We measured serum and urinary citrate, oxalate, calcium, and magnesium in 22 normal subjects and in 16 patients with malabsorption. The patients had subnormal levels of serum citrate and magnesium during fasting, subnormal 24-hour levels of urinary citrate, magnesium, and calcium, and excessive levels of urinary oxalate. Daily citrate excretion averaged only 15 per cent of normal. The hypocitraturia in the patients resulted from a subnormal filtered load of citrate and abnormally high net tubular reabsorption of the anion. An oral citrate supplement raised both the serum concentration and the filtered load of citrate to normal fasting values, but net tubular reabsorption remained abnormally high and urinary excretion abnormally low. Intramuscular magnesium sulfate, which corrected the hypomagnesemia and hypomagnesuria, had no effect on serum citrate or its filtered load. Nevertheless the injection restored net tubular reabsorption of citrate to normal and partially improved the hypocitraturia. Full correction of the hypocitraturia was achieved by combined treatment with oral citrate and intramuscular magnesium sulfate. Hypocitraturia may contribute to the formation of oxalate stones in these patients, and therefore our treatment may help to prevent this complication.

Several investigators have reported that hypocitraturia is frequent in patients with idiopathic kidney stones. In these studies, however, glomerular filtration rate, urinary tract infection, sex, diet, time of day, and medications, all potentially influential variables, were uncontrolled. Fifteen men, aged 30-52 yr, with recurrent idiopathic calcium oxalate stones and 15 normal age-matched men were studied. Patients with hyperparathyroidism, renal tubular acidosis, reduced creatinine clearance (less than 80 ml . min/1.73 M2), or urinary infection were excluded. Medications were stopped 2 weeks before the study began. A standard constant diet, furnishing 800 mg calcium and free of citrate, was fed for 20 days. During the last 10 days, 4.5 g sodium citrate were given orally. Eight-hour collections of urine were analyzed for calcium and citrate. Filtered load and net tubular reabsorption of citrate were also calculated. The 24-h urinary excretion of calcium was elevated in eight stone formers, and citrate excretion was depressed in seven. Five patients were both hypercalciuric anc hypocitraturic. The hypocitraturia resulted from excessive net tubular reabsorption of a normal filtered load of citrate. Urinary citrate was highest between 0800-1600 h, whereas calcium was highest between 1600-2400 h; both components were lowest between 2400-0800 h. The diurnal profiles of urinary calcium and citrate were similar in the stone formers and in the normal men. Oral sodium citrate did not influence urinary citrate in either group. These data suggest that in adult men, hypocitraturia may be a common predisposing factor for calcific nephrolithiasis.

Dietary protein and NaCl are the precursors of about 60% of the urinary osmoles (urea and NaCl). This investigation tested the hypothesis that in patients with dieabetes insipidus, intake of dietary protein and salt will directly influence the degree of polyuria. Four subjects with pituitary and one with nephrogenic diabetes insipidus were studied. All medications were discontinued. To provide diets ranging between "low-solute" and "high-solute," protein was varied in increments from 40 to 130 g/day and NaCl was varied simultaneously from 0.5 to 10 g/day. In all patients, each increment in protein and salt caused a prompt increase in 24-hr urinary osmoles in the form of urea, Na+, and Cl-. The 24-hr urine volume likewise increased progressively. Average increase in urine osmoles and volume from low- to high-solute diet was +224% and +127%, respectively. In four of the five patients, Reduction of protein/salt intake from habitual dietary at home to the recommedded daily allowance caused a 50 to 100% reduction in the magnitude of polyuria.

A B S T R A C T The effect of human growth hormone (HGH) on the N, P, Na, and K balance, and on the body weight (BW) of three groups of subjects was measured. In group I were nine cases (age 6-69) with HGH deficiency; in group II, eight cases (age 9-79) with normal endogenous HGH; in group III, four cases with myotonic dystrophy (age 45-51). After a 7 day control period, the hormone was administered for 7 days. Each subject was tested with three doses of HGH: dose A, 0.0168 U/kg BW"' per day; dose B, 0.0532 U/kg BW3'4 per day; dose C, 0.168 U/kg BW314 per day.In group I, the responsiveness to HGH declined with age. Two subjects aged 6 yr responded to all three doses of HGH with positive balances in N, P, Na, and K and increases in BW. At ages 15-17, responses were obtained only to doses B and C in three cases, and only to dose C in two cases. Two subjects, aged 42 and 69, responded only to dose C. Not only did the threshold dose increase with age in group I, but the magnitude of the responses declined with age as well.Patients of group II were less responsive to all doses of HGH than were patients of group I at comparable age. None responded to dose A or dose B. All responded to dose C, but the increments in balances and in BW stimulated by this dose were only one-third to one-half as great as in HGH-deficient subjects of similar age.Three patients of group III responded to all three doses of HGH, and one responded to doses B and C. The responses were similar in magnitude to those in the

A B S T R A C T Metabolic balance studies were conducted in seven boys with Duchenne-type muscular dystrophy, and in six normal boys of similar age, during a 12 day control period and during a 12 day period of treatment with human growth hormone (HGH) at the following doses: 0.0168, 0.0532, and 0.168 U/kg body weight (BW)f per day (doses A, B, and C, respectively). In five of the six normals, dose C caused positive balances in N, P, Na, and K; doses B and A had anabolic effects in two and one normal subjects, respectively. In six of the seven Duchenne cases, dose C caused negative balances of N and K, and sometimes of P. Negative balances were produced in three of the Duchenne subjects by dose B, and in one by dose A. None of the dystrophy cases exhibited an anabolic response to any dosage of HGH tested.The release of endogenous HGH in response to insulin, after 2 days' pretreatment with diethylstilbestrol, was similar in both groups of subjects. In the course of these tests, a marked anabolic effect of diethylstilbestrol in the Duchenne patients was apparent. Therefore metabolic balance studies were repeated, in both Duchenne and normal cases, during a 12 day control period and during 12 days of treatment with diethylstilbestrol (0.106 mg/kg BW1 per day). In three of the normal children, diethylstilbestrol had no effect on the elemental balances; in two cases, a retention of Na was observed. In all seven Duchenne cases, diethylstilbestrol caused positive balances in N. P, Na, and K. Ethinyl estradiol (0.0106 mg/kg BW1 per day) produced positive N, P, Na, and