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Lupus nephritis: current update
Ramesh Saxena, Tina Mahajan, Chandra Mohan
Arthritis Research & Therapy , 2011, DOI: 10.1186/ar3378
Abstract: Lupus nephritis (LN) is a major cause of morbidity and mortality in patients with systemic lupus erythematosus (SLE). The general consensus is that 60% of lupus patients will develop clinically relevant nephritis at some time in the course of their illness [1]. Prompt recognition and treatment of renal disease is important, as early response to therapy is correlated with better outcome [2]. The present review summarizes our current understanding of SLE pathogenesis, summarizes how the disease is diagnosed and treated, and expands on new emerging therapies.Most SLE patients develop nephritis early in the course of their disease. The vast majority of patients who develop nephritis are younger than 55 years, and children are more likely to develop severe nephritis than are elderly patients [3]. In a recent retrospective study, male sex, young age (<33 years), and non-European ancestry were found to be determinants of earlier renal disease in patients with SLE. Asian, African Caribbean, and African American ethnicities may present with more severe nephritis than other ethnic groups [4].Proteinuria is the characteristic feature of renal disease in lupus. In a comprehensive review of LN, proteinuria was reported in 100% of patients, with nephrotic syndrome being reported in 45 to 65% [5]. Microscopic hematuria was found to occur in about 80% of patients during the disease course, invariably associated with proteinuria. Macroscopic hematuria is rare in LN. Hypertension is not common but is present more frequently in patients with severe nephritis. About one-half of all patients with LN will have a reduced glomerular filtration rate, and occasionally patients present with acute kidney injury. Renal tubular function is often disturbed, resulting in urinary excretion of Tamm-Horsefall proteins, light chains and β2-microglobulin [5].Ideally, urinary protein excretion is gauged using a 24-hour urine collection. Although universally practiced, variable results may occur over a s
Systematic review and meta-analysis of randomised trials and cohort studies of mycophenolate mofetil in lupus nephritis
R Andrew Moore, Sheena Derry
Arthritis Research & Therapy , 2006, DOI: 10.1186/ar2093
Abstract: The prevalence of systemic lupus erythematosus (SLE) varies with age, gender, and ethnicity, and the highest rates occur in young adult women, particularly of Afro-Caribbean origin, who are in peak childbearing years [1-4]. Nephritis complicates SLE in a significant minority of patients and is associated with renal failure and increased mortality. The tendency for people of Afro-Caribbean origin to have a worse prognosis may be due, at least in part, to poor socio-economic status [5]. In the 1950s, patients with class IV nephritis rarely lived longer than 5 years, whereas now more than 80% survive with good renal function for more than 10 years [6].The World Health Organization (WHO) classification for lupus nephritis is based on the histological appearance, with progressive changes to the glomerulus and tubulo-interstitium with increasing severity (Additional file 1). Milder disease (WHO classes II and IIIa) affects approximately 35% to 50%, whereas more serious classes IIIb, IV, and V affect 45% to 60% [7]. A significant minority of patients with class III disease (focal segmental proliferative glomerulonephritis) show worsening renal function and may progress to class IV lupus nephritis. Class IV (diffuse proliferative glomerulonephritis) usually presents with clinical evidence of renal disease, including oedema, hypertension, sediment, and worsening renal function with proteinuria. Class V (diffuse membranous glomerulonephritis) involves patients with laboratory and clinical features of nephrotic syndrome.The aim of treatment is first to stop disease progression (induction phase) and then prevent recurrence (maintenance) while minimising the adverse effects. More specifically with lupus nephritis, the aims of treatment are to reduce the risk of end-stage renal disease, reduce renal and extra-renal lupus activity or symptoms, and reduce the mortality risk.Treatment with immunosuppressive therapy is better than prednisolone monotherapy at preserving renal function
