William A. Briggs

Influenza Vaccination in Kidney Transplant Recipients: Cellular and Humoral Immune Responses

Influenza infection in renal transplant recipients may cause either morbidity and mortality or acute allograft rejection; thus, routine annual influenza vaccination should be considered. We have studied the humoral and cellular immune responses to influenza virus antigens before and after trivalent vaccine administration in 13 patients and 16 control subjects. The patients, nine of whom were either on alternate-day or low-dose daily steroid therapy, showed highly significant serum hemagglutination-inhibition antibody responses to each influenza virus strain, There was no significant change in mean lymphocyte stimulation index to any influenza virus strain after vaccination in either group. There was no correlation in the patient group between hemagglutination-inhibition antibody titer or response, or lymphocyte stimulation index or response, and the degree of allograft function or dose or duration of immunosuppressive therapy. The vigorous antibody response and the evidence of cellular immunity support the efficacy of influenza vaccination in these patients.

Hypoxemia during Hemodialysis Using Acetate versus Bicarbonate Dialysate

To evaluate the extent and cause(s) of dialysis-related hypoxemia, we studied 10 patients, 7 days apart using acetate (AC) and bicarbonate dialysate (HCO3). We measured arterial blood gases, WBC, minute ventilation (VE) and inspired and expired gas concentrations and calculated the respiratory quotient (R) and the alveolar-arterial oxygen difference (A-a)DO2 before and during hemodialysis. 8 patients developed hypoxemia. Arterial PO2 (PaO2) dropped similarly at 30 min from 93 +/- 5 to 78 +/- 6 (p less than 0.05) and 89 +/- 4 to 79 +/- 5 mm Hg (p less than 0.05) with AC and HCO3, respectively. R and VE decreased during AC (p less than 0.05). (A-a)DO2 increased at 30 min and correlated with the drop in PaO2 during both AC (r = 0.68, p less than 0.025) and HCO3 (r = 0.76, p less than 0.025). The fall in PaO2 also correlated with the fall in WBC count for both AC and HCO3 (r = 0.63, p less than 0.005). The increase in arterial pH during HCO3 (up to 7.45 +/- 0.01) was significantly greater than that during AC (up to 7.42 +/- 0.01) (p less than 0.025), and coincided with a relative decrease in VE. We conclude that (1) HCO3 does not prevent hypoxemia, and (2) hypoventilation V/Q abnormalities and increase in arterial pH, contribute variably to dialysis related hypoxemia depending on the type of dialysate and the time during dialysis.

Comparability of Insulin Binding to Erythrocytes and Monocytes from Hemodialysis Patients and Healthy Subjects

Most studies relating alterations in insulin receptor binding to abnormalities of glucose tolerance in humans have used peripheral blood monocytes for the in vitro assay of insulin-binding kinetics. S

Immune-Complex Nephritis (ICN) with Hepatitis-Associated Antigen (HAA) in Chronic Hepatitis.

Excerpt Three patients with chronic hepatitis with either HAA or anti-HAA antibody and glomerulonephritis were studied to determine the relationship between these two disease processes. All had ele...

Glucose Tolerance, Insulin Release, and Insulin Binding to Monocytes in Kidney Transplant Recipients

In order to evaluate glucose tolerance following renal transplantation, intravenous glucose tolerance tests (IVGTT), with evaluation of hormonal responses to the intravenous glucose load and percent specific 125I-insulin binding to peripheral blood monocytes, were studied in eight clinically stable kidney transplant recipients. For comparison purposes, identical studies were done in eight control subjects and seven clinically stable hemodialysis patients. One transplant recipient was glucose intolerant, with fasting hyperglycemia, elevated HbA1C, and abnormal glucose decay constant. Impaired pancreatic insulin release appeared to be the major factor accounting for his glucose intolerance. The seven glucose-tolerant transplant recipients had significantly increased insulin release during IVGTT compared to control subjects, and significant correlations were found among insulin release, glucose decay constant, and fasting blood sugar in those patients. Insulin binding to monocytes was significantly greater in transplant recipients than control subjects due to an increase in insulin binding capacity per cell. A significant correlation was found between percent specific 125I-insulin binding and steroid dose, expressed as mg/kg body weight/day, in those patients. Thus, chronic steroid administration does not cause glucose intolerance in transplant recipients who manifest steroid-associated increases in pancreatic insulin release and cellular insulin binding capacity.