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Introduction: Glomerulonephritis (GN) with crescents and IgA deposits in kidney biopsy poses a frequent diagnostic and therapeutic dilemma because of multiple possibilities., Methods: Native kidney biopsies showing glomerular IgA deposition and crescents (excluding lupus nephritis) were identified from our biopsy archives between 2010 and 2021. Detailed clinicopathologic features were assessed. One-year clinical follow-up on a subset of cases was obtained., Results: A total of 285 cases were identified, and these clustered into IgA nephropathy (IgAN, n  = 108), Staphylococcus or other infection-associated GN/infection-related GN (SAGN/IRGN, n  = 43), and antineutrophil cytoplasmic antibody-associated GN (ANCA-GN, n  = 26) based on a constellation of clinicopathologic features, but 101 cases (group X) could not be definitively differentiated. The reasons have been elucidated, most important being atypical combination of clinicopathologic features and lack of definitive evidence of active infection. Follow-up (on 72/101 cases) revealed that clinicians' working diagnosis was IgAN in 43%, SAGN/IRGN in 22%, ANCA-GN in 28%, and others in 7% of the cases, but treatment approach varied from supportive or antibiotics to immunosuppression in each subgroup. Comparing these cases as "received immunosuppression" versus "non-immunosuppression," only 2 features differed, namely C3-dominant staining, and possibility of recent infection (both higher in the no-immunosuppression group) ( P  < 0.05). Renal loss was higher in the non-immunosuppression subgroup, but not statistically significant ( P  = 0.11)., Conclusion: Diagnostic overlap may remain unresolved in a substantial number of kidney biopsies with glomerular crescents and IgA deposits. A case-by-case approach, appropriate antibiotics if infection is ongoing, and consideration for cautious immunosuppressive treatment for progressive renal dysfunction may be needed for best chance of renal recovery., (© 2022 Published by Elsevier Inc. on behalf of the International Society of Nephrology.)

Background: BK virus (BKV) is an important cause of renal dysfunction in kidney transplant (KTX) recipients. Immunosuppression intensity is a major risk factor for BKV replication in these patients. The prevalence of BKV replication in immunosuppressed patients with granulomatosis with polyangiitis (GPA) and microscopic polyangiitis (MPA) without transplant is not known. Methods: Consecutive patients (n = 37) with a diagnosis of GPA (n = 25) or MPA (n = 12) without history of KTX were evaluated for plasma BKV replication by quantitative PCR (group A). Descriptive data were collected. BKV replication in this nontransplant immunosuppressed vasculitis cohort was compared with a historical cohort of vasculitis KTX recipients (group B). Results: Group A patients had mean disease duration of 75 months. Mean age was 57 years and 54% were female. Mean time from vasculitis onset to BKV testing was 36 months, and 19/37 patients were tested within 24 months of induction therapy. At the time of BKV testing, 73% were on prednisone (P) with azathioprine, mycophenolate mofetil (MMF), methotrexate or leflunomide. None of the nontransplanted vasculitis patients had detectable plasma BKV. Among 35 patients in group B, 16 were tested for BKV; 5/16 (31%) had detectable virus in plasma at a mean of 6 months after TX (p = 0.002). Most (94%) were on maintenance therapy with MMF, P and tacrolimus. Conclusion: Immunosuppressed patients with GPA/MPA without KTX had no evidence of plasma BKV. However, BKV was common in GPA/MPA patients after KTX, suggesting that replication may be related to differences in immunosuppression, alloimmune activation or differences in host defense mechanisms. © 2013 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Glomerular diseases (GD) are characterized by lesions of the glomerular basement, which may be or may not be accompanied by inflammation and cellular hyperplasia. They are mainly classified as primary or secondary to a systemic disease. They are also classified as proliferative or non-proliferative diseases depending on the cellular infiltrate. Minimal change disease, focal segmental glomerulosclerosis and thin membrane disease are non-proliferative, usually primary, glomerular diseases. Nephrotic syndrome is mainly the clinical syndrome that accompanies these GD. Proliferative GDs comprise IgA and IgM nephropathy, and crescentic GDs with or without immunodeposits. Secondary proliferative GDs include systemic lupus erythematosous GD, vasculitides, and post-infection GDs. Non proliferative secondary GDs encompass diabetic nephropathy, amyloidosis, HIV nephropathy. Recent data on many aspects of GDs, i.e. pathogenesis and pathophysiology, diagnosis, therapy and other are briefly discussed in the present review. [ABSTRACT FROM AUTHOR]

