Titlebook: Atlas of Renal Pathology; R. A. Risdon,D. R. Turner Book 1980 Springer Science+Business Media Dordrecht 1980 pathology

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https://doi.org/10.1007/978-3-642-23684-6lectively termed glomerulonephritis. Such changes may be primary or part of a systemic disease, but the initial damage to the kidney occurs in the glomeruli. Although tubular and interstitial lesions may also develop and are often extensive, these are regarded as secondary phenomena.

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4.3 Collection of Biokinetic Data,identification., although light microscopy may enable one to identify a range of non-specific abnormalities. More recently, it has been noted that anti-basement membrane antibody from patients with Goodpasture’s syndrome will not bind to the glomeruli of patients with Alport’s syndrome..

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Renal Infarction, Cortical Necrosis and Tubular Necrosis,ial infarction, atrial fibrillation or infective endocarditis. Occlusion may also be due to local causes within the renal arterial system such as atherosclerosis or thrombosis associated with periarteritis.

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4.5 Doses to Patients in Diagnostics,stitium (oedema and/or fibrosis, often with inflammatory cell infiltration) and the tubules (tubular atrophy and loss). These lesions may result from direct damage to tubules or interstitium, orfrom vascular insufficiency. Sometimes a combination of factors is involved and frequently the exact mechanisms are obscure.

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