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A white Bengal tiger was determined to have a central retinal lesion and a central visual defect. Because of the known association between feline central retinal degeneration (CRD) and taurine deficiency in domestic cats, plasma concentrations of taurine were measured in this tiger. Serum concentrations of taurine, methionine, and cystine also were measured in white Bengal tigers, orange Bengal tigers, taurine-sufficient domestic cats, and taurine-deprived and tissue-taurine-depleted visually impaired cats with CRD. Hepatic and brain enzymes responsible for taurine synthesis were identified in tissue specimens from an orange Bengal tiger. Serum taurine concentrations were lower in white vs orange tigers, but were not as low as those in cats with CRD. Thus, we concluded that taurine depletion did not account for the central retinal lesion in the white Bengal tiger.

The beta-amino acid transport capabilities of rat renal epithelium were assessed using brushborder membrane vesicles (BBMV). Taurine, a metabolically inert sulfur-containing amino acid, was studied with emphasis on the renal adaptation to dietary sulfur amino acid alteration. Three isoproteinic diets were given to Sprague-Dawley rats: low-sulfur-amino-acid diet (LTD), normal-sulfur-amino-acid diet (NTD), and high-taurine diet (HTD). Our studies demonstrated that taurine is actively transported into membrane vesicles by a sodium-dependent transport system. This transport is enhanced by hyperpolarization with valinomycin and decreased by dissipation of the sodium gradient by gramicidin. On LTD (compared to NTD), plasma taurine, urinary taurine, and fractional excretion of taurine were reduced. On HTD (compared to NTD), plasma taurine, urinary taurine, and fractional excretion of taurine were elevated. In vitro studies in BBMV from NTD animals revealed a Km of 40 microM and Vmax of 102 pmoles/mg protein/30 sec. Other beta-amino acids significantly inhibited BBMV taurine accumulation. BBMV taurine uptake was enhanced after LTD (compared to NTD) and diminished after HTD (compared to NTD). These studies indicate that a renal adaptation to dietary alterations in sulfur-containing amino acids occurs and that the luminal brushborder membrane participates in the adaptation. Renal adaptative mechanisms to dietary change may serve to help conserve amino acids during deprivation and to excrete amino acids during periods of excess.

This study examines the effect of a low sulfur amino acid diet (LTD) and a high taurine diet (HTD), compared with a normal diet, on the plasma, urine, muscle, brain and renal cortex levels of taurine in immature and adult rats. Milk taurine from lactating dams reflected the taurine content of the diet, being low in LTD-fed and high in HTD-fed animals. Nursing pups (7, 14 and 21 d old) often had plasma, urine and tissue--renal cortex, heart, skeletal muscle--levels of taurine related to dietary exposure, a situation also found in adult animals. These diets did not influence the urinary excretion of the sulfur-containing alpha-amino acids methionine and cystine but a sulfur aminoaciduria of immaturity was evident. By contrast, the content of taurine in brain was constant regardless of dietary intake of sulfur amino acids. An age-related decline in brain taurine content was found--as noted by others--but this too was influenced by diet. This dual finding of brain taurine constancy despite wide differences in sulfur amino acid intake and changes in the renal handling of taurine as influenced by diet suggest that the renal adaptive response serves to maintain the stability of brain taurine content.

The abdominal muscle deficiency syndrome ("prune belly syndrome"(, a symptom triad of aplasia of the abdominal wall musculature, malformations of the urinary tract, and cryptorchism, is described from the urologist's point of view, citing nine cases. With modern diagnostic procedures the early detection of the correct diagnosis in the usually very young patients is possible. While the urologic symptomatology is due to the malformations in the urinary tract, the life expectancy depends mainly on the degree of renal function impairment. Combat of infection together with proper operative repairs are the treatments of choice to date. Instrumental procedures should be limited as much as possible. The survival changes following kidney transplantation appear promising.

Serum-1,25-dihydroxyvitamin-D3 (1,25-[OH]2D3) was subnormal in children receiving long-term glucocorticoid treatment for various glomerular diseases, including nephrotic syndrome. In children with chronic glomerulonephritis not treated with glucocorticoids who had similar serum-creatinine with glucocorticoids who had similar serum-creatinine concentrations, serum-1,25-dihydroxyvitamin-D3 concentrations resembled those in healthy controls, indicating that glomerular renal disease per se does not account for reduced serum-1,25(OH)2DE concentrations in steroid-treated patients. The reduction in concentration of this most active vitamin-D metabolite correlated with the dose of steroid administered and with reduction in forearm bone mineral content measured by the photon absorption technique. Reduced serum-1,25-(OH)2D3 concentration may be important in the pathogenesis of steroid-induced osteopenia.