Kidney transplantation ( KTX) is the treatment of choice for patients with end-stage renal disease ( ESRD) due to ANCA-associated vasculitis ( AAV). Recurrent ANCA-associated glomerulonephritis ( GN) occurs after KTX and may adversely affect allograft survival. Cyclophosphamide ( CYC) combined with glucocorticoids has been the cornerstone of treatment for recurrent GN. Rituximab ( RTX), a B-cell-depleting monoclonal antibody, is approved for remission induction in AAV. We report the clinical presentation and outcomes of five KTX recipients treated with RTX for biopsy-confirmed recurrent GN. The median age at the time of KTX was 26 years (four Caucasian, three females). All patients were in remission with four being ANCA positive at time of KTX. Recurrent GN occurred at a median of 26 months post- KTX. All relapses were treated with RTX and glucocorticoids. Four patients achieved disease remission; the fifth patient was refractory to treatment with RTX and CYC. Follow-up biopsies ( n = 3) showed resolution of active GN in two patients and persistent active GN in one patient. RTX is an alternative to CYC for remission induction in recurrent AAV-associated GN in KTX patients. [ABSTRACT FROM AUTHOR]

Background: Renal biopsies provide important diagnostic and prognostic information in ANCA associated glomerulonephritis. A new classification for prognostication of pauci-immune glomerulonephritis (GN) based on four categories (Mixed, Crescentic, Sclerotic and Focal) was proposed by an international working group of renal pathologists (IWGRP). The goal of our study was to apply the proposed classification system to a United States cohort of vasculitis patients and determine the association of IWGRP class with estimated glomerular filtration rate (eGFR) at one year. Methods: Seventy-six cases of pauci-immune glomerulonephritis diagnosed from 1995 to 2011 from a single center were identified for this retrospective study. Clinical data were collected by abstraction from medical records. Histology was reviewed by a pathologist and classified according to the new classification. MDRD formula was used to calculate eGFR. We correlated IWGRP class to renal function at presentation and at one year. ×2, ANOVA, and linear regression analysis were performed as appropriate. Results: Renal biopsies were categorized as focal: n = 20, crescentic: n = 18, mixed: n = 27, sclerotic: n = 11. The baseline e-GFR was lowest in the crescentic class and highest in the focal class. In linear regression analysis investigating e-GFR at 1 year; age and baseline e-GFR were independent predictors of e-GFR at 1 year. Conclusions: The e-GFR at diagnosis and age were predictors of e-GFR at 1 year. Pathologic class at diagnosis may also be a helpful tool in risk stratification at diagnosis. [ABSTRACT FROM AUTHOR]

A subset of patients with crescentic glomerulonephritis (CGN) is characterized serologically by the presence of antineutrophil cytoplasmic antibody (ANCA) and anti-glomerular basement membrane antibody (anti-GBM) called 'double positive' disease. The clinical significance of the occurrence of both antibodies is not clear. This study aims to describe the clinical and histologic characteristics and outcomes of CGN in a US cohort of double positive (DP) patients and compare them to patients with anti-GBM disease only or ANCA only (ANCA-associated vasculitis (AAV)). Renal biopsies with a diagnosis of CGN with either pauci-immune or linear immunofluorescence were selected and classified as AAV, anti-GBM disease, or DP based on serologic testing at the time of biopsy. Data on demographics, clinical presentation, treatment, and outcome were obtained by chart review. Six patients with anti-GBM disease, 9 with DP disease, and 18 AAV patients matched for year of diagnosis with DP were identified. Extrarenal disease manifestations were more prominent in the DP patients. The DP patients had severe renal dysfunction at presentation with eight of nine patients requiring dialysis at presentation. Renal biopsy findings of DP patients were similar to anti-GBM disease with majority of glomeruli showing cellular crescents. Eighty-nine percent of patients were treated with immunosuppressive therapy and 78 % with plasmapheresis. At 1 year, all nine DP patients reached end-stage renal disease. We conclude that the DP patients share extrarenal manifestations similar to AAV patients while the renal manifestations resemble anti-GBM patients clinically and histologically. The renal prognosis of DP patients remains poor despite treatment. [ABSTRACT FROM AUTHOR]

Ameboma refers to the rare development of an inflammatory, ulcerated, exophytic mass in the gastrointestinal tract that can resemble carcinoma. Typically it presents as a right lower quadrant abdominal mass, Patients may also present with diarrhea or constipation and associated systemic symptoms, including weight loss and fever. In this article we present a young man with a background of ANCA associated vasculitis, who presented with fresh lower gastrointestinal bleeding during hospital admission for severe covid-19 pneumonia which turned out to be caecal aemboma. This case is highlighted for its rarity, the diagnostic challenge, and for the major role of colonoscopy as a diagnostic tool for this pathology., Competing Interests: None declared., (© 2022 The Authors.)

