anti-glomerular basement membrane disease/albumin

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Chloride channel ClC-5 binds to aspartyl aminopeptidase to regulate renal albumin endocytosis.

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ClC-5 is a chloride/proton exchanger that plays an obligate role in albumin uptake by the renal proximal tubule. ClC-5 forms an endocytic complex with the albumin receptor megalin/cubilin. We have identified a novel ClC-5 binding partner, cytosolic aspartyl aminopeptidase (DNPEP; EC 3.4.11.21), that

Reduced tubular degradation of glomerular filtered plasma albumin is a common feature in acute and chronic kidney disease.

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Tubular epithelial cells take up and degrade plasma albumin filtered by the glomerulus. Tubular damage resulting in reduced albumin uptake or degradation has been suggested as one mechanism contributing to albuminuria in kidney disease. This study investigated whether tubular albumin uptake or

Characteristics of albumin processing during renal passage in anti-Thy1 and anti-glomerular basement membrane glomerulonephritis.

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Recent studies have shown that glomerular-filtered albumin appears to be processed by two distinct cellular pathways. The major pathway, a high-capacity retrieval pathway, returns most of the filtered albumin to the blood supply intact. The albumin not taken up by the retrieval pathway is degraded

Factors affecting the glomerular protein leak after polyclonal activation in the HgCl2-induced model of anti-GBM disease in the brown Norway rat.

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The administration of the polyclonal activator HgCl2 (1 mg/kg i.p.) to Brown Norway (BN) rats on days 0, 2, 4 and 7 resulted in the cyclical production of anti-glomerular basement membrane (GBM) antibodies, the first peak of which occurred at day 14 with a smaller peak at day 26. Glomerular anti-GBM

Comparison of double filtration plasmapheresis with immunoadsorption therapy in patients with anti-glomerular basement membrane nephritis.

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BACKGROUND Double filtration plasmapheresis (DFPP) and (IA) are both used to clear antibody. However, the clinical efficacy and safety of DFPP in patients with anti-glomerular basement membrane (anti-GBM) disease are unclear. METHODS The 28 enrolled patients diagnosed serologically and

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