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Background: Transplant education in dialysis centers can increase access to kidney transplant; however, dialysis center transplant barriers are common, and limited research identifies the most effective transplant education approaches., Methods: We surveyed transplant educators in 1694 US dialysis centers about their transplant knowledge, use of 12 education practices, and 8 identified education barriers. Transplant wait-listing rates were calculated using US Renal Data System data., Results: Fifty-two percent of educators orally recommended transplant to patients, 31% had in-center transplant discussions with patients, 17% distributed print educational resources, and 3% used intensive education approaches. Distribution of print education (incident rate ratio: 1.021.151.30) and using >1 intensive education practice (1.001.111.23) within dialysis centers were associated with increased wait-listing rates. Several dialysis center characteristics were associated with reduced odds of using education strategies leading to increased wait-listing. Centers with greater percentages of uninsured patients (odds ratio [OR]: 0.960.970.99), in rural locations (OR: 0.660.790.95), with for-profit ownership (OR: 0.640.770.91), and with more patients older than 65 years (OR: 0.050.110.23) had lower odds of recommending transplant, while centers with a higher patient-to-staff ratio were more likely to do so (OR: 1.011.031.04). Language barriers (OR: 0.480.640.86) and having competing work priorities (OR: 0.400.530.70) reduced the odds of distributing print education. Providers with greater transplant knowledge were more likely to use >1 intensive educational strategy (OR: 1.011.271.60) while providers who reported competing work priorities (OR: 0.510.660.84) and poor communication with transplant centers (OR: 0.580.760.98) were less likely to do so., Conclusions: Educators should prioritize transplant education strategies shown to be associated with increasing wait-listing rates.

Background: Kidney transplant is the best treatment for most end-stage renal disease (ESRD) patients, but proportionally few ESRD patients receive kidney transplant. To make an informed choice about whether to pursue kidney transplant, patients must be knowledgeable of its risks and benefits. To reliably and validly measure ESRD patients' kidney transplant knowledge, rigorously tested measures are required. This article describes the development and psychometric testing of the Knowledge Assessment of Renal Transplantation (KART)., Methods: We administered 17 transplant knowledge items to a sample of 1294 ESRD patients. Item characteristics and scale scores were estimated using an Item Response Theory graded response model. Construct validity was tested by examining differences in scale scores between patients who had spent less than 1 and 1 hour or longer receiving various types of transplant education., Results: Item Response Theory modeling suggested that 15 items should be retained for the KART. This scale had a marginal reliability of 0.75 and evidenced acceptable reliability (>0.70) across most of its range. Construct validity was supported by the KART's ability to distinguish patients who had spent less than 1 and 1 hour or longer receiving different types of kidney transplant education, including talking to doctors/medical staff (effect size [ES], 0.61; P < 0.001), reading brochures (ES, 0.45; P < 0.001), browsing the internet (ES, 0.56; P < 0.001), and watching videos (ES, 0.56; P < 0.001)., Conclusions: The final 15-item KART can be used to determine the kidney transplant knowledge levels of ESRD patients and plan appropriate interventions to ensure informed transplant decision making occurs.

We investigated the effects of a newly synthesized cardiotonic agent, TA-064, on helical strips of isolated canine cerebral, coronary, femoral, mesenteric, and renal arteries. TA-064 had no effect on isolated arterial strips under resting tension. When the arterial strips were partially contracted with prostaglandin F2 alpha, TA-064 caused markedly significant concentration-related relaxations in coronary arterial strips. However, the maximum relaxation induced by TA-064 in renal, mesenteric, and femoral arterial strips was only one-third or less of the coronary artery. On the other hand, cerebral arterial strips generated negligible responses to TA-064. Relaxation of renal, mesenteric, and femoral arteries was not potentiated by pretreatment with 10(-5) M phenoxybenzamine. The concentration-response curve for TA-064 in coronary artery was shifted to the right to a similar extent by exposure to 2 X 10(-7) M propranolol and 2 X 10(-7) M metoprolol. On the other hand, relaxation of renal arterial strips was only slightly attenuated by metoprolol but was inhibited by propranolol. Droperidol (3 X 10(-5) M) failed to significantly alter the concentration-response curve for TA-064 in coronary artery. These results indicate that TA-064 causes coronary arterial vasodilatation mediated by beta 1-adrenoceptors. It would further appear that the same mechanism may be responsible for the positive inotropic action of TA-064.

The effects of dobutamine on helical strips of isolated canine cerebral, coronary, mesenteric, and renal arteries was investigated. Dobutamine contracted only renal arterial strips under resting condition. When renal and mesenteric arterial strips were partially contracted with prostaglandin F2 alpha (PGF2 alpha), dobutamine caused further concentration-related contraction, while coronary arterial strips were relaxed. Cerebral arterial strips, on the other hand, did not significantly respond to dobutamine. After treatment with 10(-5) M dl-phenoxybenzamine hydrochloride (POB) for 1 h, dobutamine-induced contractions of partially precontracted mesenteric and renal arterial strips were converted to relaxations. Relaxations of coronary arteries were not potentiated by the alpha-antagonist, but were attenuated by treatment with 10(-6) M propranolol and 10(-6) M metoprolol to a similar extent. On the other hand, relaxations of mesenteric and renal arterial strips were not inhibited by metoprolol but by propranolol. Droperidol (3 X 10(-5) M) failed to significantly alter the concentration-response curve for dobutamine. These results suggest that dobutamine causes vasoconstriction mediated by apha-adrenergic receptor and vasodilatation mediated by beta 1- and beta 2-adrenoceptors. Dobutamine does not appear to act on dopamine receptors.