uraemic syndrome and single kidney

Creatinine clearance and microalbuminuria were measured before and after an oral protein load in 17 children with a history of haemolytic uraemic syndrome, 11 with a single kidney, and 15 controls, all of them normotensive and without evidence of renal damage, to look for indirect evidence of glomerular hyperfiltration. While creatinine clearance increased significantly after the protein load in controls, it did not change in patients with either haemolytic uraemic syndrome or a single kidney. Basal microalbuminuria was significantly higher in those with haemolytic uraemic syndrome when compared with those with a single kidney and controls. It increased significantly in all groups after a water load; this increase was significantly higher in haemolytic uraemic syndrome. After the protein load microalbuminuria returned to baseline. In conclusion, children with a history of haemolytic uraemic syndrome have an abnormal renal functional reserve like children with a single kidney. Only patients with haemolytic uraemic syndrome exhibited an increased microalbuminuria, however, suggesting that it may be the expression of a pathophysiological mechanism involved in haemolytic uraemic syndrome and not in single kidney, that could account for their different prognosis. their renal functional reserve, suggesting that all their remaining nephrons were functioning at a maximal rate. He suggested that glomerular hyperfiltration might have played a pathogenetic part in the further derangement of their renal functional reserve. Further support for this contention may be drawn from experimental observations demonstrating an increase of the glomerular filtration rate in single remaining nephrons after renal ablation.5 Glomerular hyperfiltration may produce alterations in the glomerular capillary permeability,5 8 9 leading to increased urinary albumin excretion in the microalbuminuric range. 10 Microalbuminuria has thus been suggested as an early marker of hyperfiltration. " 12 The present study was undertaken to search for indirect evidences of glomerular hyperfiltration in patients with a history of haemolytic uraemic syndrome. Past morphological studies performed on kidneys of these patients during the acute phase indicated that the glomerular involvement is in fact focal and leads to a reduction in the number of their functioning nephrons. Thus results obtained in children with haemolytic uraemic syndrome were compared with those obtained in a special control group of children with a known cause of reduced renal mass such as single kidney. None of the children included in this study showed evidence of impairment in their renal function as determined by conventional methods. Hospital de Nifios 'Ricardo Gutierrez', Buenos Aires, Argentina E M Pereistein B G Grunfeld R B Simsolo Hospital Italiano, Buenos Aires, Argentina M I Gimenez C A Gianantonio Correspondence to: Dr E M Perelstein, La Pampa 3635, 1430 Buenos Aires, Argentina. Accepted 30 March 1990 The haemolytic uraemic syndrome, characterised by the triad of acute renal failure, microangiopathic haemolytic anaemia and thrombocytopenia, is the main cause of acute renal failure in late infancy and early childhood. Although more than 95% of patients survive the acute phase of the disease and most of them, moreover, recover initially normal renal function, some of these patients may develop chronic renal failure in later stages of life. Haemolytic uraemic syndrome is the leading cause of chronic renal failure in childhood and adolescence in Argentina. Mechanisms responsible for the progression of renal failure in these patients remain obscure. Glomerular hyperfiltration has been postulated as a universal mechanism implicated in the deterioration of kidney function.5 6 This hypothesis has stimulated the search for a method of early assessment of hyperfiltration in humans. Bosch et al introduced the concept of renal functional reserve as the capacity of the kidney to increase its level of glomerular filtration rate after an oral protein load.7 He reported that patients with overt renal disease had lost Patients and methods