Objectives: T regulatory cells (Tregs) are a heterogeneous group of immunoregulatory cells that dampen self-harming immune responses and prevent the development of autoimmune diseases. In anti-neutrophil cytoplasmic autoantibody (ANCA) vasculitis, Tregs possess diminished suppressive capacity, which has been attributed to the expression of a FOXP3 splice-variant lacking exon 2 in T cells (FOXP3Δ2 CD4 + T cells). However, the suppressive capacity of Tregs varies between subsets. We evaluated the frequency of Treg subsets in ANCA vasculitis as a potential explanation for diminished suppressive capacity., Methods: We developed a custom mass cytometry panel and performed deep immune profiling of Tregs in healthy controls, patients with active disease and in remission. Using these data, we performed multidimensional reduction and discriminant analysis to identify associations between Treg subsets and disease activity., Results: Total Tregs were expanded in ANCA vasculitis, which was associated with remission and the administration of rituximab and/or prednisone. The frequency of FOXP3Δ2 CD4 + T cells did not distinguish disease activity and this population had high expression levels of CD127 and lacked both CD25 and Helios, suggesting that they are not conventional Tregs. The frequency of CXCR3 + , CD103 + and CCR7 + Tregs distinguished disease activity, and the combination of the frequency of these three Treg subsets segregated active patients from patients in remission and healthy controls. From these three subsets, the frequency of CXCR3 + Tregs distinguished patients with active disease with renal involvement., Conclusion: Treg heterogeneity can discriminate disease activity and should be explored as a biomarker of disease activity in ANCA vasculitis., Competing Interests: The authors declare no conflict of interest., (© 2022 The Authors. Clinical & Translational Immunology published by John Wiley & Sons Australia, Ltd, on behalf of Australian and New Zealand Society for Immunology, Inc.)

The advent of COVID-19, caused by the SARS-CoV-2 virus, has resulted in over 541 million cases with 6.32 million deaths worldwide as of June 2022. The devastating consequences of this global pandemic resulted in the expedited generation of mRNA-based vaccines such as the Pfizer-BioNTech and Moderna vaccines. Although the vaccines have been effective, with recent data indicating greater than 95% effectiveness, rare complications have been reported, including manifestations of autoimmune phenomena. Herein, we report a rare case of Granulomatosis with polyangiitis (GPA) in an active duty military male soon after receiving the first dose of the Pfizer-BioNTech COVID-19 vaccine., Competing Interests: The authors declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article., (© The Author(s), 2022.)

Cardiovascular disease is a complication of systemic inflammatory diseases including anti-neutrophil cytoplasm antibody-associated vasculitis (AAV). The mechanisms of cardiovascular morbidity in AAV are poorly understood, and risk-reduction strategies are lacking. Therefore, in a series of double-blind, randomized case-control forearm plethysmography and crossover systemic interventional studies, we examined arterial stiffness and endothelial function in patients with AAV in long-term disease remission and in matched healthy volunteers (32 each group). The primary outcome for the case-control study was the difference in endothelium-dependent vasodilation between health and AAV, and for the crossover study was the difference in pulse wave velocity (PWV) between treatment with placebo and selective endothelin-A receptor antagonism. Parallel in vitro studies of circulating monocytes and platelets explored mechanisms. Compared to healthy volunteers, patients with AAV had 30% reduced endothelium-dependent vasodilation and 50% reduced acute release of endothelial active tissue plasminogen activator (tPA), both significant in the case-control study. Patients with AAV had significantly increased arterial stiffness (PWV: 7.3 versus 6.4 m/s). Plasma endothelin-1 was two-fold higher in AAV and independently predicted PWV and tPA release. Compared to placebo, both selective endothelin-A and dual endothelin-A/B receptor blockade reduced PWV and increased tPA release in AAV in the crossover study. Mechanistically, patients with AAV had increased platelet activation, more platelet-monocyte aggregates, and altered monocyte endothelin receptor function, reflecting reduced endothelin-1 clearance. Patients with AAV in long-term remission have elevated cardiovascular risk and endothelin-1 contributes to this. Thus, our data support a role for endothelin-blockers to reduce cardiovascular risk by reducing arterial stiffness and increasing circulating tPA activity., (Copyright © 2022 International Society of Nephrology. Published by Elsevier Inc. All rights reserved.)