Secondary oxalosis is a complication of renal failure. Since oxalate is excreted by the kidney, the severity of oxalate deposition has been directly related to the duration of renal failure. We report a patient with acute renal failure on hemodialysis who received daily ascorbic acid (an oxalate precursor) via parenteral alimentation. He developed widespread secondary oxalosis, which was especially prominent in the kidneys and pancreas. This oxalate burden may have contributed to the complications seen during his hospital course. The provision of ascorbic acid to patients with renal failure should be carefully monitored to avoid accelerated development of secondary oxalosis.

A boy aged 4.5 years with prune-belly syndrome and associated urethral stenosis, oligohydramnios, imperforate anus and vesicosigmoid fistula is described. In contrast to the anticipated poor prognosis, vesicostomy and divided transverse colostomy performed after birth followed by prophylaxis of infection and bicarbonate supplementation have resulted in a good outcome. The vesicosigmoid fistula might have served in utero as a "natural diversion" protecting from pressure-induced renal damage. It is suggested that the main determinant of prognosis in PBS is the presence and degree of kidney dysplasia at birth as reflected by the neonatal renal function after performance of an indicated urinary diversion procedure rather than the presence of severe associated anomalies.

Vitamin D2 or D3 are prohormones that are converted in the liver and kidney to three metabolites, all having biological activity. the most prevalent circulating metabolite is 25(OH)D, and when its level falls, osteomalacia and rickets result. The second most prevalent metabolite is 24,25(OH)2D which may be a mineralizing hormone and which may impair PTH secretion, although wide controversy prevails over its function. Calcitriol circulates at levels a thousand-fold less than 25(OH)D and is the most active metabolite in terms of calcium absorption from the gut and mobilization of calcium and phosphate from bone. Clinical defects in this system result from abnormalities of vitamin D metabolism or from end-organ resistance to these hormones. Many disorders of demineralization can now be understood more clearly, and treated with a greater understanding of the underlying pathophysiology. Nonetheless, many new questions about the role of various vitamin D metabolites have now arisen.

Isolated renal tubules were prepared from newborn and adult Sprague-Dawley rats. They were used to study the uptake and accumulation of the beta-amino acid, taurine, by renal epithelium. Initial rate as well as steady-state kinetics were studied. Initial rate studies revealed heterogeneity of uptake in newborn and adult tubules. Slower uptake was present in the newborn in the low-affinity system. Slowed efflux was found in neonatal tissue. Newborn tubules in contrast to adult tubules demonstrated uptake under anaerobic conditions. Adult and newborn tissues showed decreased uptake of taurine when incubated with beta-alanine. Physiologic taurinuria, be it in the rat or man, may be due to less rapid initial uptake and/or efflux from ren in neonatal tissue. Newborn tubules in contrast to adult tubules demonstrated uptake under anaerobic conditions. Adult and newborn tissues showed decreased uptake of taurine when incubated with beta-alanine. Physiologic taurinuria, be it in the rat or man, may be due to less rapid initial uptake and/or efflux from ren in neonatal tissue. Newborn tubules in contrast to adult tubules demonstrated uptake under anaerobic conditions. Adult and newborn tissues showed decreased uptake of taurine when incubated with beta-alanine. Physiologic taurinuria, be it in the rat or man, may be due to less rapid initial uptake and/or efflux from renal epithelium.

Renal cortex slices from newborn, 2-week, and 4-week-old Sprague-Dawley rats had reduced initial rates of taurine uptake compared to adult slices after short (less than 30 min) incubation periods. From birth onward, steady-state accumulation occurred by at least two sodium-dependent uptake systems. The first system had an "apparent Km1" = 0.1 mM and a Vmax varying from 1.8 to 5.1 mumoles/ml ICF/120 min at four ages. The second uptake mode had an apparent Km2 = 12-16 mM and a Vmax of 45 mumoles/ml ICF/120 min. Efflux of taurine was reduced in slices from younger animals possibly accounting for taurinuria. Only other beta-amino acids inhibited accumulation. Anoxia inhibited uptake at high concentration ( greater than 1.0 mM) at each age, but taurine accumulation at low concentrations ( less than 0.4 mM) was relatively protected from anoxia in neonatal ( less than 36 hr of age) tissue. Preincubation in taurine-free medium for 120 min enhanced low concentration, but not high concentration uptake in neonatal and 2-week slices. After preincubation in dibutyryl cyclic AMP (dbcAMP) enhanced uptake of taurine was found in adult cortex, but not in neonatal cortex. The ontogeny of renal taurine transport in cortex slices appeared to involve faster initial uptake rates and faster efflux as well as greater dependence on aerobic metabolism with maturation. Age-related differences in the response to preincubation and cyclic nucleotides were also indicative of maturation events in renal tubular amino acid transport.

