Acute viral hepatitis (C - genotype 6a and B) acquired during kidney transplantation by two patients and review of the literature.

Two patients were contaminated by hepatitis during kidney transplantation from unrelated living donors, performed abroad in 2006. One patient died from fulminant hepatitis C (the first case of virus genotype 6a diagnosed in Israel) 2 months after transplantation and the other developed acute hepatitis B with YMDD to YVDD mutation necessitating life-long antiviral therapy. The dilemma of antiviral therapy in transplant recipients is discussed in this paper. Patients awaiting kidney transplantation by far outnumber the kidneys available for cadaver transplantation. International trade with living non-related kidneys has therefore become common. Comorbid conditions, although significant, are often ignored. After transplantation, the first patient presented with a picture of fulminant hepatitis C; immunosuppressive medication was tapered rapidly. This patient subsequently died from hepatic failure. The patient with active hepatitis B with YVDD mutation is receiving ongoing treatment by lamivudine and adefovir.

Clinical and genetic characterization of an autosomal dominant nephropathy.

Autosomal dominant familial nephropathies with adult onset, no macroscopic cysts, and progressive deterioration include medullary cystic disease (ADMCKD) as well as other less specific entities. We studied a kindred of Jewish ancestry in which 15 members (both male and female) have suffered from chronic renal failure. The first evidence of renal involvement was observed between 18 and 38 years. It included hypertension followed by progressive renal insufficiency. No polyuria, anemia, gout, hematuria, nor proteinuria were seen. An average of 4.5 years elapsed from diagnosis to end-stage renal disease. Renal pathology at early stages of the disease showed extensive tubulointerstitial fibrosis and global glomerulosclerosis. Linkage analysis was performed at the two known loci of ADMCKD, on Chromosomes 1 and 16. Linkage to the chromosome 16 locus was excluded. However, linkage to the chromosome 1q21 locus of ADMCKD was established with a maximum two-point LOD score of 3.82 to D1S394. The disease interval could be narrowed to about 9 cM/7.4 Mb between D1S1156 and D1S2635. Multiple-point linkage analysis revealed a maximum LOD of 4.21, with a broad peak from markers D1S2858 and D1S2624. This report establishes linkage between a familial nephropathy characterized by hypertension and progressive renal failure to the locus described for ADMCKD, a disease classically associated with macroscopic corticomedullary cysts, salt-losing tubulointerstitial nephropathy, and anemia. This finding broadens the clinical spectrum of ADMCKD positioned on chromosome 1q21 locus.

Aspergillus peritonitis in continuous ambulatory peritoneal dialysis patients.

Aspergillus peritonitis is a rare and serious cause of peritonitis in continuous ambulatory peritoneal dialysis (CAPD) patients. We report 3 cases of aspergillus peritonitis in CAPD which were successfully treated by catheter removal and amphotericin. Two of the 3 patients returned temporarily to CAPD, but were subsequently transferred to hemodialysis because of membrane failure. A novel finding in 2 of the 3 cases was a positive Limulus amebocyte lysate test, despite negative bacterial cultures. We discuss the possible relevance of this finding to the diagnosis of aspergillus infections and emphasize the importance of early catheter removal for successful treatment of this condition.

Severe Coombs'-negative autoimmune hemolytic anemia in a kidney transplant patient.

BACKGROUND/AIM: Few cases are found in the literature regarding autoimmune hemolytic anemia which is Coombs' test positive in kidney transplant patients, although hemolytic uremic syndrome due to cyclosporin and FK506 has been well described. In the following, we describe a case of severe life-threatening Coombs' test negative autoimmune hemolytic anemia after kidney transplantation. METHODS: Soon after undergoing renal transplantation, the patient presented with hemolytic anemia. Kidney biopsy, routine Coombs' test, gel filtration and flow-cytometric assay were undertaken. RESULTS: Kidney biopsy ruled out hemolytic uremic syndrome; although Coombs' test and gel filtration assay were negative, flow cytometry revealed circulating antierythrocytic autoantibodies. CONCLUSIONS: Our findings indicate that flow cytometry may be an efficient method in the diagnosis of hemolysis of unknown origin in transplant patients. We further hypothesize that the underlying mechanism of autoimmune hemolytic anemia is related to the passenger B lymphocytes in the graft.

Renal transplant dysfunction due to severe aorto-iliac atherosclerosis in the presence of patent renal transplant artery.

We report a case of progressive deterioration in renal function and decreased renal graft perfusion induced by extensive aorto-iliac atherosclerotic lesions proximal to a patent renal graft artery. Significant improvement in kidney graft function followed left axillo-femoral bypass graft surgery, which to the best of our knowledge, has never been performed previously for permanent maintenance of renal transplant perfusion.