Antineutrophil cytoplasmic antibody (ANCA) associated vasculitis comprises a rare entity of disorders that affects primarily small and medium-sized blood vessels. Since first documented in 1897, we have come a long way trying to understand the pathogenesis and finding an optimal treatment regimen. The pathogenesis of ANCA vasculitis is not well understood and despite many advances in treatment, the morbidity and mortality remains high. Over the last decade, there have been many advancements toward elucidating the pathogenesis, optimizing current therapies, and discovering new medicines. Presently, one trend is aimed at minimizing the adverse effects of glucocorticoids by reducing their use without sacrificing efficacy and safety. A new medicine targeting the alternative complement system has emerged and intends to replace glucocorticoids. Here, we review three articles that describe these new trends in the management of ANCA vasculitis., (Copyright © 2022 Elsevier Inc. All rights reserved.)

Coronavirus disease 2019 (COVID-19) pandemic is responsible for widespread morbidity and mortality. The vaccination against the severe acute respiratory syndrome coronavirus 2 (SARS-COV-2) infection, the cause of the COVID-19 pandemic, is currently ongoing across the globe. Rapid vaccination is of paramount importance to mitigate this pandemic. Although considered safe in general, these vaccines have their share of rare adverse events. We report a case of antineutrophil cytoplasmic antibody (ANCA)-associated pauci-immune crescentic glomerulonephritis 15 days post 2 nd dose of a killed COVID-19 (COVAXIN™ -BB152 V) vaccine. We hypothesize that vaccination triggered a systemic immune response in a susceptible patient to develop ANCA-associated vasculitis (AAV), leading to rapidly progressive glomerulonephritis (RPGN)., Competing Interests: There are no conflicts of interest., (Copyright: © 2022 Indian Journal of Nephrology.)

Antibodies to myeloperoxidase (MPO) and proteinase 3 (PR3) have been demonstrated to mediate anti-neutrophil cytoplasmic antibody (ANCA)-associated disease. For membranous nephropathy, antibodies to the podocyte-expressed phospholipase A2 receptor (anti-PLA2R) are highly associated with disease activity and have been reported in at least 70% of patients with idiopathic membranous nephropathy (IMN). We present a case of a 56-year-old male with a 1 year history of hypertension, leg edema, and proteinuria, who presented with advanced renal failure and was found to have both ANCA-associated glomerulonephritis (GN) and IMN on kidney biopsy. Consistent with the idea that this is due to the chance occurrence of two independent diseases, we found both anti-MPO and anti-PLA2R antibodies in the patient's sera. Treatment with methylprednisolone, plasmapheresis, and cyclophosphamide resulted in improvement in kidney function and proteinuria, together with the simultaneous decrease in both autoantibodies. This is the first demonstration of two pathogenic antibodies giving rise to ANCA-associated GN and IMN in the same patient. It confirms the importance of classifying disease based upon the underlying mechanism, in addition to renal histopathology, to both optimize therapy and predict prognosis. [ABSTRACT FROM PUBLISHER]

Introduction. Churg–Strauss syndrome (CSS) is a small vessel systemic vasculitis associated with asthma and eosinophilia that causes glomerulonephritis (GN) in ∼25% of patients. Rituximab (RTX) is a chimeric anti-CD20 monoclonal antibody that depletes B cells and is effective in numerous autoimmune diseases including antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis. We aim to evaluate the safety and efficacy of RTX in inducing remission of renal disease activity in patients with CSS.Methods. We conducted a single-center, open-label pilot study using RTX (375 mg/m2/week × 4) for induction of remission in CSS patients with renal involvement [defined as having >25% dysmorphic red cells, red blood cell casts or pauci-immune GN on biopsy]. Written informed consent was obtained from all individuals. Patients were eligible if they were untreated, had failed glucocorticoid therapy or had failed glucocorticoid dose reductions because of disease relapses. The primary outcome was remission of renal disease activity defined as stability or improvement of creatinine clearance, absence of active urinary sediment and reduction of the glucocorticoid dose to <50% of the average dose received over 3 months before enrollment or <10 mg/day (whichever is smaller) at 6 months. Patients were followed up for 1 year.Results. Only three patients (two females; ages 54, 55 and 65) were enrolled. All patients had positive myeloperoxidase-ANCA and renal involvement. Two patients had biopsy-proven pauci-immune crescentic GN. All achieved the primary end point of renal remission within the first 3 months and remained in renal remission during the year following RTX treatment. One patient experienced a nonrenal relapse (eye and joint involvement) at 6 months coinciding with the reconstitution of CD19+ cells and eosinophilia. He was retreated with RTX and achieved remission within 6 weeks. No major adverse effects were recorded.Conclusions. In this pilot study, RTX was safe and successful in controlling renal disease activity in three patients with CSS. This agent deserves further study in CSS. [ABSTRACT FROM PUBLISHER]

