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 The Urinary System
Glomerular Diseases Clinical features, Diagnosis, Management, Prognosis, The term glomerulonephritis signifies glomerular inflammation (not infection) and can be considered as primary when the major problem appears to start in the glomerulus and secondary when involvement is part of a systemic disease. Examples of systemic disease that may cause glomerulonephritis are systemic lupus erythematosus (due to deposition of immune complexes containing DNA and anti-DNA antibodies), diabetes mellitus (due to widespread microangiopathy), chronic infections (malaria, hepatitis B, Syphilis) or certain tumours (presumably tumour antigen-antibody complexes). The introduction of percutaneous renal biopsy provided a detailed histogical classification which has further expanded following development of immuno-histological techniques (e.g., direct immunoflulorescence) and electron microscopy. It is now recognised that there is poor correlation between the clinical presentation and the histological appearance and only a few patients can be diagnosed accurately on clinical presentation. Glomerulonephritis may be classified according to pathologic changes observed on light and electron microscopy into three main groups:
In the majority of patients with glomerulonephritis there is clear histological evidence of inflammation; in other such as minimal change nephropathy, there is no evidence of an inflammatory process. In some circumstances, the cusative factors are known and the pathogenesis understood, in other we still don't know much. When an antigen excites antibody formation there is, normally, an excess of antibody and the antigen-antibody complexes so formed are large, insoluble and readily removed mainly by liver Kupffer cells and splenic macrophages. When the complexes are relatively small and soluble, they may circulate for long periods and eventually become deposited in glomerular capillary walls. This situation usually occurs when there is a modified immune response and relative antigen excess or antigen-antibody equivalence. It is possible therefore that patients who develop immune complex glomerulonephritis suffer from some minor defect of their immune system restricting antibody production resulting in the formation of abnormal complexes. The site of deposition within the glomerulus depends on the size, solubility and electrical charge of the particles, and upon the electrical charge of the capillary basement membrane, but may be subendothelial, subepithelial and mesangial. Following interaction of antigen and antibody an inflammatory response develops with accumulation of inflammatory cells and subsequent damage of the glomerular filtration membrane. In a number of instances of glomerulonephritis the causal antigen is known but it has become apparent that no single agent produces a uniform glomerular response. furthermore, even in well-defined forms of glomerulonephritis the rate of progression of the disease varies greatly from patient to patient. It is likely that most glomerulonephritis results from some environmental factor, such as viral or bacterial antigens, acting in a genetically susceptible patient who is relatively immuno-incompetent due to inherited or acquired factors. Four main pathogenetic mechanisms are recognised:
Clinical features: < BACK TO TOP >
Diagnosis: < BACK TO TOP >
Management < BACK TO TOP >
Prognosis < BACK TO TOP >
(source :
Dr Zoran Pletikosa) |
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