By R. A. Risdon, D. R. Turner (auth.)
This e-book is meant as a realistic bench guide phological abnormalities in renal ailments, and for the medical institution pathologist who needs to have the place acceptable those were illustrated. entry to an easy informative account of renal even supposing the most emphasis is at the pathology, pathology, rather for the translation of the proper medical features of the stipulations cov percutaneous needle biopsy specimens. I n addition ered are integrated in popularity of the truth that we belief it will likely be important to physicians operating renal illness is a space during which correlation of the within the box of renal sickness, for whom the interpre medical and histopathological findings is especially tation of renal biopsy fabric is at once appropriate to big in achieving an educated prognosis. sufferer administration. while a accomplished insurance extra appro priate to a bigger textual content has no longer been tried, the Acknowledgements textual content has been deliberate to offer an sufficient account of the extra very important non-neoplastic sickness seasoned we wish to thank the technical employees of the cesses and their pathological appearances within the Histopathology Laboratories of The London Hos kidney. issues of hassle in interpretation and dif pital scientific collage, The clinic for ailing Chil ferential prognosis are lined either within the textual content and in dren, nice Ormond highway, and Guy's health center the illustrations.
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6. Spitzer. R. , Vallota, E. H .. , Sudora, E.. Stitzel. , Davis, N. C. and West. C. D. (1969). Serum C31ytic system in patients with glomerulonephritis. Science, 164, 436-437. 7. Peters. D. , Williams, D, C .. Charlesworth, J. , BoultonJones, J. , Sisson:;, J. G. , Evans, D. , Kourilsky, O. and Moret-Maroger, L. (1973). Mesangiocapillary nephritis, partial lipodystrophy and hypocomplementaemia. Lancet, 2, 535-538. 8. Turner, D. R.. Cameron, J. , Ogg, C. S.. Evans, D. J .. Trafford, A. J. P. and Leibowitz, S.
Cells outside the glomerular capillary basement membrane) causing obliteration of the urinary space (so-called 'capsular crescent' formation) and affecting at least 80% of un sclerosed glomeruli. This extracapillary cell proliferation is often so marked that the associated glomerular tuft is compressed and obscured. 1 Mesangiocapillary glomerulonephritis. The glomerulus is enlarged and shows accentuated lobulation of the tuft. There is both diffuse thickening of the walls of tuft capillary loops and mesangial cell proliferation.
34 RENAL INFARCTION, CORTICAL NECROSIS AND TUBULAR NECROSIS nant animals with a single dose of endotoxin. Clinical evidence of DIC may be found in conditions such as bacteraemic shock and obstetric emergencies which may be associated with renal cortical necrosis. However, DIC and fibrin deposition within glomerular capillaries may occur in the absence of renal cortical necrosis so that the development of this lesion probably also requires a degree of vascular spasm. Acute Tubular Necrosis This may be due to: (i) Direct poisoning of the tubular epithelium mainly affecting proximal convoluted tubules (the nephrotoxic lesion), or (ii) Acute ischaemic damage affecting all parts ot the renal tubules (the tubulorrhexic lesion), or to a combination of (i) and (ii).
Atlas of Renal Pathology by R. A. Risdon, D. R. Turner (auth.)