No abstract available Copyright © 2010 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Antibodies recognizing the complement of the middle of PR3 (cPR3m) occur in ∼∼30% of PR3-anti-neutrophil cytoplasmic autoantibodies (ANCA)-vasculitis patients and immunization of animals with a peptide complementary to the middle of PR3 (cPR3m) induces not only anti-complementary PR3 antibodies, but also anti-PR3 antibodies derived through an anti-idiotypic response. PR3 epitopes recognized by patient ANCA, however, are not restricted to the middle of PR3. This prompted us to test for antibodies that react with proteins complementary to the terminal regions of PR3 (cPR3C and cPR3N) in PR3-ANCA patients. Anti-cPR3C reactivity was detected in 28% of patients but anti-cPR3N reactivity in only 15%. Ranked anti-cPR3C and anti-cPR3m reactivity correlated in the cohort, whereas there was no significant relationship between cPR3C and cPR3N reactivity. Serial samples from 3 patients' revealed that anti-cPR3C and anti-cPR3m reactivity followed a similar pattern over time. Serial samples from a fourth patient demonstrated an anti-cPR3N response without concurrent cPR3m or cPR3C reactivity. Epitope determination by mass spectrometry identified a 13-amino acid sequence on cPR3C that contained a common binding site recognized by antibodies from three patients. This peptide sequence contains a ''PHQ'' motif which was reported to be the basis for cross-reactivity of anti-cPR3m antibodies with plasminogen. Why these antibodies are detected in only ∼∼30% of the patients remains unclear. The data reveal that it is not due to lack of inclusion of flanking regions of complementary PR3 during screening. Instead, quite unexpectedly, the data demonstrate that patients' antibodies react with a restricted epitope that exists in both cPR3m and cPR3C. [ABSTRACT FROM AUTHOR]

We report a rare case of Hydralazine-induced ANCA associated glomerulonephritis with alveolar hemorrhage in the setting of acute Clostridium Difficile Infection. A 71-year-old Caucasian woman with hypertension, who was being treated with hydralazine 25 mg twice a day for six years, presented to the hospital with diarrhea, nausea, vomiting and anemia. She had acute kidney injury and urinalysis showed proteinuria, dysmorphic RBCs, and rare RBC cast. She was found to have Clostridium difficile colitis which was successfully treated. She became hypoxemic; CT scan findings showed bilateral pulmonary infiltrates. Broncho-alveolar lavage was consistent with pulmonary hemorrhage. Kidney biopsy revealed focal segmental necrotizing and diffuse crescentic glomerulonephritis, pauci-immune type (ANCA-associated). Hydralazine was discontinued and the patient was treated with corticosteroids, intravenous cyclophosphamide and plasmapheresis. To our knowledge, hydralazine-associated low complement in the setting of C-diff infection has not been previously reported. This is considered a potentially life-threatening condition requiring immediate discontinuation of the offending medication and expedited lifesaving measures. [ABSTRACT FROM AUTHOR]

One of the rare causes of secondary vasculitides is malignancy. Hematological malignancies produce secondary vasculitis more frequently than solid malignancies. Here in we report a case of acute myeloid leukemia presenting with anti-neutrophil cytoplasmic antibody-positive vasculitis. This case highlights the importance of looking for underlying malignancies, especially leukemias in patients presenting with features of systemic vasculitides. [ABSTRACT FROM AUTHOR]

