926 has not, so far, been shown to produce heterophile antibody.4 Unlike other causes of an "LM.-hke illness", the production of heterophile4 antibody seems specific to infection by EpsteinBarr virus. We feel that Smith’s explanation of the findings of his case-i.e., severe adenovirus infection in a patient immunosuppressed by recent LM.-is more reasonable than that given by Schumacher et al. It would seem unwise to conclude that adenovirus type 7 produces heterophile antibody. Departments of Hæmatology and Bacteriology, Ninewells

D. O. HO-YEN D. PARRATT

Hospital,

Dundee DD1 9SY

DIALYSIS FOR RENAL FAILURE IN TORONTO

ambulatory

SIR,-Continuous

peritoneal

dialysis

(C.A.P.D.)5.6 is now accepted by many centres around the world, and the seems a

of infection (1 episode every 7.3 patient months) worthwhile price to pay for the many advantages of

rate

their population or their method of doing fluorescence tests enables them to make this statement. In Oxford, 36 patients with no c.M.v. antibodies detectable by immunofluorescence and who were given a kidney from a c.M.v. seronegative donor have remained uninfected. 70% of 33 seronegative patients given a kidney from a c.M.v. seropositive donor became infected between 19 and 78 days later. No patient was given a c.M.v. seropositive blood-transfusion, so the infection must have come from the donated kidney. The use of an initial serum dilution of 1:8 would make Neild and Southee’s test no more sensitive than the complement-fixation test criticised. For more accurate results it is advisable to start serum dilutions at a titre of 1 : 2. The possibility of preventing c.M.v. infection in seronegative recipients by giving them kidneys from seronegative donors is most applicable to areas where a high proportion of the population are seronegative, as in Oxford. In areas where few people are seronegative, as in the population served by Guy’s, primary infection must be uncommon and there is little incentive to make a serious attempt to prevent it. Virology Laboratory and Renal Transplant Unit,

J. O’H. TOBIN M. J. WARRELL P. J. MORRIS

Churchill Hospital,

Headington, Oxford DIALYSIS PATTERNS IN TORONTO

1976-78 ISLET AUTOANTIBODIES IN HUMAN PANCREATIC TRANSPLANT RECIPIENTS

SIR,-It is well established that autoimmune mechanisms play a role in the destruction of the islet B-cell in patients

can

*3f of patients m 1978 were transplanted before dialysis. this form of

In

Canada, at least twenty centres now The final place ofc.A.P.D. in the manrenal disease will be established once the agement of infection-rate improves and the long-term effects have been clarified. However, trends in chronic dialysis in Toronto may be indicative of future patterns of management. The table shows the numbers of new patients admitted to five teaching hospitals in Toronto during 1976, 1977, and 1978. Allocation to hxmodialysis has become less frequent while peritoneal dialysis has become more common, and a similar pattern is seen in patients trained for home dialysis. D. G. OREOPOULOS D. R. WILSON G. A. DEVEBER S. S. A. FENTON Toronto Western Hospital, C. SAIPHOO University of Toronto Nephrology C. WILLIAMS Coordinating Committee,

treat

therapy.

patients by

C.A.P.D.

end-stage

Toronto, Ontario M5 T 2S8, Canada

M. JOHNSON

with insulin-dependent diabetes mellitus: insulitis and autoantibodies against islet tissue are characteristic features of the onset of diabetes. 1-4 In addition, lymphocytes sensitised to pancreatic antigens have been found in diabetic patients.5.6 Under these circumstances, the transplantation of islet tissue might be thought futile since the graft would suffer the same fate as the autologous B-cell. However, Dr Andersson has now reported (March 17, p. 581) that mice with diabetes caused by cytotoxin-induced insulitis could be permanently cured by intrasplenic transplantation of syngeneic islets. There was no sign of an inflammatory reaction in the grafted islets. We have addressed ourselves to this question clinically by studying two insulin-dependent diabetic patients who received cadaveric, vascularised, segmental pancreatic grafts. Islet-cell antibodies2 were not detected either at transplantation or at any postoperative examination including those at rejection (days 43and 51). There were no morphological signs of insulitis. In one of the patients we also looked for islet-cell surface antibodies4 without finding any evidence of "reimmunisation". Autoantibodies against islet B-cells should thus not pose a

problem in human pancreatic transplantation. of Medicine and Karolinska Institute,

Departments

Surgery,

Huddinge Hospital, Huddinge, Sweden Department of Immunology, Middlesex

Hospital,

London WC1

CYTOMEGALOVIRUS INFECTION AND RENAL TRANSPLANTATION

Department of Histology, Umea University, Umeå, Sweden

SIR,-In the last paragraph of their letter Dr Neild and Mr Southee (March 17, p. 604) state that previous reports of cyto-

megalovirus (c.M.v.) infection transmitted by donor kidneys must be interpreted with great caution. We do not feel that 4 Evans. A. S. Am J med. Sci. 1979, 276, 325. 5. Popovich, R P., Moncrief, J W., Decherd, Ann intern Med. 1978, 88, 449.

J B., Bomar, J B., Pyle, W K.

6. Oreopoulos, D G., Robson, M., Izatt, S., Clayton, S., deVeber, G. A Trans. Am Soc artif. intern. Organs, 1978, 24, 484

ROLF GUNNARSSON CARL-GUSTAV GROTH

G. FRANCO BOTTAZZO

ÅKE LERNMARK

1. Gepts, W Diabetes, 1965, 14, 619. 2. Bottazzo, G F., Florin-Christensen, A., Doniach, D. Lancet, 1974, ii, 1279 3 Lendrum, R., Walker, G., Gamble, D. R. ibid. 1975, i, 880. 4. Lernmark, A, Freedman, Z. R., Hoffman, C, Rubenstein, A H . Steiner. D. F., Jackson, R I. , Winter, R. J., Traisman, H. S New Engl J Mea

1978, 299, 375. Nerup, J., Ortved Andersen, O., Bendixen, G., Egeberg, J., Poulsen, J E Diabetes, 1971, 20, 424. 6. MacCuish, A. C., Jordan, J., Campbell, C. J., Duncan, L J. P. Irvine, W. J. Lancet, 1974, ii, 1529 5