Twenty-two women aged 13 to 44 years (mean, 22 years) with toxic shock syndrome (TSS) were hospitalized in Madison, Wis, between Aug 1, 1977, and Sept 1, 1980. Disease onset occurred during menses in 21 patients; all recovered. Notable sequelae included vocal cord paralysis and impaired finger sensation in two patients and recurrent disease in three. Coagulase-positive staphylococci were grown from the cervix or vagina in 11 of 12 women cultured. Previously undescribed features included vulvar cellulitis, hypocalcemia, hypophosphatemia, hypocholesterolemia, hyponatremia, lymphocytopenia, hypoferrinemia, and late convalescent hair and nail loss. Patients requiring dopamine hydrochloride had worse renal function, longer hospitalizations, and higher total serum bilirubin levels, and clinical onset earlier in menses. Originally reported in children, TSS now appears to be primarily a disease of menstruating women in whom recurrences are possible.

Serum 25-hydroxyvitamin D (25-OH-D) and 1,25-dihydroxyvitamin D (1,25-(OH)2D) and bone mineral content by the photon-absorption technique were determined in eight patients with X-linked hypophosphatemic rickets treated for at least 24 months with oral sodium phosphate and high-dosage ergocalciferol (vitamin D2). Mean 25-OH-D2 level was 129.5 +/- 67.5 ng/mL (mean +/- SD); the level of 25-OH-D3 was 10.5 +/- 5.8 ng/mL. These values were significantly higher than in normal subjects (total 25-OH-D mean of 27 +/- 10 ng/mL). Serum 1,25-(OH)2D was 16.9 +/- 8.5 pg/mL (mean +/- SD) in the eight patients, significantly lower than 47 +/- 16 pg/mL in 27 age-matched controls. Values indicative of significant demineralization were found in seven of the eight phsophate-treated patients, who had no radiologic evidence of rickets. These results suggest that any theory of the pathogenesis of this disorder must account for inappropriate renal vitamin D metabolism and for renal hyperphosphaturia. The failure of high-dosage oral phosphate and ergocalciferol to fully correct demineralization may suggest a role for calcitriol (1,25-(OH)2D3) as a therapeutic agent.

In 10 patients with renal tubular acidosis, seven with type I and three with Fanconi syndrome, simultaneous measurements of vitamin D metabolites and electrolytes were made. No marked abnormalities of calcidiol2, calcidiol3, 24,25(OH)2D, or calcitriol were found in these patients, whose mean serum HCO3 was 18 +/- 3 mM/L (SD). Further, no relationship between serum HCO3 and calcitriol could be found. These results suggest that either vitamin D deficiency may be required before any alterations in the production of calcitriol are seen, or that the effects of acidosis in animals may not be reflected in humans. Further, it appears less likely that the bone disease found in renal tubular acidosis is related to abnormalities in vitamin D metabolism resulting from systemic acidosis, but that bone disease is more likely related to the acidosis and hypercalcuria prevalent in this disorder.

Rickets, hypocalcemia, hypophosphatemia, and hyperparathyroidism were found in a low-birth-weight premature infant. The concentration of plasma calcitriol (1,25-dihydroxyvitamin D) was 145 pg/mL. With additional exogenous calcitriol (37.5 ng/kg/24 hr) given for eight weeks, the biochemical abnormalities were corrected and healing of rickets was evident. Three months later, while receiving only 400 IU of ergocalciferal daily, the patient had normal levels of serum calcium, phosphate, and alkaline phosphatase with a serum calcitriol concentration of 36 pg/mL. These observations suggest that rickets of prematurity may involve a malabsorption of calcium and phosphorus with an elevated calcitriol level needed to overcome this inadequate absorption. Additional doses of calcitriol may be of benefit in these infants, although it must be given carefully. Furthermore, the role of phosphate supplementation in these infants requires consideration.

