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IntroductionSpontaneous bladder rupture is an extremely rare clinical event that is associated with urinary ascites and apparent acute renal failure. This event is difficult to diagnose clinically, even with advanced techniques such as computed tomography; however, the timely diagnosis of this condition is critical. Here, we report a case of a patient who experienced a spontaneous intraperitoneal bladder rupture 10 years after postoperative pelvic irradiation for the treatment of uterine cancer. In this report of a rare case, we describe the contribution of the appearance of mesothelial cells in the urine to the diagnosis of this condition.Case presentationOur patient was a 71-year-old Asian woman who experienced lower abdominal pain and vomiting of two days duration. On admission, abdominal computed tomography showed intraperitoneal fluid collection and her blood tests revealed acute renal failure and hyperkalemia. She underwent hemodialysis and a transurethral catheter was inserted. The transurethral catheter was removed three days after her admission. Four days after the catheter removal, her symptoms recurred and her serum creatinine and blood urea nitrogen levels were elevated. We noted the presence of mesothelial cells in her urine, which led to a diagnosis of intraperitoneal bladder rupture. She underwent surgical repair of her bladder and hyperbaric oxygen therapy, and was discharged after her renal function returned to normal.ConclusionUrine analysis is a simple and non-invasive test and we believe that a thorough urine analysis may contribute to the early diagnosis of an intraperitoneal bladder rupture. We think that the findings presented in this case report will significantly enhance our understanding of the etiology of bladder rupture. Moreover, these case findings may help nephrologists and urologists to rapidly diagnose this condition.

The "nutcracker" phenomenon results from compression of the left renal vein between the superior mesenteric artery and the aorta. The main features of this phenomenon are non-glomerular haematuria on urinalysis and stenosis of the left renal vein with dilatation of the vein distal to the stenosis. The characteristics of two patients with the "nutcracker" phenomenon complicated by immunoglobulin A nephropathy were compared with those of 10 patients showing only the "nutcracker" phenomenon. Patients with the "nutcracker" phenomenon complicated by immunoglobulin A nephropathy showed aggravation of haematuria after upper respiratory infections, urinary red cell morphology indicating haematuria of glomerular origin, elevation of serum IgA, persistence of proteinuria, and granular casts in the urine. The coexistence of immunoglobulin A nephropathy was suspected when these characteristics were observed in patients with the "nutcracker" phenomenon. In such cases, a renal biopsy is needed for a final diagnosis.

Human T-cell leukaemia virus type-1 (HTLV-1) is known to cause adult T-cell leukaemia. The prevalence of anti-HTLV-1 antibody in haemodialysis patients has been reported to be higher than that in the general population. The anti-HTLV-1 antibody-positive rate in patients with primary glomerulonephritis in the Nagasaki district, an endemic area of HTLV-1, was evaluated. The antibody-positive rates in patients with primary glomerulonephritis (9.9%) and in haemodialysis patients (18.4%) were significantly higher than the rate in general blood donors (6.6%). Of 142 patients with primary glomerulonephritis, 14 (9.9%) were positive for the antibody; histological evaluation of these patients showed minor glomerular abnormality in one, mesangial proliferative glomerulonephritis in eight (IgA nephropathy in six and non-IgA nephropathy in two), membranous nephropathy in three, and crescentic glomerulonephritis in two. Evaluation of 10 antibody-positive patients by immunofluorescent microscopy showed immunocomplex-type nephritis in nine, suggesting the involvement of HTLV-1-associated antigen in the development and progression of glomerulonephritis.

SUMMARYIgA nephropathy (IgAN ) is the commonest cause of glomerulonephritis and clinical exacerbation of IgAN is frequently associated with mucosal infection. T-cell receptorcd ( TCRcd+) cells are increased in both the circulation and in renal biopsies of patients with progressive IgAN. We examined the hypothesis that specific peptides within the 65 000 MW heat-shock protein (hsp) might stimulate TCRcd cells and play a part in the immunopathogenesis of IgAN. We studied T-cell proliferative responses stimulated by overlapping peptides derived from the sequence of mycobacterial 65 000 MW hsp. Three T-cell epitopes have been identified ( peptides 51-65, 71-85 and 281-295). The three peptides have a synergistic eÂect and they stimulate significantly higher proliferation of T cells in patients with IgAN than in disease or healthy controls. This response was inhibited by monoclonal antibodies (mAb) to TCRcd+ and human leucocyte antigen (HLA) class I, but not by mAb to HLA class II. The involvement of TCRcd+ cells was confirmed by up-regulation of the proportion of TCRcd+ cells when stimulated with the three specific peptides. We suggest that IgAN might be associated with mucosal infection by a variety of micro-organisms and that peptides within the microbial hsp cross-react with the homologous human hsp which may stimulate TCRcd+ cells and play a part in the pathogenesis of IgAN.