Oliver Wrong

From a background as a "salt and water" physician, he made detailed clinical observations and scientifically imaginative connections which were the basis of numerous advances in the molecular biology of the human kidney.

Though academic in his leanings, he was a compassionate physician who established a warm rapport with patients (though not with his students), a link he regarded as the keystone of his research.

[citation needed] He belonged to a generation of idealistic young doctors responsible for the establishment of the UK's National Health Service in the post-War years.

[4] After internships in Toronto and at Massachusetts General Hospital with Alexander Leaf, he was appointed University Tutor in Medicine at Manchester Royal Infirmary.

Wrong had a parallel interest in the role of the large intestine in salt and water balance and developed much of his own experimental work into a short monograph published in 1981.

The original paper by Wrong and Davies examined the effect of the 'short ammonium chloride loading test' on acid excretion by the kidney.

These developments in the molecular biology of the kidney may be traced back in large part, though not exclusively, to Wrong's original 1959 paper.

These were rolled-up ribbons of semi-permeable tubing which could be eaten at breakfast and examined on retrieval distended with faecal fluid allowing comparison of gastrointestinal solute transport in normal subjects and those with kidney failure.

[16] Wrong, based on his own additional clinical work, discovered that this was a new hereditary disease and with his co-workers Norden and Feest reported it as a form of the renal 'Fanconi Syndrome'.

[17] This clinical work was put on a very firm basis by Thakker, Scheinman and Wrong and colleagues who determined that mutation of the chloride channel gene CLCN5 was the cause of many, though not all, of these disorders including one of the two original patients described by Dent and Friedman.

It became clear that several similar clinical conditions were, on the basis of genetic analysis, the same as that which Wrong had originally termed 'Dent's Disease' in honour of his late mentor.

Wrong, who had been diagnosed with idiopathic pulmonary fibrosis seven years earlier, was working on his final paper when admitted to Intensive Care Unit at UCH, the hospital at which he had spent most of his professional life.

The paper, published posthumously, describes a variant of autosomal dominant distal RTA, due to SLC4A1 mutations, originally found in SE Asia.