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  • membranoproliferative glomerulonephritis
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  • glomerulonephritis,membranoproliferative
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  • membranoproliferative
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  • membranoproliferative glomorulonephritis
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CMPGN chronic membranoproliferative glomerulonephritis
MPGN membranoproliferative glomerulonephritis
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MPGN Membranoproliferative glomerulonephritis
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  • membranoproliferative glomerulonephritis
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membranoproliferative glomerulonephritis <pathology> A kidney disorder which results in kidney dysfunction. Inflammation of the glomeruli result from an abnormal immune response and the deposition of antibodies within the kidney (glomerulus) ultrastructure.
Membranoproliferative glomerulonephritis has been divided into two different types in the basis of where the antibodies are deposited in the glomerulus. MPGN type I, the more common type, deposits antibodies in the subendothelial layer of the basement membrane, whereas type II deposits antibodies in the bottom layer of the basement membrane.
Symptoms include cloudy urine (pyuria), decreased urine output, swelling and hypertension. This disorder often results in end-stage renal disease.
Acronym: MPGN
(26 Mar 1998)
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glomerulonephritis, membranoproliferative Chronic glomerulonephritis characterised histologically by proliferation of mesangial cells, increase in the mesangial matrix, and a thickening of the glomerular capillary walls. The wall thickening is sometimes said to be a result of the interposition of mesangial cytoplasm or matrix between the basement membrane and the endothelium of the capillary wall. It is often divided into types I and II, and sometimes III. Pathogenesis is not well understood, but some types are thought to involve the immune system, with the complement system, in particular, being implicated.
(12 Dec 1998)
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  • membranoproliferative - »õâ
  • membranoproliferative glomerulonephritis - »õâ
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  • Membranoproliferative glomerulonephritis (type II) - »õâ
  • Membranoproliferative GN I - »õâ
  • Membranoproliferative GN II - »õâ
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membranoproliferative g. a chronic glomerulonephritis characterized by mesangial cell proliferation and irregular thickening of the glomerular capillary wall. There are two subtypes: Type I is marked by subendothelial electron-dense deposits and classical complement pathway activation, and Type II (called also dense deposit disease) is marked by heavy electron-dense deposits in the glomerular basement membrane and alternative complement pathway activation involving C3 nephritic factor. Both types occur in older children and young adults and follow a slowly progressive course with irregular remissions ultimately resulting in renal failure. Called also chronic hypocomplementemic g., lobular or lobulonodular g., and mesangiocapillary g.
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