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BACKGROUND: Carpal tunnel syndrome (CTS) is a major complication in long-term haemodialysis patients and is thought to be a form of haemodialysis-associated amyloidosis. CTS may be due to the deposition of amyloid as well as local inflammatory process in the carpal tunnel. Although macrophage-like cells infiltrating the tenosynovium of carpal tunnel are known to express mRNA for adhesion molecules, the level of expression of adhesion molecules on peripheral blood mononuclear cells (PBMC) in patients with CTS is unknown. METHODS: We compared the expression of very late activation antigen (VLA-4) on PBMC by flow cytometry in 14 patients on haemodialysis (6-21 years) with CTS, nine on haemodialysis (1-6 years) but without CTS and six patients on chronic ambulatory peritoneal dialysis (CAPD, 1-5 years) without CTS. RESULTS: The expression of VLA-4 on peripheral lymphocytes was not different among the groups. However, the FACScan fluorescence histogram of VLA-4 expression on peripheral monocytes showed a bimodal pattern in the CTS group, and the rate of the high intensity portion of the expressed VLA-4 on monocytes was significantly higher in CTS than other groups (P<0.05). The observed differences were not based on differences in the type of the dialysis membrane. We also examined the adhesion of PBMC to fibronectin-coated plates. The number of adherent PBMC was significantly higher in patients with CTS than in other groups (P<0.05). CONCLUSION: Our results suggest that increased expression of VLA-4 on peripheral monocytes and augmented adhesion capacity of PBMC to fibronectin may be involved in the development of CTS in haemodialysis patients.

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A case of systemic lupus erythematosus (SLE) associated with minimal change nephrotic syndrome (MCNS) in a 25-year-old female is described. The patient suddenly manifested butterfly rash and proteinuria was first pointed out on March, 1994. On admission, her skin biopsy indicated SLE. Subsequently, she developed nephrotic syndrome. Urinalysis showed heavy proteinuria (4.1 g/day), with no other abnormalities in the urinary sediment. Immunological examination revealed positive antinuclear antibody at a titer of 1:80 with a speckled pattern. Anti-ssDNA and anti-SS-A antibodies were positive, but other antibodies were negative. Serum complement (CH50) was within the normal range (30.5 U/ml). The renal biopsy showed no apparent cellular proliferation or increase of extracellular matrices in glomeruli by light microscopy. Slight deposition of IgG, IgM, C3 and C1q was focally seen in the mesangium and capillary wall by immunofluorescence. Electron microscopic examination revealed small and scattered dense deposits in the mesangium, subepithelium and subendothelium, associated with diffuse fusion of the foot processes of epithelial cells along the glomerular basement membrane. According to the WHO classification, the histological features were compatible with those of lupus nephritis (LN), class Ib. The patient was treated with PREDNISOLONE, Mizorbine and Dilazep, resulting in the disappearance of proteinuria and a normal serum level of total protein. The association of LN and MCNS is very rare. We also investigated the relationship between the intensity of proteinuria and histological types of 53 cases with LN examined in our laboratory. The cases with heavy proteinuria were mostly classified as WHO-Class IV and Class V. We report here a case of LN associated with MCNS and also review the literatures.

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IgA nephropathy (IgAN) is the commonest cause of glomerulonephritis and clinical exacerbation of IgAN is frequently associated with mucosal infection. T-cell receptor gamma delta (TCR gamma delta+) 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 TCR gamma delta 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 effect 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 TCR gamma delta+ and human leucocyte antigen (HLA) class I, but not by mAb to HLA class II. The involvement of TCR gamma delta+ cells was confirmed by up-regulation of the proportion of TCR gamma delta+ 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 TCR gamma delta+ cells and play a part in the pathogenesis of IgAN.

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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.

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The beta 1 integrin family, major adhesive receptors for the extracellular matrix (ECM), have been reported to be present in normal and diseased kidneys. Attachment of glomerular cells to ECM is mediated by beta 1 integrins. Several members of the beta 1 integrins are referred to as VLA (very late activation) antigens. Peripheral mononuclear cells also express VLA antigens in both resting and activated states. We examined the expression and function of VLA antigens on peripheral lymphocytes and monocytes in patients with IgA nephropathy using monoclonal antibodies (mAbs) specific for VLA alpha-chains. Peripheral lymphocytes from patients with IgA nephropathy expressed VLA-4 alpha and 5 alpha, but not VLA-1 alpha, 2 alpha or 3 alpha. Peripheral monocytes from patients with IgA nephropathy expressed VLA-2 alpha, 4 alpha and 5 alpha, but not VLA-1 alpha or 3 alpha. The expression of VLA adhesive receptors was observed in healthy individuals. Adhesion assay to fibronectin revealed augmented adhesion of mononuclear cells in IgA nephropathy (P < 0.05), and this increased adhesion was inhibited by mAbs to VLA-4 alpha and 5 alpha. The expression of beta 1 integrins in IgA nephropathy was similar to that of healthy individuals, but the function of these molecules in terms of adhesion to fibronectin though VLA-4 and VLA-5 is increased in these patients. These findings suggest that the activation of fibronectin receptors on peripheral mononuclear cells plays an important role in the pathogenic process of IgA nephropathy.

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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.

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