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Screening of patients referred to a Renal Clinic in Western Scotland over a period of 6 months revealed that 18 patients out of a total of 127 had a history of analgesic abuse, defined as a total consumption of phenacetin or salicylate in excess of 1 Kg. A further 8 patients with analgesic abuse were admitted to the Renal Unit with uraemia and electrolyte disturbance. Renal function was assessed in the whole group of 26 patients; creatinine clearance was significantly reduced in almost all, and a relationship was demonstrated between creatinine clearance and the total dose of phenacetin ingested. Renal concentrating power was markedly reduced in most, and in general the degree of impairment was worst in those with low creatinine clearances. The findings on intravenous pyelography are described; it was not possible in any case to distinguish the appearances from those found in chronic pyelonephritis. Isotope renogram was abnormal in 17 out of 21 patients, and in 4 patients there was delay in the excretory phase of the renogram despite an apparently normal intravenous pyelogram. Half of the patients studied had bacteriological evidence of urinary tract infection, and 11 out of 26 had varying degrees of anaemia; types of anaemia seen included haemolytic anaemia, sideroblastic anaemia and hypochromic anaemia. In general, the clinical picture in patients with a history of analgesic abuse was fairly non-specific, although there are several associations of signs and symptoms which now suggest that this diagnosis should be considered.

THE association between the abuse of analgesics containing phenacetin and chronic interstitial nephritis with renal papillary necrosis is now well established (Spuhler and Zollinger, 1953;Larsen and Moller, 1959;Nordenfelt and Ringertz, 1961 ;Reynolds and Edmondson, 1963;Dawborn et al., 1966; Prescott, 1966). Less well known is the oxidant effect of phenacetin causing acute hzemolysis in susceptible persons, notably those with red cell glucose-6-phosphate dehydrogenase (G6PD) deficiency (Houston and Barlow, 1959;Gilles and Ikeme, 1960;Harley, 1961 ;Harley and Robin, 1962; Dodion-Fransen, 1963). The combination of phenacetin intoxication and acute hzmolytic renal failure with subsequent papillary necrosis has not been reported. Finally, chronic ingestion of phenacetin has been shown to cause sideroblastic anzmia in a few patients (Dacie and Mollin, 1966), but this has not been described as a complication of acute analgesic overdosage.Case Report.-A 33-year-old West-Indian Negro male was admitted to another hospital in June 1969, 3 hours after taking 100 Codeine Compound tablets. As each tablet of Codeine Compound contains 250 mg. of Phenacetin, 250 mg. of Aspirin and 8 mg. of Codeine, a total of 25 g. of Phenacetin, 25 g. of Aspirin and 800 mg. of Codeine was ingested. Five months previously he had taken a small amount of the same type of tablet without any ill effects. He was not admitted to hospital on that occasion. In the past he had had occasional episodes of epigastric pain relieved by antacids,and headaches for which he took various analgesics, reputedly in small quantities. He had had no previous symptoms of loin pain, renal or ureteric colic or hsmaturia. There was no past history of any untoward reactions following drug ingestion by the patient or his family.On admission he was fully conscious, but depressed. He was neither anamic (Hb. 90 per cent, 13.3 g. per cent), nor icteric, and there were no abnormal physical findings. His urine was recorded as being " reddish " in colour. The blood urea and serum salicylate levels were not measured at this time. A stomach washout was performed on admission. This was followed by the intravenous infusion of 2 : litres of dextrose-saline over 24 hours combined with a single initial dose of 60 mg. of frusemide, which produced a good diuresis (Fig. 1). He remained well, normotensive and maintained a satisfactory urine output while receiving 3 litres of oral fluids daily. On the 3rd day he started vomiting and became oliguric. There was no response to an infusion of 500 ml. of 10 per ceid mannitol. At this time his blood urea was 109 mg./100 ml., his serum was stained deep brownish-red by methsnrdbumin and oxyhsmoglobin, and the serum salicylate concentration was 21 mg./100 ml. By the 4th day he was icteric and anuric, the hzmoglobin had fallen to 60 per cent (8.9 g. per cent) and the blood urea had risen to 174 mg./ 100 mi. Oliguric renal failure due to acute intravascular haemolysis was diagnosed and he was transferred to the

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