The neutrophil serine protease proteinase 3 (PR3) is a main autoantigen in anti-neutrophil cytoplasmic antibody-associated vasculitis. PR3 surface presentation on neutrophilic granulocytes, the main effector cells, is pathogenically important. PR3 is presented by the NB1 (CD177) glycoprotein, but how the presentation develops during neutrophil differentiation is not known. An N-terminally unprocessed PR3 (proPR3) is produced early during neutrophil development and promotes myeloid cell differentiation. We therefore investigated if PR3 presentation depended on NB1 during neutrophil differentiation and if PR3 and proPR3 could both be presented by NB1. In contrast to mature neutrophils, differentiating neutrophils showed an early NB1-independent PR3 surface display that was recognized by only two of four monoclonal anti-PR3 antibodies and occurred in parallel with proPR3, but not PR3 secretion, suggesting that the NB1-independent surface PR3 was proPR3. PR3 gene expression preceeded NB1. When the NB1 receptor was detected on the surface, a mode of PR3 surface display similar to mature neutrophils developed together with the degranulation system. Ectopic expression studies showed that NB1 was a sufficient receptor for PR3 but not proPR3. ProPR3 display on the plasma membrane may influence the bone marrow microenvironment. NB1-mediated PR3 presentation depended on PR3 N-terminal processing implicating the PR3–N-terminus as NB1-binding site. [ABSTRACT FROM AUTHOR]

Anti-neutrophil cytoplasm antibody (ANCA)-associated vasculitides are rare autoimmune diseases that can often be life threatening. They particularly affect the kidneys and lungs but can also affect many other organs. Various hypotheses have been proposed to explain the loss of tolerance against ANCA antigens (present in granules of neutrophils and monocytes); however, clear mechanisms remain elusive. Clinical observation, in vitro studies and newly developed animal models implicate ANCAs in disease pathogenesis and relevant mechanisms are now being characterized. Abnormalities in patient's T-cell populations exist and the increasingly recognized role of B cells in ANCA-associated vasculitis is also discussed. [ABSTRACT FROM AUTHOR]

Immunosuppressive treatment is a critical procedure in dialysis patients, in whom an increased risk of infection is already present. Haemodialytic treatment increases the patient's susceptibility to bacterial infection, mainly by impairing polymorphonuclear leukocyte phagocytosis, but it can also restore the patient's immunological defences by improving the T‐cell function, which is reduced by pre‐dialysis uraemia. Patients on dialysis usually continue the immunosuppressive treatment that had been established for the illness that caused their renal failure [e.g. systemic lupus erythematosus (SLE) or renal vasculitis]. Less frequently, patients on dialysis need immunosuppression for immunological or inflammatory diseases that appear ‘de novo’ after initiation of dialysis. SLE and antineutrophil cytoplasmic antibody (ANCA)‐related vasculitides are immunological illnesses that frequently cause end‐stage renal failure (ESRF). A reduction in serological and/or clinical activity is usually observed in SLE patients after they reach ESRF, but a similar or increased frequency of extrarenal relapse episodes in lupus patients after the beginning of the dialysis, compared with the pre‐dialysis period, has also been described. Frequency of relapse episodes in patients on dialysis treatment for ANCA‐related vasculitides varies from 10 to 30% per patient/year in different reports, and it is higher than the frequency of relapses after renal transplantation; anti‐rejection therapy seems to be the most likely protective factor in these conditions. The treatment of relapse episodes in SLE or ANCA vasculitis in dialysis‐dependent patients is usually not different from treatment of relapses in patients with dialysis‐independent renal function. However, the risk of severe infection caused by immunosuppressive treatment is relevantly higher in dialysis patients. Furthermore, there is a lack of prospective controlled studies indicating the optimal management of immunosuppressive protocols in dialysis patients. A particularly careful assessment of the patient's risks and benefits is necessary in deciding how long immunosuppressive treatment should last after acute or rapidly progressive renal damage, that should require dialysis treatment, in patients with SLE or ANCA vasculitis. In the above conditions, the risks of prolonging immunosuppressive treatment must be balanced against the relatively good prognosis offered to these patients by dialysis and renal transplantation. In a retrospective review of 24 patients receiving long‐term steroid therapy (>3 months) in our dialysis unit in the past 5 years, we found relevant clinical differences in the patients receiving steroid treatment compared with 24 controls. Steroid‐treated patients showed less favourable nutritional conditions, with lower serum albumin and body mass index vs non‐steroid‐treated patients; moreover, C‐reactive protein values were persistently higher in the steroid‐treated group. Steroid treatment in these patients was usually performed at the beginning of regular dialysis, as a continuation of the treatment that started before the initiation of dialysis. Only two patients, who needed a prolonged low‐dose steroidal treatment to control a malnutrition–inflammation–atherosclerosis (MIA) syndrome, started steroids many years after beginning dialysis. Steroid treatment was effective in improving the nutritional condition and inflammatory symptoms in these two patients after all conventional measures had failed. [ABSTRACT FROM PUBLISHER]