. However, at the individual level there are too many false-positive and false-negative results, making this parameter no more meaningful than serum creatinine levels alone or even in association (as tested in logistic discriminant analysis). In addition, it seems that the variations in S-IL-2R are patly related to renal function itself, as suggested by the correlation between S-IL-2R levels and serum creatinine levels. This association may explain the increase in S-IL-2R that can be observed without T cell activation. In conclusion, S-IL-2R may not be of major interest in discriminating between rejection of kidney and CsA-induced nephrotoxicity episodes in kidney allograft recipients.     

Histologic resolution of documented hemosiderosis in a renal transplant recipient

A 33-year-old cadaveric renal transplant recipient showed complete histologic resolution of hemosiderosis by liver biopsies obtained pre- and post-transplantation. Although there have been reports in the past of progression of hemosiderosis to hemochromatosis to severe liver failure in the renal transplant population, the correlation has never been clear. This is the first case report of complete resolution of hemosiderosis as documented histologically by liver biopsies in a cadaveric renal transplant recipient.     

Hepatic candidiasis in a kidney transplant recipient treated successfully with amphotericin B and itraconazole.

The incidence of hepatic candidiasis is difficult to estimatebecause of diagnostic difficulties. Its frequency was