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Arthritis Care Res (Hoboken). Jun;71(6) doi: /acr Epub Apr A Novel System to Categorize the Symptoms of Systemic. Biomark Med. Aug;11(8) doi: /bmm Epub Aug 3. Novel biomarkers for systemic lupus erythematosus. Zeng J(1), Wu. Nefrol., ahead of print Epub Nov 14, Involvement of the kidneys by lupus nephritis (LN) is one of the most severe clinical manifestations Development of a novel renal activity index of lupus nephritis in children and young adults.

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Construction of a frailty index as a novel health measure in systemic lupus erythematosus. J Rheumatol. [Epub ahead of print]. VIEW MORE. 16 February. Epub /12/ eng. 2. Lahita RG. The role of sex hormones in systemic lupus erythematosus. M. The multi-faceted influences of estrogen on lymphocytes: toward novel immuno-interventions strategies for autoimmunity management. There are many new therapeutic directions for the disease systemic lupus erythematosus (SLE). Despite this Rheumatology (Oxford) [ePub ahead of print ].

Altered gene expression usually accompanies these functional alterations [ 6 ]. Expression signatures in SLE have been addressed primarily in the peripheral blood compartment, where pioneering work by the Pascual group first described the interferon signature [ 7 ] [ 8 ]. These genes are inducible by the cytokine in vitro and have since been subdivided as being targets of type I or II interferon [ 9 ]. Many of these are simultaneously induced in subsets of cells including T and B cells [ 10 ] and monocytes [ 11 ] providing evidence for shared signaling abnormalities in peripheral blood mononuclear cells.

Alterations in expression reveal patient subtypes marked by induction of genes involved in protein folding on the endoplasmic reticulum, high levels of ribosomal protein genes, or the previously identified interferon signature alone. Substantial differences in T cell expression in men and women were also found.

Highlighted genes could represent biomarkers informative for disease management and may also direct investigation into other T-cell driven autoimmune conditions. This methodology is amenable to study of any disease with great variability of symptom presentation if highly relevant tissue can be obtained for transcriptome sequencing.

Blood was similarly obtained from 4 similarly aged healthy female controls.

Written informed consent was obtained from all participating subjects and all clinical investigation was conducted according to the principles expressed in the Declaration of Helsinki. Heatmaps were generated using median-normalized expression data with Gene-e and NMF clustering was performed on the Genepattern server, both provided by the Broad Institute. Online supplemental files contain methods with specific program commands and R scripts which were implemented in R studio S1 Text.

As controls we prepared specimens from 4 healthy women aged 25 to None of the patients were receiving therapy with biological agents Table 1.

To evaluate the cell-type purity of the samples we checked non-T cell marker expression. Of the epitopes used to collect T cells by rosette negative selection, only one had expression above background. Most analysis was carried out on the top quartile of expression in the genome genes which included high and medium classes. Loss of immune tolerance is the initial trigger for SLE.

The glomerulus is the most severely affected structure in the nephrons of individuals with LN. Additionally, clinical findings do not predict the clinical development or the prognosis of patients with the disease. Therefore, kidney biopsy becomes an essential measure at assessing tissue involvement, categorizing LN, and choosing the course of therapy. A possibly ideal additional criterion is renal biopsy showing immune-complex-mediated nephritis with complement deposition associated with varying degrees of cell injury.

Patients with SLE may present with numerous renal disorders not linked to LN, such as thrombotic microangiopathy, amyloidosis, immune-complex-mediated tubulointerstitial nephritis, ascending tubulointerstitial infection, opportunistic renal infection, and drug-induced nephrotoxicity.

Other immunological criteria include: Complement system protein levels decrease in response to the activation of the classical complement pathway by IC deposited locally. Serum creatinine is not particularly relevant in the diagnosis or assessment of LN. Hematuria, red blood cell casts, and leukocyturia are generally suggestive of active glomerulonephritis in infection-free individuals.

Proteinuria is one of the diagnostic criteria for LN, although its absence does not rule out active LN. Kidney histopathology is a valuable input in guiding treatment.

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In some cases, particularly for pediatric patients with active renal injury, serial renal biopsies may be clinically relevant. LN is characterized by the following features: Adapted from Jennette et al. Treatment with immunosuppressants is generally recommended to manage extrarenal manifestations. Proliferative LN classes III and IV is caused by the deposition of IC in the subendothelial space of the glomerular capillaries, either alone or in combination with the deposition of IC in the mesangial region.

