Early onset of ganciclovir-resistant cytomegalovirus infection in a lung-transplant recipient

Ganciclovir resistance in cytomegalovirus (CMV) is an increasing problem in lung-transplant recipients with adverse clinical outcomes. We experienced the successful treatment of ganciclovir-resistant CMV infection in a lung-transplant recipient still receiving CMV prophylaxis. A 24-year-old woman with lymphangioleiomyomatosis underwent a living-donor lobar lung transplantation. She was a primary CMV mismatch (D+/R?) patient. She recovered from her postoperative complications, and was about to be discharged. However, she suffered ganciclovir-resistant CMV infection during prophylactic therapy. She was successfully treated with foscarnet, and is now alive without recurrence 18 months after surgery.     

Early onset of ganciclovir-resistant cytomegalovirus infection in a lung-transplant recipient.

Ganciclovir resistance in cytomegalovirus (CMV) is an increasing problem in lung-transplant recipients with adverse clinical outcomes. We experienced the successful treatment of ganciclovir-resistant CMV infection in a lung-transplant recipient still receiving CMV prophylaxis. A 24-year-old woman with lymphangioleiomyomatosis underwent a living-donor lobar lung transplantation. She was a primary CMV mismatch (D+/R-) patient. She recovered from her postoperative complications, and was about to be discharged. However, she suffered ganciclovir-resistant CMV infection during prophylactic therapy. She was successfully treated with foscarnet, and is now alive without recurrence 18 months after surgery.     

Polyomavirus nephropathy in native kidneys of a solitary pancreas transplant recipient

BACKGROUND: Latent polyomavirus (PV) infection of the urinary tract can be reactivated by immunosuppression. When this occurs in the renal allograft, permanent loss of allograft function can occur. Polyomavirus reactivation could potentially affect the native kidneys of nonrenal transplant recipients and cause renal dysfunction. METHODS: This article describes a case of PV nephropathy in the native kidneys of a solitary-pancreas transplant recipient. This patient had a progressive increase in serum creatinine. Screening urine cytology showed numerous cells with cytopathic changes suggestive of polyomavirus infection. RESULTS: Biopsy of the native kidneys of this patient showed renal tubular cells with intranuclear inclusions characteristic of PV infection, which was confirmed by immunohistochemistry. Electron microscopy showed intranuclear viral particles. Patchy inflammation and fibrosis also were noted. CONCLUSION: Polyomavirus reactivation can occur in the native kidneys of nonrenal solid organ transplant recipients. This should be considered in the differential diagnosis of renal impairment in these patients. The effects of PV reactivation on long-term native kidney function are not known.     

Systemic Epstein-Barr virus infection associated with membranous nephropathy in children

Epstein-Barr virus (EBV) infection can cause diverse renal manifestations ranging from microscopic hematuria to acute renal failure. Membranous nephropathy (MN) is an uncommon and usually secondary cause of nephrotic syndrome in children, and has been reported after chronic infections and antigenemia. We report two pediatric cases of secondary MN associated with acute and chronic systemic EBV infection. Patient 1 had a liver transplant for cirrhosis due to biliary atresia and developed chronic EB viremia. Membranous nephropathy occurred 3 years later and with aggressive therapy has partially subsided, in temporal association with a drop in blood EBV PCR levels. The other patient had a primary immunodeficiency and developed a lymphoproliferative disorder attributed to EBV. Nephrotic syndrome developed at initial presentation and was associated with MN on biopsy. The patient cleared the virus from blood, which was associated with eventual resolution of the MN. We postulate that EB viremia in patients lacking a fully competent immune system, but without a renal allograft, may create a susceptible environment for chronic systemic EB antigenemia that can then lead to immune-complex MN in the kidney. The association of EBV with renal histological changes consistent with MN has been suggested but not directly described before.     

BK virus subtype 1 infection associated with tubulointerstitial nephritis in a renal allograft recipient

The BK polyomavirus (BKV) infects most of the human population, but clinically relevant infections are usually limited to individuals who are in an immunosuppressed state. The significance of BKV infection was investigated in a 50-year-old man who underwent cadaveric kidney transplantation and was treated with tacrolimus, mycophenolate mofetil and prednisolone. By staining renal biopsy specimens with a monoclonal antibody against BK large T antigen, we were able to observe the relationship between the appearance of the BKV antigen and the extent of immunosuppression in this patient. We also determined that BKV belonged to genotype I by analysis of viral DNA from the patient's urine.     

