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The incidence of neonatal HSV infection is approximately one case per 7,500 del iveries: The occurrence o f HSV infections in two infants born within a one-month period to mothers who had been living together in the same commune is highly unlikely to be fortuitous. HSV viruses were cultured from both infants and serotyping proved that they were of the genital type II. There is substantial evidence that this type is transmitted exclusively in adults through sexual contact? A likely explanation for our case would involve a common male source o f the virus, venereal transmission to the mothers in the third trimester near term, and the subsequent infection of the infants during parturition. Neither infant manifested signs or symptoms of a prenatal infection. There is reasonable clinical evidence o f in one mother (No. 1) a localized genital viral infection and in another mother (No. 2) a systemic viral illness presumably both from HSV within one month prior to the births of their children. The acquisition of HSV infection by the mothers must have occurred late in gestation, since infectious virus persists in the urogenital canal for on the average only 27 days in primary infection and for only 16 days in nonprimary infections. If the mothers shed viruses in their urogenital tracts at delivery, the infants had at least a 40% risk of becoming infected. ' The risks are significantly less if the mothers were infected earlier in gestation. Overall, only one in 28 infants born to mothers who have had HSV genital infection at some point in gestation will acquire neonatal disease? Thus, it is likely that our infants acquired their infection during parturit ion passing through an infected canal.

Systematic exclusion of all previously described causes of hypertension in children established idiopathic essential hypertension associated with suppressed plasma renin activity as an apparently distinct entity here reported for the first time in a child. Additional features of this condition include normal rates of excretion of aldosterone, normal levels of plasma aldosterone which were not suppressed in response to mineralocorticoid administration, and an abnormally low salivary sodium-potassium ratio.

Cefazolin has not been studied before in children with renal insufficiency. A single dose of 7 mg/kg was administered to 10 children (1½-16 yr) with varying degrees of renal impairment (Grp I), and to 10 children (7-14 yr) undergoing hemodialysis (Grp II). Serum half-life (T/2) in hours was calculated from disappearance curves and creatinine clearance was obtained (ml/min/1.73 m2). In Grp I one child had a ClCr of 57 ml/min and a T/2 of 4.8 hr. Three children with ClCr of 15-25 ml/min had a T/2 of 19-23 hr. Four children had a ClCr of 8-10 ml/min and had a T/2 of 29-40 hr. Two children with ClCr less than 5 ml/min had T/2 values greater than 58 hr. Normal adults have T/2 of 1.8-1.9 hr. Studies have shown adults with ClCr of 40-60 ml/min to have T/2 of about 5 hrs. Adults with lower ClCr had less prolongation of T/2 than did the children. The drug did not alter the tubular reabsorption of phosphate or the clearance of uric acid. In Grp II the T/2 was 8.25-29.5 hrs. A value of 6.5 hrs. has been reported for adults. The T/2 increased as the efficiency of dialysis, estimated by per cent reduction of BUN and creatinine, fell. T/2 of cefazolin is prolonged in children with renal insufficiency and the degree of prolongation is comparable to adults when the ClCr is only moderately reduced. As the ClCr falls further, the T/2 increases more among the children. T/2 for children on hemodialysis varies with the efficiency of dialysis. Supported in part by NIH grants RR-75 and RR-5624.

Renal blood flow has been measured in children of age 1½ to 16 years, by injecting 133Xe into the renal artery at the time of aortography or surgery. The rate of washout of radioactivity was monitored on magnetic tape and the resultant data analyzed by graphic analysis using a semi-automatic method of plotting and computing the rates and fraction of blood flow perfusing the outer and inner cortical regions of the kidney. The number, type, and results of the studies follows: 1) In 8 normal kidneys, RBF's were similar to adult values. 2) In 53 studies of RBF in children with congenital heart disease, RBF's were reduced in both cyanotic and acyanotic heart disease, were further reduced when heart failure was present (8 patients) and fell after angiography (19 patients). 3) Following renal biopsy drops in RBF may occur in intact kidneys, but not in the transplanted kidney (4 patients). 4)In chronic renal disease outer cortical blood flow is diminished. 5) 31 measurements of RBF in donor kidneys upon insertion and/or following transplantation suggest that this technique may have some value in predicting both the immediate and subsequent function of the graft. 6)In 5 patients with renal vascular hypertension, 133Xe measurements of RBF were helpful in determining secretory rates of renin in both kidneys. Supported NIH grants RR-75, RR-5624 and HE-12651.

The efficacy of ATG (ATGAMR-Upjohn Co.) in prolonging patient + cadaver renal allograft survival was studied in 21 patients,age 5 to 19 yrs receiving transplants from May 1977 to Oct.1979. Of the 9 patients randomly selected to receive ATG, 3 were given a fixed dose for the 28 day period of therapy; the daily doses of 3 were altered in relation to the percentage of rosette forming cells. Six of the selected patients received the full course of therapy; 1 patient had a positive skin test to ATG; 2 had untoward reactions to the first (and only) administered dose. Of those receiving ATG 1 had irreversible rejection 1 mo after transplantation, and 1 kidney was rejected after 3 mo. Three control patients experienced irreversible rejection within 1 mo, + 2 kidneys were rejected after 3 mos. All patients except 1 experienced threatened rejection episodes during the first mo. One patient died at 2 wks and 2 died within 1 yr after transplantation. All 3 were controls. The 5 treated patients with functioning allografts 4 mos to 2 yrs after surgery had creatinine clearances from 42 to 91 m1/min/1.73M2; 7 controls had clearances from 22 to 120 m1/min/1.73M2. Conclusions: Although the number of patients was very small, there appeared to be no correlation between patient and graft survival and ATG therapy. There was a correlation between graft survival and HLA matching.

Peritoneal dialysis was performed in 7 uremic children (4 months to 18 years). Rates of diffusion of Na, K, Cl, PO4, urea, creatinine, and uric acid were similar to adult diffusion curves. With the exception of uric acid diffusion, no age related differences were found. Peritoneal urea and creatinine clearnces paralleled the rate of exchage of dialysis fluid. Actual urea clearance values were within the range of clearance values obtained in adults dialysed at similar rates. Data to compare creatinine clearances in adults to children is not avialble over the range of dialysis volumes utilized in their studies. Estimation of urea production based on the average daily rise in BUN revealed similar production rates per kg body weight in all ages. These studies demonstrate no intrinsic age-related differences in the kinetics of peritoneal dialysis. Thus, there is no necessity to correct peritoneal clearances to cither 70 kg body weight or 1.73 M2, in order to compare children to adults. The greater ‘efficiency’ of peritoneal dialysis in children can be ascribed to a smaller body pool size in children relative to adults. Therefore, at a give clearance rate, the amount of material in the pool diminishes at a faster rate in children than in adults. Moreover, since peritoneal clearance increases as the rate of dialysis increases, no single clearance value for a given individual exists but rather a family of values related to the rate of dialysis. (Supported in part by NIH grants RR-5624. HD-2870 and FR-75.)