Evidence has been presented by several investigators that functional capacity of the kidney in the premature and young infant is lower than in older children and adults. Schoenthal (1) using urea clearance, McCance and Young (2) urea and inulin clearances, Barnett (3) inulin clearance, and

Earlier publications questioned the reliability of measurements of renal plasma flow in young infants, since the extraction ratios for para-aminohippurate (EPAH) used were those obtained in adults (1-3). It was suggested that the use of these high values for EPAH to determine renal plasma flow and filtration fraction might not be valid and could account for the high filtration fraction reported in infants under a year of age (1)(2)(3)(4)(5). This high fraction was interpreted to indicate that the rate of glomerular filtration is greater in comparison to renal plasma flow than that in adults. The present study was designed to measure EPAH in young infants in order to arrive at the true value for renal plasma flow and calculated filtration fraction. METHODSFifteen children between 8 days and 10 years old were studied; eight were under 3 months, and seven between 5 months and 10 years old. Pertinent clinical and laboratory data are listed in Tables I through IV. Forty-five minutes before testing, eight of the fifteen patients were given a sedative; ' five were infants (no. 1 and 5-8) and three were older children (no. 10, 11, and 15). Inulin2 and para-aminohippurate (PAH) were administered in normal saline or 5% dextrose in water after base-line control venous blood determinations were made. The diluent and the intervals from the mixing of PAH with the diluent to the end of the test are recorded in Tables II and III. Saline as the diluent for the PAH injection was used in four infants and in two children. Five per cent dextrose in water was the diluent in four infants and in seven children. Two infants and two children were I Chlorpromazine, 6.25 mg per ml; promethazine, 6.25 mg per ml; and meperidine hydrochloride, 25.00 mg per ml. The dose was 1 ml per 20 pounds of body weight, up to a maximum of 2 ml.2 Kindly supplied by the General Diagnostics Division, Warner-Chilcott Laboratories, Morris Plains, N. J. studied with both diluents. All blood samples were collected in heparinized tubes. Inulin and PAH were given to maintain arterial blood concentrations above 25 mg per 100 ml for inulin and below 4 mg per 100 ml for PAH. These values were not always obtained, but in the four infants given PAH in normal saline, the level of renal arterial PAH was over 3.1 mg per 100 ml in only one period of Patient 1. A no. 10 French catheter was placed in the bladder for urine collections. The femoral artery and vein were catheterized with Birds Eye catheters no. 5, 6, or 7. Under direct fluoroscopic supervision, the right renal vein was entered, and an attempt was made to enter the right renal artery; if it was unsuccessful, arterial blood samples were obtained from the aorta close to the renal artery. Spot films were taken to demonstrate the location of catheters before collections were made. Measurements of glomerular filtration rate and effective renal plasma flow measurements were made in three infants and in one older child. Complete emptying of the bladder was obtained by instilling air, and blood was withdrawn simultaneo...

The majority of infants who were prescribed antireflux drugs did not meet diagnostic criteria for gastroesophageal reflux disease.

SUMMARY Early differences in hemodynamic variables and vasoactive substances between progeny of hypertensive and normotensive parents were sought in normotensive children aged 10-17 years. Forty-two black and 34 white children of hypertensive parents (cases) and an age-balanced group of 20 black and 45 white children of normotensive parents (controls) underwent exercise stress testing. Blood pressure, heart rate, urinary electrolytes, kallikrein, and prostaglandin E-like material, plasma renin activity, and norepinephrine were measured before, during, and after exercise. Analyses compared the findings of four subject groups: black cases with black controls, white cases with white controls, black cases with white cases, black controls with white controls. Based on a family history of hypertension, significant familial differences were found: Black cases "were larger" (p = 0.003) when compared to black control subjects and had higher resting systolic, dlastolic, and maximum exercise diastolic blood pressures, and higher postexercise plasma renin activity (p = 0.04); white cases also were larger (p = 0.004) in comparison with white controls and had higher postexercise heart rates, higher preexercise urinary prostaglandin E-like material, and lower plasma norepinephrine after exercise (p < 0.05). Significant racial differences were noted in heart rate, blood pressure, urinary electrolytes, and other biochemical substances. Among the cases, black/white comparisons showed that blacks had lower postexercise heart rates, and higher resting and maximum exercise systolic and diastolic blood pressures (p < 0.04 for these comparisons). Additionally, blacks had higher preexercise urinary sodium excretion, lower preexercise urinary potassium excretion (p < 0.003), and lower plasma renin activity before and after exercise (p < 0.003). Finally, urinary kallikrein excretion before and after exercise was lower in blacks (p < 0.03). While blood pressures were similar among the black and the white controls, comparisons revealed that the blacks had higher preexercise sodium and potassium excretion (p < 0.005), lower plasma renin activity at all levels of activity, and lower plasma norepinephrine 10 minutes after exercise (p < 0.05). Thus, significant intraracial and interracial differences in physiological and biochemical variables, thought to be related to the development of hypertensive diseases, have been detected in normotensive children categorized according to a family history of hypertension. With use of these variables, the black case children can be separated from the other three groups and may have increased risk for the development of adult onset hypertension. 57Considerable information has been published concerning the familial aggregation of hypertension. Paffenbarger et al. 5 in 1968 reported that a parental history of hypertension was correlated with the development of the disorder in youths followed into later years. Familial aggregation of blood pressures through childhood was established by Zinneretal. 6 in 1971. ...

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