Immunoglobulin A nephropathy associated with hepatitis A virus infection.

Renal involvement in association with nonfulminant hepatitis A virus (HAV) infections have been reported infrequently and when present have been characterized by mild proteinuria, microscopic hematuria and slight urinary sediment abnormalities. Acute renal failure and nephrotic syndrome are extremely rare complications. This report describes a case of acute renal failure and nephrotic syndrome following a nonfulminant course of HAV infection with biopsy proven immunoglobulin A nephropathy. The cause of acute renal failure in this case is primarily due to tubulointerstitial nephritis secondary to pigment toxicity.     

Polyomavirus nephropathy in kidney transplantation

Polyomavirus nephropathy has become an important complication in kidney transplantation, with a prevalence of 1% to 8%. Unfortunately, the risk factors for polyomavirus nephropathy and renal allograft loss are not well defined. The definitive diagnosis is made through assessment of a kidney transplant biopsy. Recently, noninvasive urine and serum markers have been used to assist in polyomavirus nephropathy diagnosis and monitoring. Primary treatment is immunosuppression reduction, but must be balanced with the risks of rejection. No antiviral treatments for polyomavirus nephropathy have been approved by the Food and Drug Administration. Although cidofovir has shown in vitro activity against murine polyomaviruses, and has been effective in some patients, it is associated with significant nephrotoxicity. Graft loss due to polyomavirus nephropathy should not be a contraindication to retransplantation; however, experience is limited. This review presents potential risk factors, screening, diagnostic and monitoring methods, therapeutic management, and retransplantation experience for polyomavirus nephropathy.     

Polyomavirus nephropathy in renal transplantation: a clinico-pathological study

Polyomavirus (PV) nephropathy is a rare cause of graft dysfunction, but it may accompany acute rejection (AR), resulting in complications with respect to its diagnosis and treatment. To examine the validity of tubulitis and inflammatory phenotype in the diagnosis of concurrent AR, we reviewed the renal histology of ten biopsy samples from nine patients with PV nephropathy, and the immunohistochemistry from eight samples. Tubulitis was present in seven patients and was associated with AR in six. The degrees of tubulitis and interstitial inflammation were higher in biopsy samples with AR than in those without, but the degree of tubulitis was not related to the degree of interstitial inflammation. Virally infected cells were rare in the samples with no, or mild, tubulitis, but did not increase with the degree of interstitial inflammation. Immuno-phenotyping of inflammatory cells did not show any T-cell dominance in AR: T cells were dominant over B cells in three of six samples with AR and both samples without AR. Although the degrees of tubulitis and interstitial inflammation were higher in the AR subjects, the presence of tubulitis or inflammatory phenotype was not helpful in the diagnosis of concurrent AR. Further studies will be required to find a better marker for coexisting AR in patients with PV nephropathy and to establish strategies for treatment.     

IgA nephropathy in a child with human immunodeficiency virus type 1 infection

Infection with the human immunodeficiency virus type 1 (HIV-1) can cause a spectrum of renal disease, termed acquired immunodeficiency syndrome (AIDS) nephropathy. The most common clinical manifestations of kidney involvement in HIV-1-infected patients are proteinuria and/or nephrotic syndrome, and the histopathological pattern usually reveals focal segmental glomerulosclerosis. We describe an 8-year-old child with AIDS who presented with recurrent gross hematuria. A kidney biopsy demonstrated IgA nephropathy. This unique case indicates that the range of kidney disease in HIV-infected children may be broader than originally thought, and that these patients warrant a complete evaluation of any renal abnormality.     