Children with acquired glomerular disease were divided into two groups: Group 1 patients received short-term daily or long-term alternate-day prednisone (up to 2.7 mg/kg/48 hr); group 2 patients received no corticosteroids. Height, bone mineral content (BMC), and bone density were evaluated in the two groups and compared to those of 800 sex- and age-matched controls; BMC and bone density were assessed by the photon absorption technique. Significant demineralization was present in 18 of 25 prednisone-treated and none of the 17 nonprednisone-treated patients (P less than .001). Group 1 patients were 5.3 +/- 0.7% shorter than controls, while group 2 patients were only 1.9 +/- .8% shorter (P less than .02). Height velocity was 2.6 +/- 0.8 cm/yr in group 1 and 5.1 +/- 0.8 cm/yr in group 2 patients (P less than .05). When prednisone therapy was discontinued, six patients had an increase in height and BMC toward normal values. This study suggests that BMC and height velocity are correlated. Both appear to be influenced by alternate-day prednisone therapy rather than by glomerular disease per se.

Hypocalcemia is a common finding in TSS. This has been causally related to the hypoalbuminemia of TSS. To more clearly define the mechanism responsible for this hypocalcemia, we examined the serum concentrations of CaT, Ca+ +, iCT, albumin, and DBP in 28 women meeting the case-study definition of TSS. Mean CaT was 2.18 +/- 0.36 mM/L (S.D.), Ca+ + was 0.93 +/- 0.19 mM/L, and iCT was 1941 +/- 978 pg/ml; all were significantly different (p less than 0.01) from the normal values of CaT (2.38 +/- 0.09), Ca+ + (1.09 +/- 0.04) and iCT (less than 30 to 135). A significant inverse correlation was found between iCT and both CaT and Ca+ +, p less than 0.001. Serial values were measured in two women in whom the iCT values declined each day. Gel filtration of the iCT from two patients with the highest values suggested that some polymeric molecular species, rather than authentic CT, accounted for 90% of the circulating iCT value. No abnormalities of DBP levels were found, and no correlation with CaT, Ca+ +, or iCT was evident. The hypocalcemia of the TSS represents a reduction in both CaT and Ca+ + concentrations, which may be at least partially accounted for by the elevated iCT concentrations.

Eight children with acute leukemia in relapse were hypokalemic during their hospital course. All had accompanying hypophosphatemia, and three had mild metabolic alkalosis. Potassium chloride supplementation in each case resulted in resolution of the electrolyte and acid-base disturbances. These findings were not present in patients with conditions newly diagnosed or those in remission. The pathogenesis of the electrolyte and acidbase disturbances was not evident and was not related to antibiotic or cytotoxic drug therapy, but may have been related to the patients' poor nutritional status. Seven of the eight patients died within six months of the hypokalemic episode. Hypokalemia may be a common accompaniment of terminal leukemia.

Taurinuria is characteristic of the immature rat. The excessive taurine loss could be the result of brush border or basal lateral membrane immaturity. The beta-amino acid, taurine, and D-glucose were examined using isolated brush border membrane vesicles (BBMV), slices and tubules prepared from 28-day-old rats. In BBMV, taurine accumulation was inversely proportional to osmolarity, indicating uptake rather than binding, and taurine accumulation was Na+-dependent. BBMV from 28-day rats did not accumulate D-glucose to the same degree as in adult BBMV, and the initial rate of uptake was slower. Taurine uptake had a similar Km and Vmax in BBMV from immature rats. Despite similarities in the kinetics of taurine uptake, higher urinary taurine concentrations are found in younger rats. The efflux of taurine from slices and tubules was much slower than in adults and probably accounts for the taurinuria of young animals. A diet low in methionine and taurine (LTD) given for seven days resulted in a lower excretion and fractional excretion of taurine than in animals fed a normal sulfur amino acid diet (NTD). A high-taurine diet (HTD) causes excessive taurinuria. These patterns of excretion are reflected at the brush border membrane surface with greater uptake after the LTD and reduced uptake after the HTD. A kinetic analysis of adult and 28-day-old animal BBMV reveals that the Vmax of accumulation is altered by diet, whereas the Km remains unchanged. The Vmax is higher in BBMV from LTD animals and lower in BBMV from HTD animals.(ABSTRACT TRUNCATED AT 250 WORDS)

