Lupus Nephritis

Lupus nephritis (LN) is a glomerulonephritis caused by SLE. The clinical findings are hematuria, proteinuria in the nephrotic range and in more advanced cases, azotemia. The diagnosis is made by renal biopsy. Treatment depends on the underlying disorder and usually includes corticosteroids, cytotoxic or other immunosuppressive drugs.

Lupus nephritis is diagnosed in about 50% of patients with SLE and evolves usually within 1 year after diagnosis. However, the overall incidence is probably> 90%, as show in kidney biopsies of patients suspected of having SLE without clinical signs of kidney disease changes of glomerulonephritis.

Lupus nephritis (LN) is a glomerulonephritis caused by SLE. The clinical findings are hematuria, proteinuria in the nephrotic range and in more advanced cases, azotemia. The diagnosis is made by renal biopsy. Treatment depends on the underlying disorder and usually includes corticosteroids, cytotoxic or other immunosuppressive drugs. Lupus nephritis is diagnosed in about 50% of patients with SLE and evolves usually within 1 year after diagnosis. However, the overall incidence is probably> 90%, as show in kidney biopsies of patients suspected of having SLE without clinical signs of kidney disease changes of glomerulonephritis. Pathophysiology The pathophysiology includes u. a. Immune complex deposits with the development of glomerulonephritis. The immune complexes consist of core antigens (in particular DNA) high affinity complement-fixing IgG antibody antinuclear antibodies against DNA are typical subendothelial, intramembranous, subepithelial or mesangial deposits. Where immune complexes are deposited, immunofluorescence staining is positive for complement and for IgG, IgA and IgM in different proportions. Epithelial cells can proliferate and form crescents. The classification of lupus nephritis is based on histological findings (see Table: classification of lupus nephritis). Antiphospholipid syndrome (APLS), this syndrome can occur with or without lupus nephritis in up to one third of patients with SLE. The syndrome occurs without another autoimmune process in 30-50% of affected patients. When antiphospholipid syndrome causes circulating lupus anticoagulant microthrombi, endothelial damage and cortical ischemic atrophy. compared to the sole lupus nephritis An associated with the antiphospholipid syndrome nephropathy increases the risk of hypertension and renal failure or renal failure. Symptoms and complaints The main symptoms and complaints are those of SLE. Patients with this disease have edema, foamy urine, high pressure or a combination. Classification of lupus nephritis Category Description * Histological findings Clinical findings regarding prognosis. Renal I Minimal mesangial normal (although sometimes immune complexes are visualized by immunofluorescence or electron microscopy) No Excellent II mesangial proliferative immune complexes only in mesangial and mesangial Hy perzellularität may microscopic hematuria, proteinuria, or both Excellent III focal proliferative endocapillary and extracapillary cellular proliferation and inflammation in <50% of glomeruli, usually with a segmental distribution Usually hematuria and proteinuria may hypertension, nephrotic syndrome, and increased serum creatinine Variable IV diffuse proliferative † endocapillary and extracapillary cellular proliferation and inflammation in> 50% of glomeruli In general, hematuria and proteinuria Common Hypertension, nephrotic syndrome and increased serum creatinine Variable V membranous thickening of the glomerular basement membrane with subepithelial and intramembranous immune complex deposition usually nephrotic syndrome Sometimes microscopic hematuria or hypertension, serum creatinine usually normal or slightly elevated Bad defines VI sclerosing sclerosis of> 90% glomerular capillary Inconspicuous urinary sediment and renal disease Ends tadium or slowly rising serum creatinine Bad * Using light microscopy. † Most common form. Diagnostic urinalysis and serum creatinine (all patients with SLE) renal biopsy The diagnosis is made in all patients with SLE, especially in patients with proteinuria, hematuria, erythrocyte cylinders or hypertension. The diagnosis is made in patients with unexplained hypertension, elevated Serumkreatininspiegenl or abnormalities in the urinalysis showing clinical features suggest the SLE. A urine analysis is performed and serum creatinine measured. If abnormalities occur in both cases, is usually a kidney biopsy to confirm the diagnosis and to classify the disorder histologically. Histological Classification helps determine prognosis and guide therapy. Some of these histological subtypes correspond to other Glomerulopathies. For example, the membranous lupus nephritis is similar histologically of idiopathic membranous nephropathy and diffuse proliferative lupus nephritis is similar histologically membranoproliferative glomerulonephritis type I. The overlap between these categories are significant, and patients may progress from one class to another. Lupus nephritis Mesangioproliferativ (Class II) Figures provided by Agnes Fogo, M.D., and the American Journal of Kidney Disease Atlas of Renal Pathology (see www.ajkd.org). var model = {thumbnailUrl: ‘/-/media/manual/professional/images/lupus_nephritis_mesangial_proliferative_class_ii_high_de.jpg?la=de&thn=0&mw=350’ imageUrl: ‘/-/media/manual/professional/images/lupus_nephritis_mesangial_proliferative_class_ii_high_de.jpg?la = en & thn = 0 ‘, title:’ lupus nephritis Mesangioproliferativ (class II) ‘, description:’ u003Ca id = “v38396963 ” class = “”anchor “” u003e u003c / a u003e u003cdiv class = “”para “” u003e u003cp u003eDas upper image shows a mesangial IgM deposition (immunofluorescence with anti-IgM

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