BK virus nephropathy in a kidney transplant recipient: a case report and literature review

BK virus nephropathy (BKVN) has emerged as an important cause of allograft dysfunction and loss in kidney transplant recipients. We present a case in a 30-year-old female who underwent ABO-compatible living kidney transplant from her mother and was maintained with tacrolimus, mycophenolate mofetil and prednisolone. The serum creatinine level was stabilized about 0.9 mg/dl on postoperative day (POD) 35. On POD258, the serum creatinine increased to 1.8 mg/dl and the patient received methylpredonisolone pulse therapy under the diagnosis of acute rejection, which resulted in further increase in creatinine level from 1.8 to 2.6 mg/dl. Urine cytology showed decoy cells, but renal biopsy specimen showed no evidence of viral infection. Despite histopathological findings, positive urine and serum BKV-DNA suggested that allograft dysfunction was caused by BKVN. Therefore, the immunosuppession was reduced and gamma-globuline was given for 2 weeks. After the treatment, urine cytology became negative for decoy cells and serum creatinine level recovered to 2.0 mg/dl. On POD456, serum creatinine level was stabilized about 1.8 mg/dl and decoy cells remained negative.     

肾移植受者巨细胞病毒感染与慢性移植物肾病

目的　探讨肾移植术后早期巨细胞病毒 (CMV)感染与慢性移植物肾病 (CAN)的关系。　方法　 1999年 8月至 2 0 0 0年 12月行肾移植并随访 3年的患者 77例 ,根据术后 6个月内外周血CMV pp6 5 ( )白细胞计数的数量和持续时间 ,将其分为 :非活动性 (A组 ,n =15 )、低活动性 (B组 ,n=32 )、短期高活动性 (C组 ,n =18)和长期高活动性 (D组 ,n =12 )CMV感染 4组。 6个月后行移植肾穿剌活检 ,通过免疫荧光和逆转录聚合酶链反应 (RT PCR)比较 4组患者肾组织中转移生长因子β1(TGF β1)蛋白和mRNA的表达量 ;3年后比较 4组患者肾功能不全 (血肌酐持续 >114 μmol/L)的发生率和肌酐清除率 (Ccr)减损量 ;对肾功能不全的患者通过活检明确是否为CAN。　结果　肾移植 6个月后A、B、C组TGF β1蛋白表达量分别为 :( 5 .82± 1.32 )× 10 6、( 6 .34± 1.4 7)× 10 6和 ( 6 .5 8± 1.4 4 )× 10 6,TGF β1mRNA分别为 :0 .84± 0 .17、0 .78± 0 .15和 0 .82± 0 .16 ;D组TGF β1蛋白和mRNA表达量分别为 ( 10 .4 7± 2 .12 )× 10 6和 1.37± 0 .2 5 ,均明显高于前 3组 (P <0 .0 1)。前 3组 3年内Ccr减损量分别为 :( 5 .6± 5 .2 )、( 6 .2± 6 .4 )和 ( 5 .9± 4 .7)ml/min ;D组为 ( 15 .8± 9.6 )ml/min ,明显高于前 3组     

Antibodies to simian vacuolating virus 40 in bladder cancer patients

The occurrence of antibodies to herpes simplex virus type 2 (HSV-2) and simian vacuolating virus 40 (SV40) (two presumptive oncogenic viruses) was investigated by the technique of enzyme-linked immunosorbent assay in 233 patients with bladder cancer (200 males and 33 females) and in 466 controls (400 males and 66 females). The age of both the bladder cancer patients and controls varied from 55 to 65 years. A statistically significant association between bladder cancer and antibodies to SV40 was found in both males and females. No association between HSV-2 and bladder cancer was observed.     

IgA nephropathy associated with hepatitis B virus antigenemia

The pathogenetic ability of hepatitis B virus (HBV) antigenemia to induce IgA nephropathy was examined in 10 patients with IgA nephropathy and HBV antigenemia. They had no previous history of liver diseases and their liver function tests were normal. All were positive for hepatitis + surface antigen (HBsAg) and antibody to hepatitis B core antigen (anti-HBcAg) with high titers, thereby indicating they were persistent carriers of HBV. Immunoperoxidase studies using monospecific polyclonal antibodies revealed HBcAg and HBsAg in the nuclei and cytoplasm of glomerular mesangial cells in 8 patients. These findings suggest immune complexes involving HBcAg and HBsAg may induce IgA nephropathy in persons who carry HBV.