Human milk has been found to contain 40 to 50 IU/l of vitamin D activity. This was determined by measuring stimulation of intestinal calcium transport in the rat, an assay not subject to the errors inherent in the rat line test or calcification assay. Five vitamin D metabolites were then isolated using a combination of conventional chromatography on Sephadex LH-20 and Lipidex 5000 followed by high-performance liquid chromatography. 24,25-Dihydroxyvitamin D and 1,25-dihydroxyvitamin D were measured using binding protein assays and were found to be present at very low levels. These dihydroxylated metabolites do not contribute significantly to the total vitamin D activity. Vitamins D2 and D3 were found to be present at concentrations of 338 and 41 ng/l, respectively. This is equivalent to 14 to 16 IU/l of vitamin D activity. Human milk contains 163 ng/l of 25-hydroxyvitamin D3, which gives about 33 IU/l of vitamin D activity. Thus 25-hydroxyvitamin D3 accounts for about 75% of the biological activity observed in the calcium transport assay. Vitamin D2, vitamin D3, and 25-hydroxyvitamin D3 are responsible for more than 90% of the total vitamin D activity present. This fails to support the idea that vitamin D-sulfate or any other unknown metabolites of vitamin D provide significant vitamin D activity in human milk.

Glucocorticoids have been used extensively in the management of patients with renal disease. The beneficial effect of glucocorticoids on renal disease is probably mediated via the suppression of immune function, although some evidence exists for a direct influence of corticosteroids on glomerular function. A myriad of glucocorticoid complications have been reported, including: skin, eye, bone, blood and adipose tissue changes, as well as growth retardation, hypertension and an increased susceptibility to infection. A review of the efficacy of glucocorticoid use demonstrates benefit in a small number of glomerulonephritides (minimal change nephrotic syndrome, systemic lupus erythematosus, polyarteritis nodosa and renal transplantation). Since being introduced in the early 1950s, glucocorticoids have proven to be of limited usefulness in the treatment of glomerulonephritis.

A temperature-sensitive Escherichia coli mutant defective for the ability to utilize L-asparagine as a sole nitrogen source was isolated after N-methyl-N'-nitro-N-nitrosoguanidine mutagenesis. The mutation (asu) produces two distinct phenotypic effects. Mutant strains grow poorly at high temperature on minimal plates containing asparagine as the sole nitrogen source; this effect is greatly exacerbated by the presence of methionine. Mutant strains utilize L-asparagine as a nitrogen source three to four times more efficiently at permissive temperatures than the wild-type strains. The mutation maps at 32.4 min on the E. coli chromosome, within the E. coli cotransduction gap. Mutant strains produce normal amounts of thermo-stable L-asparaginase I activity. The mutation therefore affects a component of the asparagine utilization system other than the catabolism of asparagine within the cell; it probably affects asparagine uptake.

Analysis of the Tc-99m-DTPA renogram is usually limited to calculating the relative function of each kidney. To develop a method to determine the absolute glomerular filtration rate (GFR), various methods of analyzing the renogram were examined to determine which gave the best correlation with GFR. That regression could then be used to predict GFR without the need for blood samples. Fifty children were studied using Tc-99m-DTPA renograms and GFR measured simultaneously by plasma disappearance. The renogram variables were adjusted for detector sensitivity and for dose divided by weight, which was used as an index of plasma concentration. GFR correlated better with the slope of the second phase than with the area under the renogram curve. For the best correlation with GFR (using background subtraction and depth correction) r = .971 and the mean residual = 4.8 ml/min. For GFR normalized for body surface area (using background subtraction and no depth correction) r = .954 and the mean residual = 9.1 ml/min/1.73 m2. This method can accurately estimate GFR from the renogram in children.

In psoriatic arthritis, trauma to joints may be important in determining the site of joint involvement. We describe a child with a psoriatic arthritis in whom penetrating injury with a rose thorn led to a localized chronic synovitis which could not be distinguished clinically from psoriatic arthritis but which was effectively treated by synovectomy and removal of the remaining thorn.

