Improved Late Graft Survival and Half-Lives in Pediatric Kidney Transplantation: A Single Center Experience

We evaluated variables associated with improved late graft survival in 290 children transplanted between 11/1/1984 and 12/31/1997, and who had > 1 year graft survival. We studied the following variables: age, gender, race, primary disease (diseases prone to recurrence, i.e. hemolytic uremic syndrome, focal segmental glomerulosclerosis or oxalosis vs. others), primary vs. retransplant; donor source, acute tubular necrosis, acute rejection episodes in the first year, transplant era and discharge serum creatinine. Graft half-life was defined as the time taken for 1/2 of the grafts functioning at 1 year to fail. There were 205 living donor and 85 cadaveric transplant. The cumulative graft survival at 5 and 10 years was 88% and 75% for living donor, and 72% and 46% for cadaveric, respectively. Multivariate analyses showed a higher late graft survival to be associated with: no acute rejection episodes (risk ratio 0.16, p = 0.0001), age 2-5 years (risk ratio 0.24, p = 0.0007), living donor (risk ratio 0.46, p = 0.017), primary nonrecurrent disease (risk ratio 0.29, p = 0.001), Caucasian race (risk ratio 0.40, p = 0.006). A high half-life was seen with living donor transplant (21.3 years) and the age group 2-5 years (27.5 years). Further, living donor patients with no acute rejection episodes had the best half-life of 37.6 years, while children with hemolytic uremic syndrome, focal segmental glomerulosclerosis or oxalosis had the lowest overall half-life of 5.6 years. This study finds that living donor, no acute rejection episodes, age 2-5 years, Caucasian race and having a disease not prone to recurrence are strong predictors of late graft survival. Hence, preferential use of living donor and prevention of acute rejection episodes in the first year are key variables that can improve long-term renal graft survival in children.     

Experimental transmission of Plasmodium mexicanum by bites of infected Lutzomyia vexator (Diptera: Psychodidae)

Lutzomyia vexator is an efficient experimental vector of Plasmodium mexicanum, infecting 69.2% (9/13) of the Sceloporus undulatus lizards with as few as one bite. Sporozoites were present in the salivary glands by day 6.5 postfeed and infective by day 8 postfeed at 27 degrees C. The prepatent period was relatively long, ranging from 23 to 40 days for bite-induced infections and appears to be related to the number of sporozoites injected. The acute phase of the infection is initially exponential and rapid. All lizards (6) that were not sacrificed, died of fulminating infections from 13 to 56 days after parasites were seen in the blood films. Gametocytes from 2 experimentally infected lizards were infective to L. vexator during the course of the acute infection. The majority of P. mexicanum parasites were in erythrocytes of Sc. undulatus. Exoerythrocytic forms were observed in circulating lymphocytes and thrombocytes, lymphocytes of spleen and bone marrow, and endothelial cells of brain capillaries.     

Alterations of surfactant pools in fetal and newborn rat lungs

Preparation by the developing alveolar epithelium for the transition to air breathing and surfactant secretion at birth are critical components of neonatal survival. We combined morphometric analysis and biochemical assays of lung phospholipids to measure the amount and redistribution of lung surfactant during the perinatal period of rats. Within 10 min of the start of air breathing, there was a small increase in type II cell lamellar body content by morphometric and biochemical estimates. By 24 h, the whole lung and alveolar extracellular pool surfactant lipid had substantially increased. Subfractionation of the alveolar surfactant pool obtained at four times, from birth to 24 h of life, demonstrated a 20-fold increase in the ratio of phospholipid in a tubular myelin-rich fraction compared to a unilamellar vesicle-rich fraction. We conclude that packaging of surfactant may be very active immediately postbirth. Our results also indicate a major shift in the physical forms of extracellular surfactant during the first hours of air breathing.     

Management of chronic lunotriquetral ligament tears

Treatment of chronic disruptions of the lunotriquetral (LT) ligament is not well-defined. Eleven patients treated by LT fusion with use of a compression screw are reported. The injury frequently resulted from hyperextension of the wrist. Pain on the ulnar side of the wrist, limited motion, and tenderness over the LT joint exacerbated by ballottement were present. Standard radiographs were normal. Arthrography showed the ligamentous tear in all cases. After operation, immobilization was continued until fusion was apparent radiographically. Fusion was achieved in all cases between 2 and 5 months. Four patients were free of pain, four patients had pain only at the extremes of motion, and three patients had persistent pain. Mean wrist motion was as follows (preoperative/postoperative): flexion (53 degrees/45 degrees), extension (60 degrees/49 degrees), radial deviation (17 degrees/21 degrees), and ulnar deviation (25 degrees/18 degrees). Maximum grip strength as a percentage of the uninjured side was 73% preoperatively and 59% postoperatively. LT tears can exist de novo or as part of the ulnar impaction syndrome; a method for differentiation is presented.     

Early effects of tetraethylammonium chloride on the contractile properties of isolated rabbit basilar arteries

The acute vascular effects of tetraethylammonium chloride (TEA) were examined on annular segments of rabbit basilar arteries. Contractions induced by the potassium channel blocker were compared with those obtained for potassium chloride, 5-hydroxytryptamine (5-HT) and norepinephrine (NE). The greater magnitude of the contractions was of the following order: [K+] greater than 5-HT greater than TEA greater than NE. High concentrations of TEA alone (10(-2) M) generated spontaneous oscillatory contractions in cerebral vessels that were normally quiescent. Low concentrations of TEA (10(-8)-10(-6) M), which had no vasomotor properties per se, enhanced the contractile response of submaximal concentrations of 5-HT (10(-7) M) and NE (3 X 10(-6) M) and attenuated the contraction produced by 60 mM [K+]. An increased vascular response to the amines was still evident up to 3 h after the addition of TEA despite frequent rinsing with fresh buffer solutions. On arteries precontracted with TEA (10(-2) M), but not high [K+], the subsequent addition of 5-HT (10(-7) M) still induced a powerful constriction. Repeated concentration-response curves for [K+] were reproducible and, in the presence of TEA (10(-8) or 10(-6) M), the curve was displaced to the right in a competitive manner. A higher concentration of TEA (10(-4) M) was devoid of any blocking properties on the [K+]-induced response whereas, at 10(-3) M TEA, the response was potentiated, as evidenced by a shift of the curve to the left. Interactions between TEA and the cumulative response to 5-HT were difficult to interpret. Repeated exposures of the artery to 5-HT resulted in an increased maximal response with each determination (EAm = 127 +/- 9% and 149 +/- 14% of control values following the second and third applications, respectively). With TEA (10(-6) M), the increase in the maximal contractile effect noted previously was not observed. Contractions induced by single concentrations of TEA (10(-2) M) or [K+] (60 mM) were calcium dependent, were abolished completely in a calcium-free medium, and were depressed by the calcium antagonist nimodipine. 5-Hydroxytryptamine-induced contractions (10(-5) M) were less sensitive to withdrawal of calcium from the extracellular medium (31 +/- 6% relative to the maximal response at 4 mM calcium). Hence, an acute reduction in potassium conductance in cerebrovascular smooth muscle produced by TEA has complex, concentration-dependent effects and reproduces only part of the spectrum of effects of cisternal injection of blood on cerebrovascular reactivity.