Mycophenolate mofetil in the treatment of lupus nephritis  [cached]
Patrick FK Yong,David P D’Cruz
Biologics: Targets and Therapy , 2008,
Abstract: Patrick FK Yong1,2, David P D’Cruz21Department of Clinical Immunology, Kings College Hospital; 2The Lupus Research Unit, St Thomas’ Hospital, London, UKAbstract: Lupus nephritis is a complication of systemic lupus erythematosus, which has significant morbidity and mortality. The accepted standard of treatment for severe lupus nephritis is cyclophosphamide for induction of remission. This has significant adverse effects including severe infection and amenorrhea. In addition, although cyclophosphamide induces remission, long-term mortality does not seem to be altered. Mycophenolate mofetil (MMF) is an immunosuppressive agent originally used in solid organ transplantation, which has been compared with cyclophosphamide in trials for lupus nephritis. Randomized trials with MMF have been relatively small, although pooled data seem to suggest that it is at least as effective as cyclophosphamide in inducing remission. In addition, MMF has also been associated with a reduced risk of infection and amenorrhea, although this finding is not universal. MMF appears to be associated with more diarrhea compared with cyclophosphamide. MMF is likely to be a useful treatment for lupus nephritis, although available trial data are limited due to the small size of previous studies. A large trial (the Aspreva Lupus Management Study) is currently underway to attempt to establish the place of MMF in treatment of lupus nephritis.Keywords: mycophenolate mofetil, lupus nephritis, systemic lupus erythematosus
Actualidad en el tratamiento de la nefritis lúpica proliferativa Update on the treatment of proliferative lupus nephritis
González Luis Alonso,José Fernando Molina,Gloria María Vásquez
Revista Colombiana de Reumatología , 2009,
Abstract: La nefropatía lúpica (NL) es una causa importante de morbilidad y mortalidad en pacientes con lupus eritematoso sistémico (LES) la cual tiene un impacto directo en la supervivencia de estos pacientes. El uso de un tratamiento inmunosupresor agresivo ha mejorado la supervivencia renal y de los pacientes. Los objetivos de esta terapia inmunosupresora son la obtención de una remisión temprana, evitar la aparición de exacerbaciones y la progresión a insuficiencia renal crónica con la mínima toxicidad posible. El tratamiento con pulsos intravenosos mensuales de ciclofosfamida y de glucocorticoides (el régimen del Instituto Nacional de Salud) como tratamiento de inducción y la administración a largo plazo de pulsos venosos de ciclofosfamida o con azatioprina ha llegado a ser el tratamiento estándar de la NL proliferativa severa. El micofenolato mofetil es una alternativa a la ciclofosfamida en el tratamiento de inducción y de mantenimiento de la NL proliferativa. Existen otras opciones terapéuticas para la NL resistente como regímenes más agresivos de ciclofosfamida (a expensas de una mayor toxicidad), inhibidores de la calcineurina, gamaglobulina hiperinmune intravenosa, inmunoadsorción y terapias dirigidas contra la célula B. Lupus nephritis (LN) is an important cause of morbidity and mortality in patients with systemic lupus erythematosus (SLE). The use of aggressive immunosuppressive treatment has improved both patient and renal survival. The objectives of this therapy should be to achieve a prompt renal remission, to avoid renal flares and progression to chronic renal failure with minimal toxicity. Treatment with monthly intravenous cyclophosphamide and glucocorticoids (National Institute of Health regimen) as induction treatment and long-term administration of venous pulses of cyclophosphamide or azathioprine has become standard treatment for severe proliferative LN. Mycophenolate mofetil is an alternative to cyclophosphamide for induction and maintenance therapy of proliferative LN. There are other therapeutic options for resistant LN as more aggressive ciclophosphamide regimens, but at the expense of more toxicity, calcineurin inhibitors, intravenous immunoglobulin, immunoadsorption and therapies that selectively target B cells.
