Renal Tubular Damage in Infantile

Introduction The natural history of acute tubular necrosis in adults has been well documented, but accounts of the condition in infants and children are rare. Most of the descriptions of tubular necrosis in the paediatric literature refer to older children (Riddell, 1951; Kaplan and Fomon, 1953; Wagner, 1954), but Pratt (1948) described two cases due to sulphonamides, aged 10 months and 18 months, and Jonsson (1951) published three fatal cases of severe asphyxia neonatorum with oliguria and raised blood urea, but at autopsy in Jonsson's cases there were haemoglobin casts in the distal tubules with no degeneration of the tubular epithelium. Doxiadis (1947) described tubular changes in some fatal cases of gastro-enteritis, but the details of the renal histology given are insufficient to make it clear whether he was dealing with acute tubular necrosis or with some type of nephrocalcinosis. The pathological aspect of renal disorders in early life associated with circulatory disturbances has been fully reviewed by Zuelzer, Charles, Kumetz, Newton and Fallon (1951) who showed that various types of acute renal failure not uncommonly develop in severely dehydrated children. They described a range of vascular complications affecting the kidney, including 'lower nephron nephrosis' (acute tubular necrosis). In many of their cases diarrhoea and vomiting appeared to have been the precipitating symptoms. Carre and Squire (1956) published three cases of anuria with tubular necrosis, which were studied in great detail. The cause of the anuria was uncertain in the first case, and was thought to be due to sulphonamides and a penicillin reaction respectively in the other two cases. Recent work (Oliver, MacDowell and Tracy (1951) and Van Slyke (1954)) has indicated that, apart from certain poisons, renal ischaemia is the probable cause of most cases of acute tubular necrosis, and that the ischaemia is itself a response to certain circulatory disorders associated with severe shock. In children, acute gastro-enteritis is probably the commonest cause of dehydration and shock, and it is surprising that there have been no reports of the clinical recognition of tubular damage in this condition. The only observations on this subject are those of Calcagno and Rubin (1951) and of Kerpel-Fronius, Varga, Kun and V6n6czky (1954). Calcagno and Rubin (1951) produced evidence of failure of water reabsorption during the acute phase of dehydration and shock in two severe cases, but found that complete recovery occurred within 24 hours and five days respectively. KerpelFronius et al. (1954) stated that it was often some days or even weeks before complete restoration of renal function occurred. Two cases with evidence of tubular damage are here reported in full, together with a retrospective survey showing that minor degrees of renal damage are not uncommon in gastro-enteritis.