Intially corticotropin (ACTH) and cortisone were used only to induce diuresis in children with the nephrotic syndrome, though occasional remissions were produced.1-7 Most of these early trials were of short duration and the amounts of drugs administered were small because of limited supplies and the occurrence of side-effects such as edema, hypertension, and hypokalemia. The demonstration that such changes could be prevented or minimized by means of diets rigidly restricted in sodium and high in potassium 8 enabled us and others 9,10 to undertake more prolonged administration of large amounts of corticotropin and adrenocortical steroids in the hope of influencing the course of the underlying disease. Materials and MethodsDuring the past five years we have treated a total of 106 instances of nephrotic syndrome in children. All had persistent and usually massive proteinuria on admission. Each patient was treated in essentially the same way, and no attempt was made to exclude those with hypertension, formed elements in the urine, or azotemia. Data on 30 of these children have been reported earlier.8 Seventytwo were initial attacks ; the remainder represented exacerbations. From the information in Tables 1A and IB it can be calculated that the mean age at which the initial episode of nephrotic syn¬ drome occurred in the group of 72 children was 4 years 4 months, with \y2 to 2y2 years the com¬ monest age of onset and a range of 4 months to 13 years 7 months in the remainder. There were more boys than girls, 45 versus 27, and the latter were somewhat older at the first manifestation (4 years 9 months versus 4 years 2 months). Symptoms or signs of nephrotic syndrome, or both, had been present for one week to four years prior to hospitalization for the first course of corticotropin, with a mean duration of 27 weeks. This interval was much shorter, averaging four weeks, in patients who developed an exacerbation while under observation in the dispensary. A his¬ tory of an infection prior to or coincident with the first episode of nephrotic syndrome was obtained in 40 of the 72 patients, with upper respiratory in¬ fection in 34, unexplained fever in 3, varicella in 2, and rubeola in 1 (Table 1A). In the 18 patients admitted one to six times with a total of 34 exac¬ erbations, recrudescence followed an upper re¬ spiratory infection in 12 instances, bronchitis in 1 and was unassociated with any recognized infec¬ tion in the remaining 21 (Table IB). Beta-hemo¬ lytic streptococci were isolated from nose and throat cultures in only a minority of the initial and the subsequent attacks, 12% and 6%, respec¬ tively.

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Reports describing trials of exchange resins in removing cations from the gastrointestinal tract of experimental animals have been limited to toxicity studies and to measurements of the relative magnitudes of the oral intake and the stool output (1-3). In the experiments presented in this paper changes in serum, urine, and stool components, as well as the external and internal balances of certain electrolytes and of nitrogen have been determined in dogs receiving a carboxylic cation exchange resin in one of two forms. The chemical and physical characteristics of these agents have been described in detail in the introductory paper (4). MATERIALS AND METHODSMongrel female dogs, maintained on a commercial feed ("Friskies") 1 and allowed free access to water, received a carboxylic cation exchange resin in the hydrogen or the sodium form for periods of seven to 11 days. In some instances beef extract or milk and sugar were used to enhance palatability, but many animals nonetheless lost weight partly or entirely as a consequence of anorexia induced by the regimens employed. Since this occurred to an equal degree when control and recovery periods of comparable length were alternated with resin periods it represented a common denominator in our experiments. The beginning and the end in each interval of the study were marked by catheterization of the urinary bladder, measurement of body weight and withdrawal of venous blood for analysis of blood nonprotein nitrogen (NPN) and sugar, and of serum carbon dioxide content, chloride, sodium, potassium, calcium, phosphorus and water, using previously described methods (5-7). The pH of anaerobic samples of serum was determined by means of the glass electrode. Food and resin intake, stool and urine output as well as any vomitus or rejected food were collected, measured, and analyzed separately for nitrogen, sodium, potassium and chloride content (8-10). Stools were removed from the cage and weighed immrediately. Procedures for partitioning the external balances into extracellular and cellular components have been described only in part in previous publications (11)(12)(13)(14)(15)(16)(17) and are therefore appended in detailed form.1 Content per 100 g.: Na, 17.6 meq.; K, 10.2 meq.; Cl, 162 meq.; and N, 3.42 g.With but minor exceptions all findings have been subjected to conventional statistical analyses (18). In the case of the body weight and the serum constituents values observed at the end of each control, experimental, or recovery interval were subtracted from those present at the start of the particular period under scrutiny and expressed as increments or decrements (±t A). After the means of these changes had been calculated (values greater than 2 S. D. were discarded) the resin and post resin values were compared with those of the control periods. Changes were considered significantly different statistically when "p" for the "t" test was 0.05 or less. Urinary and stool output and the balance data were analyzed in terms of per diem values.

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