Understanding lupus nephritis: diagnosis, management, and treatment options  [cached]
Mok CC
International Journal of Women's Health , 2012,
Abstract: Chi Chiu MokDepartment of Medicine, Tuen Mun Hospital and Center for Assessment and Treatment of Rheumatic Diseases, Pok Oi Hospital, Hong Kong, ChinaAbstract: Systemic lupus erythematosus (SLE) predominantly affects women in their reproductive years. Renal disease (glomerulonephritis) is one of the most frequent and serious manifestations of SLE. Of the various histological types of lupus glomerulonephritis, diffuse proliferative nephritis carries the worst prognosis. Combined with high-dose prednisone, mycophenolate mofetil (MMF) has emerged as a first-line immunosuppressive treatment, although data regarding the efficacy of MMF on the long-term preservation of renal function are forthcoming. Cyclophosphamide is reserved for more severe forms of lupus nephritis, such as crescentic glomerulonephritis with rapidly deteriorating renal function, patients with significant renal function impairment at presentation, and refractory renal disease. Evidence for the calcineurin inhibitors in the treatment of lupus nephritis is weaker, and it concerns patients who are intolerant or recalcitrant to other agents. While further controlled trials are mandatory, B cell modulation therapies, such as rituximab, belimumab and epratuzumab are confined to refractory disease. Non-immunosuppressive measures, such as angiotensin-converting enzyme inhibitors, vigorous blood pressure control, prevention and treatment of hyperlipidemia and osteoporosis, are equally important.Keywords: lupus, nephritis, nephropathy, glomerulonephritis, treatment, therapy, women
Intravenous Immunoglobulin in the Management of Lupus Nephritis  [PDF]
Scott E. Wenderfer,Trisha Thacker
Autoimmune Diseases , 2012, DOI: 10.1155/2012/589359
Abstract: The occurrence of nephritis in patients with systemic lupus erythematosus is associated with increased morbidity and mortality. The pathogenesis of lupus nephritis is complex, involving innate and adaptive cellular and humoral immune responses. Autoantibodies in particular have been shown to be critical in the initiation and progression of renal injury, via interactions with both Fc-receptors and complement. One approach in the management of patients with lupus nephritis has been the use of intravenous immunoglobulin. This therapy has shown benefit in the setting of many forms of autoantibody-mediated injury; however, the mechanisms of efficacy are not fully understood. In this paper, the data supporting the use of immunoglobulin therapy in lupus nephritis will be evaluated. In addition, the potential mechanisms of action will be discussed with respect to the known involvement of complement and Fc-receptors in the kidney parenchyma. Results are provocative and warrant additional clinical trials. 1. Introduction Intravenous immunoglobulin (IVIg) is a biological agent composed of polyclonal antibodies, derived from the plasma of a large pool of healthy donors [1–5]. It has been primarily used to treat hypogammaglobulinemia but has also shown promise in treating autoimmune diseases, inflammatory diseases, and cancer. It is FDA approved for the treatment of idiopathic thrombocytopenic purpura (ITP) and Kawasaki’s vasculitis. Several anecdotal reports and a few studies have shown promising results on the effectiveness of IVIg in the treatment of systemic lupus erythematosus (SLE). Its use has been widespread; however, its efficacy has not been clearly established. The precise mechanisms by which IVIg functions as an anti-inflammatory agent remains debatable (Table 1) [1, 6–8]. The presence of Ig in the preparations with specificity for variable regions of pathogenic autoantibodies (anti-idiotype responses) can allow for direct binding and neutralization of pathogenic effector functions. The effector functions of autoantibodies are mediated by receptors for constant regions of IgG (FcR) or receptors for complement components that bind to antigen antibody immune complexes. Complement receptors and FcR are expressed on lymphocytes, granulocytes, monocytes, and some parenchymal cells and can induce tissue injury once bound to immune complexes containing pathogenic antibodies. Monomeric IgG in IVIg preparations has been shown to antagonize pathologic immune complexes binding to activating FcR [9]. Alternatively, nonspecific polyclonal Ig can form immune complexes
Clinical profile of patients with lupus nephritis  [cached]
T.L. Skare,A.C. Sch?nrock
Reumatismo , 2011, DOI: 10.4081/reumatismo.2009.316
Abstract: To the Editor Lupus nephritis is the strongest predictor of systemic lupus erythematosus (SLE) patient’s morbidity and mortality with a prevalence varying from 31 to 65% according to the studied population (1). As the onset of lupus nephritis is usually silent, knowing possible association with others symptoms is useful in order to keep of better vigilance on patients with higher possibility to develop it. Pistiner et al described that lupus patients with nephritis also have an increased frequency of other severe lupus manifestations (2). According to Huong et al, in a study of 180 patients with lupus renal involvement, patients with nephritis suffered more commonly from malar rash, psychosis, myocarditis, pericarditis, lymphadenopathy and hypertension...
