The abnormal superficial radial artery does not restrict the successful creation of hemodialysis forearm arteriovenous fistula.

Anatomical variations of the radial artery are of clinical importance in end-stage renal disease patients awaiting creation of native arteriovenous fistula for hemodialysis. As radial-cephalic direct wrist fistula is a vascular access of choice, atypical localization of the distal part of the radial artery may lead to the false assumption of severe atherosclerotic lesions and prevent creation of such an access, despite good vessel conditions and convenient surgical approach. We present 7 patients with radial artery variations. In 5 patients with superficial radial artery, radial-cephalic direct wrist access was created. One patient, due to an anomaly misdiagnosis, had radial-cephalic fistula created on the contra lateral wrist. In the patient with hypoplastic radial artery brachial-basilic upper arm transposition was created.

Activated cells in urine and monocyte chemotactic peptide-1 (MCP-1)--sensitive rejection markers in renal graft recipients.

Chemokines induced during an acute immune alloresponse cause cellular infiltration of the allograft. These chemokines and cells are excreted with urine. The aim of the study was to assess the diagnostic utility of urinary excretion of monocyte chemotactic peptide-1 and certain cells involved in infiltration i.e. CD3+, CD64+ and HLA-DR+ cells. The study entailed 35 patients with acute renal rejection and 65 with a stable graft function. Urinary sediments were prepared by means of cytospin and stained with anti-CD3, anti-CD64, anti-HLA-DR labeled monoclonal antibodies. Urinary expression of MCP-1 was assayed by ELISA. In the patients with acute rejection MCP-1 level was ten-fold higher than in the patients with a stable graft function (6.1+/-3.4 vs 0.6+/-0.4 ng/mg creatinine). The number of CD3+ cells was over 5 times higher than in the non-rejection patients (13.4+/-4.6 vs 2.5+/-2.2). The number of HLA-DR+ cells was 6 times higher in the acute rejection patients (15.7+/-5.9 vs 2.5+/-2.7). The number of CD64+ cells was significantly increased in the patients during an acute rejection episode (p<0.0001). CD3+, HLA-DR+ and CD64+ cell counts strongly correlated with urine excretion of MCP-1. The counts of CD3+ and HLA-DR+ cells correlated with Banff score. The assessment of MCP-1 as well as CD3+, CD64+ and HLA-DR+ cells can provide a useful non-invasive device for the diagnosis of acute rejection. A sole assay of HLA-DR+ cell excretion provides enough specificity and sensitivity for the routine monitoring of patients after kidney transplantation, saving costs and time.

Immunocytological urinalysis and monocyte chemotactic peptide-1 in renal transplant recipients with polyomavirus replication.

In some patients polyomavirus replication induces chronic tubulointerstitial inflammation in the transplanted kidney. The aim of this study was to investigate whether immunocytological urinalysis and monocyte chemoattractant protein-1 (MCP-1) assays could be used for an early diagnosis of nephropathy for patients with polyomavirus replication. We analyzed 1189 urine sediments from 174 renal allograft recipients who were transplanted between 2000 and 2005. Decoy cells were identified by an immunofluorescence method using specific antibodies (JC/BK monoclonal antibody). A similar method was used to detect CD3(+), CD14(+), and HLA-DR(+) cells with appropriate antibodies. The urinary excretion of MCP-1 was assayed by enzyme-linked immunosorbent assay. The results of urine sediment analysis and MCP-1 concentrations were compared with those of patients with stable graft function (control group n = 65). In 17 patients (10%) decoy cells were identified in urine. In 12 patients polyomavirus DNA was detected in plasma or urine by a polymerase chain reaction method. Polyomavirus nephropathy was diagnosed in eight patients by the presence of intranuclear viral inclusions or immunohistochemical staining with SV40 large T-antigen specimens from a renal biopsy, as well as by clinical and histopathological evidence (group I). Polyomavirus replication was diagnosed in four patients by urinary excretion of decoy cells and polyomavirus DNA detection (group III). In five patients only decoy cells were found. The patients of groups I and II showed an increased number of CD3, CD14, HLA-DR surface antigen-positive cells and greater excretion of MCP-1 compared with the control group (P < .02). The number of excreted cells was higher among patients with more severe infiltration. The results of patients from group III were similar to the control group. In conclusion, increased excretion of cells with CD3, CD14, and HLA-DR surface antigens and of MCP-1 were associated with intragraft tubulointerstitial inflammation in patients with polyomavirus nephropathy. Asymptomatic polyomavirus replication was associated with hidden tubulointerstitial inflammation. Monitoring cell excretion and chemokine content may be utilized for early detection of polyomavirus-induced nephropathy.