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Background: Recurrence of immunoglobulin (Ig)A nephropathy (rIgAN) is a growing cause of kidney allograft dysfunction. This study was aimed at investigating factors associated with rIgAN and the subsequent progression to end-stage renal disease (ESRD). Methods: Retrospective study including consecutive patients with IgA nephropathy (IgAN) who received a kidney transplant in our center between 1992 and 2016 and had a renal biopsy by clinical indication. The date of detection of chronic kidney disease (CKD) 5 was used as renal outcome. Results: Eighty-six kidney transplants were performed in patients with IgAN, 38 (44%) were from living donors (related n = 26). rIgAN was diagnosed in 23 allografts (27%). Renal function and proteinuria at the end of the follow-up period were worst in the rIgAN patients compared to those without rIgAN (2.2 vs. 1.4 mg/dL, p = 0.014, and 1.16 vs. 0.49 g/day, p = 0.005, respectively). Risk of rIgAN and progression to CKD 5 decreased with patient’s age (hazard ratio [HR] 0.95, 95% CI 0.92–0.98, p = 0.002, and HR 0.97, 95% CI 0.83–0.97, p = 0.008 per year, respectively). Patients with rIgAN had a higher risk of progression to CKD 5 (HR 6.7, 95% CI 1.3–35.7, p = 0.025). Full donor-recipient mismatch in the human leukocyte antigen (HLA)-B loci decreased the risk of rIgAN (HR 0.22, 95% CI 0.06–0.76, p = 0.017). Conclusions: rIgAN was an independent risk factor for ESRD after renal allograft. Younger age increased the risk of rIgAN and CKD 5. Conversely, HLA-B mismatching was a potential protective factor for rIgAN of this glomerular disease.

A new type of amyloidosis, predominantly osteoarticular, has recently been recognized in uremic patients on hemodialysis, beta 2-microglobulin being the major constituent protein. Nowadays, it is not clear whether the amyloid deposition is limited to osteoarticular structures or whether it has a systemic character. In order to investigate the extension of dialysis amyloidosis, we studied 26 patients receiving hemodialysis treatment (mean time 12.2 years) for chronic renal failure due to nonamyloid nephropathy and who were affected by symptomatic dialysis amyloidosis. Twenty-two patients developed a carpal tunnel syndrome, and amyloid arthropathy was present in 21. Subcutaneous abdominal fat aspiration, rectal and skin biopsy, and two-dimensional echocardiography were performed in most of the patients, searching for the visceral involvement. Surgical pieces (one stomach and two colon) and three necropsies of symptomatic patients were included in the systemic investigation. Also, we studied five necropsies of patients without articular symptoms. Histological confirmation of amyloid visceral involvement was demonstrated in 15 (58%) of the 26 patients studied. When positive two-dimensional echocardiograms were included, the percentage increased to 81%. No differences in the rate of visceral involvement could be found between the two clinical groups (with and without carpal tunnel syndrome). Two-dimensional echocardiography represents the most useful tool to search for the visceral involvement of beta 2-microglobulin amyloidosis, followed by abdominal fat aspiration and rectal biopsy. Amyloid deposits were resistant to potassium permanganate treatment and reacted with antihuman beta 2-microglobulin (avidin-biotin-peroxidase method).

Carpal tunnel syndrome, peripheral arthropathy, erosive spondyloarthropathy and lytic bone lesions have all been associated with dialysis amyloidosis. Recent studies indicate that beta 2-microglobulin is the major constituent protein in this new form of amyloidosis. Dialysis amyloidosis was reported to have a local rather than a systemic involvement, although its full extent is yet to be determined. We investigated 3 patients on maintenance hemodialysis with bilateral carpal tunnel syndrome and amyloid arthropathy and found amyloid depositions in several organs. These findings suggest that, in contrast to what had been thought previously, dialysis amyloidosis could have systemic as well as visceral distribution. The amyloid deposits found were resistant against potassium permanganate treatment and reacted with anti-human beta 2-microglobulin antibody.

A 21-year-old heroin addict with right-sided staphylococcal endocarditis developed skin purpura, abdominal pain, bloody diarrhea, proteinuria and microscopic hematuria. Skin biopsy showed leukocytoclastic vasculitis with IgA deposits in dermal vessels and renal biopsy disclosed proliferative glomerulonephritis with granular mesangial IgA and fibrinogen deposition. These features are typical of Henoch-Schonlein purpura. Symptoms abated spontaneously. Since the syndrome appeared during cloxacillin therapy, both this drug or the infectious disease itself could have triggered the immune response. Henoch-Schonlein purpura is a distinct clinical entity that can complicate the course of staphylococcal endocarditis.