Understanding lupus nephritis: diagnosis, management, and treatment options
Mok CC
International Journal of Women's Health , 2012, DOI: http://dx.doi.org/10.2147/IJWH.S28034
Abstract: derstanding lupus nephritis: diagnosis, management, and treatment options Review (3674) Total Article Views Authors: Mok CC Published Date May 2012 Volume 2012:4 Pages 213 - 222 DOI: http://dx.doi.org/10.2147/IJWH.S28034 Received: 10 March 2012 Accepted: 28 March 2012 Published: 22 May 2012 Chi Chiu Mok Department of Medicine, Tuen Mun Hospital and Center for Assessment and Treatment of Rheumatic Diseases, Pok Oi Hospital, Hong Kong, China Abstract: Systemic lupus erythematosus (SLE) predominantly affects women in their reproductive years. Renal disease (glomerulonephritis) is one of the most frequent and serious manifestations of SLE. Of the various histological types of lupus glomerulonephritis, diffuse proliferative nephritis carries the worst prognosis. Combined with high-dose prednisone, mycophenolate mofetil (MMF) has emerged as a first-line immunosuppressive treatment, although data regarding the efficacy of MMF on the long-term preservation of renal function are forthcoming. Cyclophosphamide is reserved for more severe forms of lupus nephritis, such as crescentic glomerulonephritis with rapidly deteriorating renal function, patients with significant renal function impairment at presentation, and refractory renal disease. Evidence for the calcineurin inhibitors in the treatment of lupus nephritis is weaker, and it concerns patients who are intolerant or recalcitrant to other agents. While further controlled trials are mandatory, B cell modulation therapies, such as rituximab, belimumab and epratuzumab are confined to refractory disease. Non-immunosuppressive measures, such as angiotensin-converting enzyme inhibitors, vigorous blood pressure control, prevention and treatment of hyperlipidemia and osteoporosis, are equally important.
Management of Lupus Nephritis  [cached]
Merkel F,Gross O,Weber M
Saudi Journal of Kidney Diseases and Transplantation , 2000,
Abstract: Summary : Renal disease is common in systemic lupus erythematosus (SLE) and significantly influences patient prognosis. Immunosuppressive therapy has markedly improved outcome, however, it increases the risk of infection and cancer induction. Although several therapeutic regimens have proved to be effective in controlling lupus nephritis (LN), optimal therapy is still a matter of discussion. The following review summarizes our current knowledge in treating LN and discusses new aspects in pathogenesis. Hopefully, continuing progress in uncovering details about the pathogenesis of SLE might lead to more disease-specific approaches to treat the underlying immunological disorder.
Mechanisms of tissue injury in lupus nephritis
Tamara K Nowling, Gary S Gilkeson
Arthritis Research & Therapy , 2011, DOI: 10.1186/ar3528
Abstract: Nephritis is a major cause of morbidity and mortality in patients with lupus. Nephritis occurs in approximately 50% of lupus patients, but rates vary significantly between genders (men more than women) and ethnicities (more common in people of color). Men and minorities with lupus nephritis are also more likely to progress to end-stage renal disease than women or people of European ancestry. The multiple factors underlying these demographic differences are unclear at this time [1].The International Society of Nephrology revised the World Health Organization classification of lupus nephritis recently, although maintaining six classes [2]. The pathologic classes vary from mild mesangial involvement (Class I) to diffuse proliferative disease (Class IV) to membranous disease (Class V) to end-stage fibrosis (Class VI). Although most attention in lupus nephritis is focused on glomerular disease, there is also significant tubular disease that impacts prognosis and renal function [3]. For the purposes of the present review, we will primarily focus on the proliferative forms of lupus nephritis (focal proliferative, Class III disease; and diffuse proliferative, Class IV disease), highlighting several contributors to tissue injury.Much of what is known about pathogenic factors in tissue damage in lupus nephritis was derived from studies of murine models of lupus, with confirmation as possible in humans. These studies utilize multigenic models of lupus (that is, MRL/lpr, NZB/NZW, and NZM congenic strains) as well as single gene mutants (that is, DNAse 1, Nrf2, or Fcγ receptor (FCγR) knockouts) [4,5]. These models share common features of human disease such as anti-double-stranded DNA (anti-dsDNA) antibodies and proliferative nephritis, but differ in their renal cytokine/chemokine profile, cellular infiltration and acuity/chronicity of disease [5]. Thus, as in human disease, there is heterogeneity of pathogenic mechanisms in murine lupus nephritis.The presence of autoantibodies
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