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Renal biopsies obtained from 20 adult patients within 30 days after onset of acute renal failure with microangiopathic hemolytic anemia ("the hemolytic-uremic syndrome") were studied. Lesions were graded independently by two observers without knowledge of the clinical history. All patients who did not have refractory hypertension were treated with heparin. Ten of the patients died, and four developed end-stage renal failure requiring chronic dialysis. Six patients, however, had a relatively good outcome: two recovered completely and four developed mild-to-moderate chronic renal failure not requiring dialysis. The six patients with a good outcome had significantly less severe arterial intimal thickening on biopsy compared with the remaining patients with a poor outcome. The patients with a good outcome and those with a poor outcome did not differ in the severity of glomerular lesions. The clinical features did not allow a prediction of late outcome. These results suggest that early renal biopsies may be helpful in predicting prognosis in the "hemolytic-uremic syndrome." This clinical syndrome may occur either in apparently healthy people, or may complicate the course of a chronic essential hypertension.

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A B S T R A C T Serum and urine from chronically uremic patients and normal individuals were subjected to gel filtration on Sephadex-G10. The effects of the eluted fractions on the uptake of urate and para-aminohippurate by isolated cortical tubules of rabbit kidney were investigated. According to the origin of the samples, one to three major groups of fractions inhibiting both urate and para-aminohippurate transport were disclosed. The first eluted group occurred for all the samples under study. The second one was demonstrated in both sera and urines from uremic patients but only in urines from normal individuals. The third one was exclusively detected in uremic sera and urines. Among all the compounds identified, only hippuric acid, eluted in the fractions of the second group, was capable of inhibiting the uptake of urate and para-aminohippurate in vitro. The concentration for which this inhibitory effect of hippuric acid occurred was in the range of that existing in uremic sera. Indoxyl sulfate, which accumulates to very high concentrations in uremic serum, could not be disclosed in the above-mentioned fractions. This is explained by the strong adsorption of this indole derivative to Sephadex gel. Potassium indoxyl sulfate, when tested in vitro at the concentration existing in uremic serum, substantially inhibited the uptake of both urate and para-aminohippurate. In normal subjects, ingestion of hippuric acid or potassium indoxyl sulfate significantly increased fractional urinary excretion of uric acid. On the basis of these results, it is suggested that progressive retention of hippuric acid, indoxyl sulfate, and other yet unidentified inhibitors may explain the gradual increase in urinary fractional excretion of urate This work was presented in part at a symposium on uremia sponsored by the International

We studied 11 patients who had visceral abscesses and in whom acute renal failure developed. All renal biopsies showed a diffuse proliferative and crescentig glomerulonephritis. In seven patients blood cultures were repeatedly negative. Endocarditis could be ruled out in six patients. Seven patients had circulating cryoglobulins; serum complement levels were normal in seven and decreased in four; circulating immune complexes were found in the three patients studied. The evolution of the glomerulonephritis, documented by serial biopsies, closely paralleled the course of the infection. A complete recovery of renal function occurred in four cases in which a rapid and complete cure of the infection was obtained. Of five patients in whom the infection was not cured, four died, and chronic renal failure developed in one. In two patients in whom therapy was delayed, chronic renal failure also developed. Deep suppuration, even in the absence of bacteremia, may be responsible for a severe but possibly reversible glomerulonephritis with circulating immune complexes.

Renal cortex slices were incubated with amine precursors L-dopa, or L-5-HTP. Localization of synthesized amines, dopamine or serotonin, was examined by means of histofluorescence methods. Formaldehyde-induced fluorescence was present in the proximal convoluted tubule and not in the pars recta or other segments of the tubules after incubation in the presence of 10(-3) to 10(-7) M L-dopa. Tubule-induced fluorescence was not seen in the presence of an inhibitor of dopa-decarboxylase or in the absence of sodium. It was independent of innervation. It is concluded that dopamine and serotonin are accumulated and likely formed within proximal convoluted tubular cells.

L’administration de thyrocalcitonine à I’homme normal détermine une excrétion rénale accrue de phosphates et de calcium. Le coefficient de réabsorption tubulaire des phosphates est diminué. Au cours d’une perfusion de phosphates, la thyrocalcitonine diminué la quantité de phosphates réabsorbés en méme temps que le coefficient de réabsorption tubulaire. Ces faits sont attribués à une diminution de la réabsorption tubulaire de ces deux ions, les variations de la filtration glomérulaire étant insuffisantes pour en rendre compte. L’excrétion rénale des ions H⁺ n’est pas modifiée de manière reproductible. Les mêmes résultats étant observés chez deux hypoparathyroïdiens et un hyperparathyroïdien, on en conclut que l’hyperphosphaturie est indépendante d’une modification de la sécrétion de parathormone. La connaissance des effets de la thyrocalcitonine sur l’excrétion rénale des phosphates doit intervenir dans l’interprétation des temps précoces des épreuves d’hypercalcémie provoquée.