Proliferative LN presents lesions that characterize activity and chronicity.

Although other injuries may occur with LN, they are not used for classification purposes. Nevertheless, they may affect the choice of treatment. Tubulointerstitial injury: These injuries may help identify patients responsive to therapies targeting B cells, such as treatment with rituximab.

Novel biomarkers for systemic lupus erythematosus.

Vascular injuries are common and may affect patient prognosis. Five types of vascular injuries are often observed: Other possible events include endothelial edema, transmural vasculitis with fibrinoid necrosis, mesangiolysis or fibrin thrombi and, enlargement of the lamina rara interna of the glomerular basement membrane seen with the aid of electron microscopy.

Podocyte injuries are common and stem from the loss of expression of the proteins present in the slit diaphragm nephrin and podocin and the disorganization of the podocyte cytoskeleton, culminating with the flattening, effacement, and microvillus transformation of the foot processes.

Podocyte injuries may be used to identify patients potentially responsive to calcineurin inhibitors. Crescentic injuries arise from immune deposits or direct attack by inflammatory cells. LN class V originates from the subepithelial IC deposition of either immune complexes transiting through the glomerular basement membrane or immune complexes formed locally to deal with podocyte antigens. LN class VI results from the progression of lupus nephritis.

A Novel System to Categorize the Symptoms of Systemic Lupus Erythematosus.

The therapeutic regimens tested for adults with SLE, although broadly recommended for juvenile SLE, may not be enough to manage the disease in pediatric patients. However, recent guidelines for the treatment of LN in children and adolescents are broadly based on consensus documents developed for the adult population.

Single Hub and Access point for paediatric Rheumatology in Europe. Renal biopsy is required in the development of LN therapy. However, extremely ill individuals cannot always undergo renal biopsies. The first stage includes induction therapy , with the purpose of attaining remission from the acute manifestations of LN. Gonadal toxicity by oral CP therapy is greater in sexually mature males and lesser in prepubertal children.

There are two regimens for intravenous CP: Regardless of the choice of CP or MMF, the induction scheme must be administered jointly with corticosteroids.


The most commonly used corticosteroid protocols are: The ideal length of maintenance therapy is unknown.

Consensus documents have indicated a minimum duration of three years. Immunosuppression therapy with CP or MMF has been advocated, particularly for patients with nephrotic-range proteinuria. Therapy failure occurs mostly due to poor compliance to treatment.

Novel paradigms in systemic lupus erythematosus.

Therapy changes may be introduced if the patient fails to respond after three months of treatment and poor compliance has been ruled out. Although SLE is a rare disease in pediatric populations, its consequences may be severe and even fatal. Although the etiopathogenesis of LN in children and adults is similar, the disease is more severe in pediatric populations.

Studies on LN affecting children and adolescents are required to detect new prognostic markers and define specific therapeutic schemes for individuals in this age range. Systemic lupus erythematosus in children and adolescents.

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Curr Rheumatol Rep ; A Brazilian Multicenter Study. Arthritis Care Res Hoboken ; Taxonomy for systemic lupus erythematosus with onset before adulthood. Why are women predisposed to autoimmune rheumatic diseases? Arthritis Res Ther ; Lupus nephropathy in childhood: J Pediatr Rio J ; Childhood onset systemic lupus erythematosus: Int J Rheumatic Dis ; Update on Lupus Nephritis.

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Mortality in systemic lupus erythematosus. Arthritis Rheum ; American College of Rheumatology guidelines for screening, treatment, and management of lupus nephritis. Kidney disease in lupus is not always 'lupus nephritis'. Lupus nephritis biomarkers. Clin Immunol ; All things complement. Diagnostic value of serum anti-C1q antibodies in patients with lupus nephritis:Pediatr Res ; Epub Jun 6.

A review. Wallace, in Rheumatology Sixth Edition , The etiologic origins of sporadic SLE are unknown, but altered regulation of T cells is well documented [ 1 — 3 ]. B Oral MMF: Genetic determinates of SLE severity have been elusive in part because of the heterogeneity that marks the disease [ 4 , 5 ], with the majority of cases caused by genetic predisposition coupled with environmental causes.

Lupus Wallace Daniel J.