الفهرس 
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Abstract
Membranous nephropathy is the most common cause of the nephrotic syndrome in adults, accounting for about one third of cases. The natural history of patients with idiopathic membranous nephropathy varies from a spontaneous complete remission of proteinuria to rapid progression to end-stage renal disease.
IMN has a male and adult predominance with the peak incidence between 30 and 50 yr and MGN is particularly likely in patients over 50 yr of age who present with nephrotic syndrome .
Idiopathic membranous nephropathy is an immunologically mediated disease in which immune complexes deposit in the subepithelial space . The hallmark of IMN is subepithelial deposition of immunoglobulin G (IgG) together (in idiopathic MGN) with normal cellularity of the glomerular tuft. Antigen-antibody complexes can develop by the production of immune complexes in situ or by deposition
The antigens associated with primary membranous nephropathy are not known , it was recently demonstrated that antibodies (dipeptidyl-peptidase IV and neutral endopeptidase (NEP) which are expressed on the human podocytes, were produced by a pregnant woman and were transferred to her fetus , in which a severe form of membranous glomerulonephritis developed prenatally.
The complement membrane attack complex (C5b-9) triggers the biosynthesis of oxygen radical-producing enzymes within the glomerular epithelial cells. C5b-9 in sublytic quantities stimulates podocytes to produce proteases, oxidants, prostanoids, extracellular matric components and cytokines, including TGF-beta.
C5b-9 also causes alterations of the cytoskeleton that lead to an abnormal distribution of slit diaphragm protein and detachment of viable podocytes that shed into the Bowman space . These events result in disruption of the functional integrity of the glomerular basement membrane and the protein filtration barrier
of podocytes with subsequent development of massive proteinuria .
The hallmark of IMN is the nephrotic syndrome, which is characterized by
Proteinuria, hypoalbuminuria, hyerlipidemia, &a tendency for thrombosis .
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Diagnosis depends on clinical picture and investigations including exclusion of occult malignancy with the definitive diagnosis is made based on findings from a renal biopsy.
Treatment of patients with membranous nephropathy consists of supportive treatment directed at proteinuria or the nephrotic syndrome and specific immunosuppressive therapy. There is little discussion about the so-called conservative treatment of a patient with a nephrotic syndrome. This comprises reduction of edema with diuretcs and aggressive lowering of blood pressure to values below 125/75 mmHg with the preferential use of ACE-inhibitors or Angiotensin II type I receptor blockers, because of their additional antiproteinuric effects. In addition, lipid lowering agents (statins) are advised for the often prominent hypercholesterolemia. In case of a severe nephrotic syndrome , one should consider the prescription of anticoagulant drugs to prevent thrombo-embolic complications . In contrast to the generally accepted conservative treatment policy, there is much debate on the need for immunosuppressive agents as well as on which agent should be used in which patient at what time point.
The proposed treatment strategy is intended to allow individualized treatment for patients with IMN where high risk patients can be identified readily . Patients are classified into 3 groups according to their risk for progression to ESRD regarding assessment of the initial CrCl, the slope of the CrCl , and the lowest level of proteinuria during a 6-mo observation period.