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The isolated rectal gland of Squalus acanthias was stimulated to secrete chloride against an electrical and a chemical gradient when perfused in vitro by theophylline and/or dibutyryl cyclic AMP. Chloride secretion was depressed by ouabain which inhibits Na-K-ATPase. Thiocyanate and furosemide also inhibited chloride secretion but ethoxzolamide, a carbonic anhydrase inhibitor, did not. Chloride transport was highly dependent on sodium concentration in the perfusate. The intracellular concentration of chloride averaged 70-80 meq/liter in intact glands, exceeding the level expected at electrochemical equilibrium and suggesting active transport of chloride into the cell. These features suggest a tentative hypothesis for chloride secretion by the rectal gland in which the uphill transport of chloride into the cytoplasm is coupled through a membrane carrier to the downhill movement of sodium along its electrochemical gradient. The latter is maintained by the Na-K-ATPase pump while chloride is extruded into the duct by electrical forces.

Kidney transplantation from live donors achieves an excellent outcome regardless of human leukocyte antigen (HLA) mismatch. This development has expanded the opportunity of kidney transplantation from unrelated live donors. Nevertheless, the hazard of hyperacute rejection has usually precluded the transplantation of a kidney from a live donor to a potential recipient who is incompatible by ABO blood type or HLA antibody crossmatch reactivity. Region 1 of the United Network for Organ Sharing (UNOS) has devised an alternative system of kidney transplantation that would enable either a simultaneous exchange between live donors (a paired exchange), or a live donor/deceased donor exchange to incompatible recipients who are waiting on the list (a live donor/list exchange). This Regional system of exchange has derived the benefit of live donation, avoided the risk of ABO or crossmatch incompatibility, and yielded an additional donor source for patients awaiting a deceased donor kidney. Despite the initial disadvantage to the list of patients awaiting an O blood type kidney, as every paired exchange transplant removes a patient from the waiting list, it also avoids the incompatible recipient from eventually having to go on the list. Thus, this approach also increases access to deceased donor kidneys for the remaining candidates on the list.

To define better the prevalence and pathophysiology of lymphoceles following renal transplantation, we prospectively evaluated 118 consecutive renal transplants performed in 115 patients (96 cadaveric, 22 living-related, 7 secondary and 111 primary). Ultrasonography was performed post-operatively and during rehospitalizations or whenever complications occurred. Perirenal fluid collections were identified in 43 patients (36%). Lymphoceles with a diameter of 5 cm. or greater were identified in 26 of 118 cases (22%). Eight patients (6.8%) had symptomatic lymphoceles requiring therapy. The interval for development of symptomatic lymphoceles was 1 week to 3.7 years (median 10 months). Risk factors for the development of lymphoceles were examined by univariate and multivariate analysis, and included patient age, sex, source of transplants (cadaver versus living-related donor), retransplantation, tissue match (HLA-B/DR), type of preservation, arterial anastomosis, occurrence of acute tubular necrosis-delayed graft function, occurrence of rejection, and use of high dose corticosteroids. Univariate analysis showed a significant risk for the development of lymphoceles in transplants with acute tubular necrosis-delayed graft function (odds ratio 4.5, p = 0.004), rejection (odds ratio 25.1 p < 0.001) and high dose steroids (odds ratio 16.4, p < 0.001). When applying multivariate analyses using stepwise logistic regression, only rejection was associated with a significant risk for lymphoceles (symptomatic lymphoceles--odds ratio 25.08, p = 0.0003, all lymphoceles--odds ratio 75.24, p < 0.0001). When adjusting for rejection, no other risk factor came close to being significant (least p = 0.4). Therapy included laparoscopic peritoneal marsupialization and drainage in 1 patient, incisional peritoneal drainage in 4 and percutaneous external drainage in 3 (infected). All symptomatic lymphoceles were successfully treated without sequelae to grafts or patients. We conclude that allograft rejection is the most significant factor contributing to the development of lymphoceles. Therapy of symptomatic lymphoceles should be individualized according to the presence or absence of infection.