HIV knocks on the Renal Unit door in 1982

 CG Winearls FRCP Senior Registrar in Nephrology Hammersmith Hospital 1982-1986

 A case of GRID (Gay Related Immunodeficiency) was presented by a gastroenterology registrar on the Royal Postgraduate Medical School Wednesday Staff Round at the Hammersmith Hospital in 1982. All very curious, we renal doctors thought, but not really our business. The cause was not known, and the possibility of blood  borne transmission was not even mentioned. It soon became our business.

A White British man working as musician in the USA was diagnosed with ESRF in 1981 and started dialysis. In 1982 he decided to return to the UK to live in Acton West London and requested transfer from his Californian dialysis unit to the overstretched Hammersmith Hospital HD Unit. He was offered CAPD and declined, and  since he had a working AV fistula jumped the queue for an HD slot. He went on the transplant waiting list and  received a well-matched graft in 1983. Immunosuppression was with high dose steroids and azathioprine. Within a few months he developed severe oral and anogenital herpes simplex, CMV with retinitis, two episodes of Pneumocystis pneumonia and intractable candida oesophagitis. He was severely lymphopenic.  I  presented him to the self-same Staff Round as “Post transplant immunodeficiency syndrome.”   I received a sceptical and critical hearing and was told that the problem was careless overdosing of immunosuppression. The patient deteriorated. HTLV-lll was then identified as the cause of what was now called AIDS and a serological test became available through the genitourinary medicine clinic at St Mary’s Hospital in Paddington.  I took to St. Mary’s a serum sample which had been stored on admission and asked Dr Jeffries [1] whether he would be so kind as to test the sample. Two days later he phoned to report that it was positive.

The  patient was neither gay nor an intravenous drug user but had received a three unit blood transfusion in the United States. We wrote to his Californian dialysis unit but received no reply. Immunosuppression was stopped and we broke the news to him. The reaction to having an AIDS patient on the transplant ward  varied from caring to avoidance. He died. The porters were reluctant to move the body to the morgue. The case was written up.[2] [3] At the time it was thought that HIV was a risk factor for the development of AIDS but it required another factor  – in this case immunosuppression.

Not surprisingly, renal units were sensitised to the problem of blood-borne virus infections. Hepatitis B had caused havoc in the late 1960s and 1970s. In Oxford where I had previously worked as the renal unit registrar all HD patients had yellow sticky labels on their notes and had three monthly HepB antibody checks. Only one man seroconverted but was fortunately on home HD; he was not allowed to attend outpatients. No case of acute renal failure  (now AKI) could be  dialysed until the HepB result was known. The Dulwich dialysis unit, part of Kings College Hospital, run by Dr Victor Parsons was one of the few units that  would take on HepB positive ESRF patients. Isolation dialysis facilities were seldom available elsewhere.

When the HTLV-lll test became available there was a clamour for all HD patients and new referrals to be tested. This was resisted on the grounds that with “universal precautions” infection of staff or other patients would not occur.  Moreover it was pointed out that the patients would have to give consent and be counselled that there was no advantage to them knowing their HIV status as there was no treatment. This ruling was very controversial and was probably ignored. In Oxford a notice was put up in the phlebotomy room informing all new patients that they would be tested for certain viruses including Hepatitis B, CMV, EBV  and er .. HTLV-lll . [4]  There was no signed consent. The first patient to be identified as having HIV  was a young blind Type 1 diabetic who was it emerged gay; the notice of testing was not provided in Braille. He was offered  CAPD only and managed in the community. His lived with his parents but had to eat alone with his own cutlery and crockery. He died a few months later.

We were allowed to test for what was now called HIV if patients were to be put on the  transplant waiting list. If they refused the test they would not be accepted. It turned out that there were very few HIV positive ESRF patients in the UK.

We learned that in the USA nephrologists were seeing HIV patients, mostly of African American heritage, who presented with nephrotic syndrome and progressive renal impairment. Biopsies usually showed FSGS and a characteristic collapsing glomerulopathy.  This became known as HIVAN (HIV-associated nephropathy). The prognosis was hopeless and they usually died before reaching  ESRF. Later it was discovered that the risk of developing HIVAN was related to the ApoL1 gene.

Much changed with the discovery of effective anti-virals but the taboos persisted.

I became a consultant in Oxford. In 2013  I made   a visit to my native South Africa where AIDS was rampant but denied by the President, Thabo Mbeki. On my  first ward round when I got back to Oxford a patient with nephrotic syndrome and AKI  (creatinine 600µmol/L) was presented. He was a black policeman from Zululand who had accompanied his wife, a nurse, to the UK. He had been found soon after arrival to have tuberculosis which was being  treated. He had declined an HIV test. The renal biopsy showed collapsing glomerulopathy. I tried  to persuade him to have an HIV test. He declined on the grounds that a positive test would have serious consequences. He was told that he could not be treated  with HAART (highly active anti-retroviral treatment) unless we confirmed the diagnosis, he would not budge.  The SpR in Infectious Disease was sent for; the patient agreed to the test.   RAAS blockade and prednisolone was prescribed along with HAART He improved and avoided dialysis for two years. His viral load was low and his CD4 count normal. He received a kidney transplant which functioned well and he had no opportunistic infections. He returned  to South Africa and the Oxford  ID team    arranged for him to continue on HAART  there. Sadly, his wife  had also become HIV positive.

In thirty years we had  seen untreatable and fatal HIV infection become  a “no drama” and easily treated chronic infection in the renal transplant setting. Such is progress.


[1] Dr Jeffries was the virologist who helped the GUM clinic at St. Mary’s which  was caring for a large number of gay men with AIDS.

[2] Cohen J, Winearls C, Oliveira  D and Williams G. Letter Opportunistic AIDS. Lancet 1984;ii:1209-1210

[3] D B OliveiraC G WinearlsJ CohenP W IndG Williams. Case Reports: Severe immunosuppression in a renal transplant recipient with HTLV-III antibodies.Transplantation 1986 41(2):260-2.

[4] Ironically, a number of patients were later found to have Hepatitis C but there was no test at the time. Oxford had a proven cross infection in a dialysis unit.

Last Updated on October 27, 2023 by John Feehally