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Background. Renalinvolvementremainsamajordeter-minant in antineutrophil cytoplasmic autoantibody-associated small vessel vasculitis (AASV). While somepatients may develop persistent renal damage, othershave a favourable outcome.Methods. To identify patients at risk for poor renaloutcome, we evaluated 95 renal biopsies (67 initialbiopsies and 28 repeat biopsies) of 67 patients withAASV for the presence and extent of active (AI)and chronic (CI) lesions, retrospectively. AI, CI, levelsof proteinuria and dose of cyclophosphamide (CYC)were related to renal outcome.Results. Recovery of renal function in patients ini-tially dialysis dependent was associated with a lowerCI compared with patients who remained on dialysis(P

Nephrogenic adenomas are benign, tumor-like lesions within the urothelial mucosa of the urinary tract that are not uncommon in renal-transplant recipients. We investigated the origin of nephrogenic adenomas in renal-transplant recipients.Tissue sections were analyzed by fluorescence in situ hybridization with the use of probes for the X and Y chromosomes, by immunohistochemical methods with the use of antibodies to renal tubular antigens, and by lectin histochemical methods. Forty-six nephrogenic adenomas from 29 patients were analyzed.All nephrogenic adenomas in 14 female recipients of transplants from male donors and 10 male recipients of transplants from female donors showed the same sex-chromosome status as the donor kidney, but not the same sex-chromosome status as the recipient's surrounding bladder tissue. The nephrogenic adenomas from all 6 female recipients of transplants from female donors showed female chromosomes, and those from the 16 male recipients of transplants from male donors showed male chromosomes. The presence of aquaporin 1, PAX2, and lectin-binding capacity for peanut agglutinin, Lotus tetragonolobus agglutinin, and Sophora japonica agglutinin in nephrogenic adenomas indicated an origin from renal tubular cells.Nephrogenic adenomas in renal-transplant recipients are derived from tubular cells of the renal transplants and are not metaplastic proliferations of the recipient's bladder urothelium.

Background. In small vessel vasculitis and its renallimited form, idiopathic crescentic glomerulonephritis, renal damage is characterized by pauci-immune necrotizing crescentic glomerulonephritis (CGN) without histological evidence of immunoglobulin (Ig) deposition. In some patients, however, significant amounts of immune deposits may be detected. Therefore, we evaluated the clinical significance of these immune deposits in anti-neutrophil cytoplasmic autoantibody (ANCA)-associated pauci-immune CGN. Methods. Renal biopsies of 45 consecutive patients with new onset of Wegener’s granulomatosis, microscopic polyangiitis and idiopathic CGN were retrospectively evaluated by light microscopy, immunohistochemistry and electron microscopy and the findings compared with renal function and outcome. Results. Typical pauci-immune CGN was found in 37 patients (group I). In eight patients (18%; group II), however, histopathological examination revealed substantial deposition of Ig in the mesangium anduor along the glomerular basement membrane. Five of these eight patients were cANCA positive; two initially had pANCA and developed a cANCA pattern and one was pANCA positive. There were no differences between groups in age, gender, renal function or extrarenal organ involvement at the time of biopsy. However, patients in group II had significantly more proteinuria (5.4"3.1 vs 1.3"1.0 gu24 h; Ps0.016). We also observed a trend for a worse outcome with respect to renal function and mortality in group II patients; however, the differences did not reach significance. Conclusions. Our results confirm that in ANCAassociated CGN a substantial percentage of patients have evidence of Ig deposition in renal biopsies. In this subgroup, Ig deposition was associated with a significantly greater degree of proteinuria. Further investigations are necessary to define the full clinical impact of immune-complex deposition on the clinical course of renal disease in pauci-immune CGN.