Immunoglobulin A-dominant postinfectious glomerulonephritis: frequent occurrence in nondiabetic patients with Staphylococcus aureus infection.

Immunoglobin A-dominant postinfectious glomerulonephritis is a distinct clinicopathologic entity that has been linked to staphylococcal infection, including methicillin-resistant Staphylococcus aureus. An association with diabetic nephropathy has been suggested. Although the morphologic features resemble other forms of postinfectious glomerulonephritis, immunofluorescence shows dominant or codominant immunoglobulin A immune-complex deposits. We encountered 7 patients with immunoglobulin A-dominant postinfectious glomerulonephritis over 2½ years at a single center. All patients presented with renal failure and with varying degrees of hematuria, proteinuria, and hypertension. All patients had clinical infections at the time of presentation. Four patients had documented S aureus infections. Three patients had methicillin-resistant S aureus infection within 2 weeks before the renal biopsy; 2 of these had an infection with a community-associated methicillin-resistant S aureus-10 clone, equivalent to USA300. One patient had methicillin-sensitive S aureus infection. Diffuse proliferative endocapillary glomerulonephritis was found in all cases; 1 had a membranoproliferative glomerulonephritic pattern, and 1 patient had a crescentic glomerulonephritis. Immunofluorescence microscopy showed dominant immunoglobulin A subepithelial and mesangial immune complexes in 5 patients and codominant immunoglobulin A with immunoglobulin G in 2 patients. Electron microscopy revealed large subepithelial deposits ("humps") in all cases. Only 1 patient had clinical diabetes mellitus but without biopsy-proven diabetic nephropathy. Two patients died, including the patient with diabetes mellitus. Renal function improved after therapy in 5 nondiabetic patients, but full recovery was not seen during the follow-up. We confirm that immunoglobulin A-dominant postinfectious glomerulonephritis is often associated with S aureus and methicillin-resistant S aureus infections, and, for the first time, we document an association with community-associated methicillin-resistant S aureus.

Glomerular mesangial fibrillary deposits in a patient with diabetes mellitus.

Various systemic or primary glomerular diseases can result in deposition of fibrillary material in the glomerular tuft and may cause an important diagnostic challenge for the pathologists. Biopsy findings of a patient with type 2 diabetes is presented here in which striking fibrillary structures were identified in the mesangium by ultrastructural examination. The distinction between diabetic fibrillosis and fibrillary glomerulonephritis accompanying diabetic nephropathy is discussed in the setting of a literature review.

Recurrent and de novo glomerular immune-complex deposits in renal transplant biopsies.

CONTEXT: Recurrent and de novo glomerulonephritis is an important cause of renal allograft failure, but estimates of its prevalence vary widely. One reason for such variability is the inconsistency with which electron microscopy and immunofluorescence are used in assessing renal allograft biopsies. OBJECTIVE: To determine the prevalence of immune-complex deposits in all renal allograft biopsies performed during a 1-year period and to correlate their presence with clinical data. DESIGN: Our center accessioned a total of 118 renal allograft biopsies during 1 year from 88 patients. All biopsies were examined by both electron microscopy and immunofluorescence in addition to conventional light microscopy. Patient and donor characteristics were obtained as well as follow-up data for a minimum of 26 months after the index biopsy. RESULTS: Eight cases of immunoglobulin (Ig) A nephropathy were found (recurrent in 7 and de novo in 1). There were 9 instances of what we designate "IgM-positive immune deposits" without specific features of a recognized glomerulonephritis. To the best of our knowledge, the latter has not hitherto been described and may be part of a heterogeneous group of glomerulopathies. Other unexpected findings included de novo fibrillary glomerulonephritis and de novo membranous glomerulonephritis, the latter occurring at 3 months after engraftment. CONCLUSIONS: A high proportion (19.5%) of unselected renal allograft biopsies show immune-complex deposits both with and without a recognized glomerulopathy. These require both electron microscopy and immunofluorescence for detection. IgM-positive deposits of uncertain etiology are relatively frequent.

Reproducibility of the Banff schema in reporting protocol biopsies of stable renal allografts.

BACKGROUND: There is evidence that biopsy of stable renal allografts may be of value in predicting chronic allograft nephropathy, the main cause of graft loss. However, the reproducibility of such histological evaluation has not been tested in this setting. We tested the reproducibility of the Banff schema for this purpose. METHODS: We rated acute and chronic changes in 184 protocol biopsies. Individual pathologists at two different Canadian transplant centres reported independently. RESULTS: There was agreement in 73.53, 42.86, and 77.08% of cases in assigning a diagnosis of acute rejection, borderline changes (as defined in the schema), and no acute rejection, respectively. Applying kappa statistics, there was very good agreement in making the diagnosis of acute rejection vs no acute rejection (kappa 0.77). There was good inter-observer agreement in scoring glomerulitis, intimal arteritis, interstitial infiltrates, tubulitis, and arteriolar hyalinosis. Rating chronic changes also gave good inter-observer agreement (kappa=0.53, 0.65, and 0.62, respectively, for mild, moderate, and severe chronic allograft nephropathy). Agreement on transplant glomerulopathy was, however, poor. CONCLUSIONS: We conclude that the Banff classification provides a reproducible method for the histological assessment of protocol renal allograft biopsies in stable grafts. Such biopsies may be valuable in detecting subclinical rejection and early chronic allograft nephropathy and may also be used as surrogate end-points in the evaluation of therapy to prevent the latter.