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with community aspects of medical care one session aweek throughout the third year is devoted to the pri-mary-medical-care aspects of that discipline to which thestudent is at that time attached in hospital.

In the fourth year, apart from one mandatory day ofclinical work each week, the student spends the whole ofhis time studying a subject of his choice. Students areencouraged, but not obliged, to choose an area of inves-tigation with clinical as well as laboratory or epidemiolo-gical aspects. At the end they are expected to write anoriginal dissertation, and many of these have been ofhigh standard. The 5 students who elected to study im-munology and alimentary disease have contributed tothree papers (in press or published) in the British Medi-cal Journal, one in Gut, one in the Quarterly journal ofMedicine, and one in The Lancet. The fourth yearallows students to recognise the limitations of existingknowledge and of experimental method in human bio-logy, and to set the pattern for life-long learning. Howthis type of learning can be organised for a class of 130students remains to be seen.The fifth year is a year of clinical apprenticeship, with

students being given the maximum responsibility undersupervision. Most of the work in this year is undertakenin district general hospitals in the Wessex Region outsideSouthampton, providing a population base of 2* mil-lion. While this should certainly make it easier to

guarantee that no patient is overwhelmed by the needsof undergraduate teaching, Southampton students havemuch more extensive opportunities than, for example,those in McMaster for contact with patients on a one-to-one basis.The establishment of Southampton medical school

was proposed by the Royal Commission on MedicalEducation. It was sanctioned by the Government in

1967, and the school was inaugurated in 1971. Whetherits graduates will recognise and respond to the needs ofsociety more appropriately than those of other institu-tions cannot yet be judged. Perhaps, by the middle of the1980s, the enthusiasm of the young faculty will be re-warded by a demonstration that this has been achieved.

RADIATION NEPHROPATHY

SINCE 1904, when Baerman and Linser1 described theill-effects of irradiation on the kidney, evidence hasaccumulated alerting radiotherapists to this hazard.

Luxton,2 3 reporting a large clinical study, defined fivecategories of disease--acute radiation nephritis,chronic radiation nephritis, benign hypertension, malig-nant hypertension, and symptomless proteinuria. Lux-ton and his co-workers4 deduced that doses of greaterthan 2300 rads in less than five weeks would probablycause renal damage. Acute radiation nephritis accountsfor most of the other reported cases with adequate histo-logical information. The onset of hypertension and pro-teinuria may be delayed for up to 12 months; hæmaturiais uncommon. Untreated, most patients die of renal fail-

1. Baerman, G , I. ser, P Münch med Wschr. 1904, 7, 996.2. Luxton, R. W. Q. Fl Med. 1953, 22, 215.3 Luxton, R. W. Lancet, 1961, ii, 1221.4. Kunkler, P. B., Farr, R. F., Luxton, R. W. Br. J. Radiol. 1952, 25, 190.

ure within the subsequent year. A few patients go on tolate malignant hypertension (Luxton group iv), from 18months to 11 years after radiotherapy. Again, withouttreatment there is rapid deterioration.

Keane and his associates5 have lately described therenal microstructure and ultrastructure in acute radia-tion nephritis. They investigated two women withhitherto normal renal function in whom nephritis arose8 and 10 months after radiotherapy for disseminatedovarian cancer. Radiation doses were 2500 rads and2700 rads over 4 and 5 weeks. The most strikingchanges were glomerular, with increase in mesangiumand thickening and cleavage of capillary basement mem-brane. Intimal proliferation was seen in medium andsmall arteries; interstitial fibrosis and tubular damagewere prominent. Fluorescent studies, using immunoglo-bulins, C3, and fibrinogen, were negative. Neither pa-tient had an abnormal urinary sediment. In relation tothe degree of glomerular damage, proteinuria was

modest (1 g/24 h) though non-selective.6How is the damage caused ? After irradiation, replica-

tion of capillary endothelial cells (which usually happensevery 2-3 months) is delayed.7-9 Capillary-wall damagewould allow activation of the coagulation system andfurther vascular damage. This theory has experimentalsupport, 1012 and the non-specific histologicalappearances certainly resemble other nephropathies inwhich coagulation derangement is implicated. The lackof fibrinogen on fluorescent staining requires explana-tion. Vascular changes and interstitial fibrosis suggestan ischasmic ætiology—maybe a direct effect of irradia-tion on juxtaglomerular cells or (again) a coagulopathycausing thrombosis in the renal microcirculation. Radia-tion also increases the susceptibility of renal arteries tohypertensive damage,14 " perhaps compounding the

damage. Drug toxicity must be borne in mind: corti-sone causes glomerular changes in irradiated rat kid-neysl6 and chemotherapy may sensitise the kidney toirradiation-especially in children.17 18 Associationsexist between nephrotic syndrome and lymphomas19 andother cancers.20 21 Radiotherapy might activate latentdisease; but the immunological evidence is lacking.

Radiation nephropathy is now uncommon, since

damaging radiation levels can be predicted. For cases ofoverdosage, anticoagulation would be a logical ap-proach 10 22—providing that it was started early enough.Treatment of the established nephropathy is along con-ventional lines for renal insufficiency.

5. Keane, W. F., Crosson, J. T., Staley, N. A., Anderson, W. R., Shapiro,F. L. Am. J. Med. 1976, 60, 127.

6. Gang, N. F., Sarophin, M E., Madrazo, A., Churg, J. Am. J. Path. 1973,72, 141.

7. Engerman, R. L., Pfaffenbach, D., Davis, M. D. Lab. Invest. 1967, 17, 738.8. Tannock, I. F., Hayashi, S. Cancer Res. 1972, 32, 77.9. DeGowin, R. L., Lewis, L. J., Hoak, J. C., Mueller, A. L., Gibson, D. P. J.

Lab. clin. Med 1974, 84, 42.10. Kinzie, J., Studer, R., Perez, B., Potchen, E. J. Science, 1972, 175, 1481.11. Fajardo, L. F., Stewart, J. R. Lab. Invest. 1973, 29, 244.12. Khan, M. Y., Okanian, M. Am. J. Path. 1974, 74, 124.13. Ljungquist, A., Unge, G, Lagergren, C., Notter, G. Acta path. microbiol.

scand. 1971, 79(A), 62914. Wilson, C., Ledingham, J. M., Cohen, M. Lancet, 1958, i, 9.15. Asscher, A. W., Wilson, C., Anson, S. G. ibid. 1961, i, 580.16. Berdjis, C. C. Archs Path. 1960, 69, 431.17. Sagerman, R. H. J. Urol. 1964, 91, 332.18. Arneil, G. C., Emmanuel, I. C., Flatman, G. E., Harris, F., Young, D. G.,

Zachary, R B. Lancet, 1974, i, 960.19. Player, J. Stutzman, L Am. J. Med 1971, 50, 56.20. Cantrell, E. G. Br. med J. 1969, ii, 739.21. Loughridge, L. W., Lewis, M G. Lancet, 1971, i, 25622. George, C, Slichter, S., Quadracei, L., Striker, G., Harker, L. New Engl.

J. Med 1974, 29, 1111.