Twenty-three women of ages 13 to 44 years were hospitalized with illnesses fulfilling the criteria of the case definition for the toxic-shock syndrome (TSS) associated with coagulase-positive staphylococci. Disease onset occurred during menses in 22, and all were oliguric when admitted. Prolonged hypotension and a reduced central venous pressure were common features. Measurements of urine volume and creatinine clearance in eight patients identified two types of acute renal failure, oliguric and nonoliguric, and prerenal azotemia related to intravascular volume depletion. Urinary sodium excretion and measurement of the renal index (UNa divided by U/PCr) provided further support for the presence of both prerenal and intrinsic renal failure. Hemodialysis was required in one patient in whom findings on renal nuclide scan were consistent with acute tubular necrosis. Pyuria was frequent, but proteinuria and more than five erythrocytes per high-power field were infrequent. Other features included initial hyponatremia and the combination of hypoproteinemia, hypoalbuminemia, hypocalcemia and hypophosphatemia of several days' duration. The hypoalbuminemia was believed to be due to exudation of protein from the intra- to the extravascular space. The hypoalbuminemia was believed to be due to exudation of protein from the intra- to the extravascular space. The hypocalcemia was probably related to the hypoalbuminemia. The pathogenesis of hypophosphatemia in the presence of acute renal failure is unclear. Following the intravenous administration of colloids, fluids and, in seven patients, dopamine, all recovered from the acute illness.

Taurine is the major free intracellular amino acid. It has become the focus of study by many as a conjugator of bile and as a neurotransmitter and intracellular messenger. In this report we document a technique for measuring taurine in physiologic samples which is rapid, reproducible, and accurate. Any physiologic sample is first derivatized with phenylisothiocyanate (PITC) and separated by reverse phase HPLC, and then taurine is detected by UV at 254 nm. The advantages of this technique for the measurement of taurine are accuracy, small sample size, and reproducibility, and with an automated system many samples can be analyzed.

Vitamin D ingested in excess results in hypercalcemia, which is caused by excessive absorption of massive quantities of calcium by the intestine and enhanced bone resorption. The symptoms of this intoxication include feeding difficulties, polydypsia, polyuria, irritability, lassitude and poor weight gain. Because daily intakes of 400 IU (10 microg) of vitamin D2 or D3 are completely safe, and because as low as 100 IU (2.5 microg) daily may prevent rickets, it is difficult to justify recent studies that attempt to firmly establish an upper limit of daily vitamin D intake in the normal neonate. Thus, despite efforts to better understand the upper limits of daily vitamin D intake, a concentration of 100 IU (2.5 g) of vitamin D per 100 kcal ingested, as is currently recommended by the Committee on Nutrition of the American Academy of Pediatrics, seems entirely appropriate.

We evaluated oral 1,25-vitamin D3 for as long as 26 months in six prepubescent children with renal osteodystrophy previously treated with vitamin D2. Therapy was given at 14 to 41 ng per kilogram per day to correct hypocalcemia and reverse bone disease. Serum levels of 1,25-vitamin D3 were initially reduced at 15 +/- 5 pg per milliliter (mean +/- S.E.M.) and after treatment rose to 54 +/- 13. Serum calcium rose from 7.5 +/- 1.6 mg per deciliter (mean +/- S.D.) to 9.8 +/- 0.6 after one month (P less than 0.02). Alkaline phosphatase activity fell from 536 +/- 298 to 208 +/- 91 IU per liter after 12 months (P less than 0.05). Serum immunoreactive parathyroid levels fell from 900 +/- 562 microliter eq per milliliter 411 +/- 377. Healing of rickets and subperiosteal erosions was found. Remineralization of bone was demonstrated by the photon absorption technic. In four patients growth velocity, evaluated for 12 months before and after therapy, increased from 2.6 +/- 0.8 to 8.0 +/- 3.2 cm per year. Growth velocity per year increased from less than third percentile in each to the 10th to 97th percentile after therapy. Height increment ranged from 27 to 113 per cent of that expected for change in chronologic age and 40 to 114 per cent expected for change in bone age after therapy. This trial demonstrates that oral 1,25-vitamin D3 can reverse renal bone disease and increase growth in uremic children.

Little information is available on the optimal management of toxic shock syndrome and on its sequelae. The most appropriate antibiotic treatment, the efficacy of colloid infusions, and the potential role of gamma globulin preparations have not yet been completely ascertained. Coagulase-positive staphylococci associated with toxic shock syndrome had minimal inhibitory concentrations of 0.06 microgram/mL or less to rifampin, 0.25 microgram/mL or less to gentamicin, and 0.50 microgram/mL or less to both nafcillin and clindamycin. In the 36 patients studied abnormal chest roentgenograms were commoner in those who had received albumin than in those who had not. Radioimmunoassay showed antibody titers to staphylococcal enterotoxin F, a marker protein in toxic shock syndrome, of 1:4000 or more for intravenous gamma globulin (12/15 lots) and 1:40 000 or more for intramuscular gamma globulin. Major sequelae of toxic shock syndrome include late-onset rash, compromised renal function, cyanotic extremities, and prolonged neuromuscular abnormalities.