Abstract:
:We studied kidney sections from 15 cases of polyarteritis using an immunocytochemical technique to demonstrate cells containing immunoreactive renin. Ten cases of classical polyarteritis nodosa showed hyperplasia of renin-containing cells in areas of renal cortex with histological evidence of ischaemia--appearances indistinguishable from those seen in renal artery stenosis. Histologically normal cortex showed little or no immunostainable renin. In the ischaemic areas there was loss of the normal gradient of renin-containing cells from superficial to deep cortex. In many cases this gradient was abolished or even reversed; in some cases most renin-containing cells were in juxtaglomerular apparatuses. This alteration in the distribution of immunoreactive renin has only been described in renal artery stenosis in man. In five cases of microscopic polyarteritis there were fewer than normal numbers of renin-containing cells. We suggest that in classical polyarteritis nodosa, focal ischaemia causes activation of the renin-angiotensin system analogous to the changes caused by renal artery stenosis. This may be important in the pathogenesis of hypertension in this condition. By contrast, in microscopic polyarteritis, the appearances of the juxtaglomerular apparatus and the reduced amounts of immunostainable renin suggest suppression of renin synthesis.
journal_name
Histopathologyjournal_title
Histopathologyauthors
Graham PC,Lindop GBdoi
10.1111/j.1365-2559.1990.tb01137.xsubject
Has Abstractpub_date
1990-04-01 00:00:00pages
339-45issue
4eissn
0309-0167issn
1365-2559journal_volume
16pub_type
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