Summary Medication adherence is essential for the survival of kidney grafts, however, the complexity of the medication-taking regimen makes adherence difficult. Little is known about barriers to medication-taking and strategies to foster medication-taking. This cross-sectional study involved semi-structured interviews with 82 kidney transplant recipients approximately 2 months post-transplant on medication-related adherence, barriers to medication-taking, and strategies to foster medication-taking. Although self-reported adherence was high (88%), qualitative analysis revealed that half of the patients (49%) reported experiencing at least one barrier to medication-taking. The most common barriers were: not remembering to refill prescriptions (13%), changes to medication prescriptions or dosages (13%), being busy (10%), forgetting to bring medicines with them (10%), and being away from home (10%). The most common strategies to foster medication-taking were: maintaining a schedule of medication-taking (60%), organizing pills using pillboxes, baggies, cups (42%), bringing medicines with them (34%), organizing pills according to routine times (32%), and relying on other people to remind them (26%). Understanding the range of barriers to adherence and strategies kidney recipients devised to promote medication-taking may help transplant clinicians to better educate transplant recipients about appropriate medication-taking, mitigate the risk of medication nonadherence-related rejection, and may help inform patient-centered interventions to improve medication adherence.
Fibrotic disorders of the renal, pulmonary, cardiac, and hepatic systems are associated with significant morbidity and mortality. Effective therapies to prevent or curtail the advancement to organ failure, however, remain a major clinical challenge. Chronic kidney disease, in particular, constitutes an increasing medical burden affecting >15% of the US population. Regardless of etiology (diabetes, hypertension, ischemia, acute injury, urologic obstruction), persistently elevated TGF-β1 levels are causatively linked to the activation of profibrotic signaling networks and disease progression. TGF-β1 is the principal driver of renal fibrogenesis, a dynamic pathophysiologic process that involves tubular cell injury/apoptosis, infiltration of inflammatory cells, interstitial fibroblast activation and excess extracellular matrix synthesis/deposition leading to impaired kidney function and, eventually, to chronic and end-stage disease. TGF-β1 activates the ALK5 type I receptor (which phosphorylates SMAD2/3) as well as non-canonical (e.g., src kinase, EGFR, JAK/STAT, p53) pathways that collectively drive the fibrotic genomic program. Such multiplexed signal integration has pathophysiological consequences. Indeed, TGF-β1 stimulates the activation and assembly of p53-SMAD3 complexes required for transcription of the renal fibrotic genes plasminogen activator inhibitor-1, connective tissue growth factor and TGF-β1. Tubular-specific ablation of p53 in mice or pifithrin-α-mediated inactivation of p53 prevents epithelial G/M arrest, reduces the secretion of fibrotic effectors and attenuates the transition from acute to chronic renal injury, further supporting the involvement of p53 in disease progression. This review focuses on the pathophysiology of TGF-β1-initiated renal fibrogenesis and the role of p53 as a regulator of profibrotic gene expression.
Preemptive ganciclovir therapy administered daily during courses of treatment with antilymphocyte antibodies reduced the excessive occurrence of cytomegalovirus disease in renal transplant recipients who were positive for cytomegalovirus antibody. This approach, which links the most potent immunosuppression to intensive antimicrobial therapy, allows preventive therapy to be given to those patients at greatest risk for developing infectious complications. These patients are likely to benefit most from the preventive strategy.
Previous studies indicate that obesity is a risk factor in renal transplantation. However, these analyses did not control for variable donor factors that may strongly influence outcome. To control for donor variables such as age, cause of death, procurement techniques, preservation methods, cold ischaemia time and implantation technique, we analysed patient and graft survival in recipients of paired kidneys, derived from the same procurement procedure, preserved in the same manner, subjected to similar cold ischaemia time and implanted by the same surgical team. Between June 1992 and August 1999, 28 procurement procedures provided kidneys which were transplanted into one obese and one non-obese recipient. Body mass index (BMI) was calculated as kg/m2. Recipients were classified as obese (BMI > 30) or non-obese (BMI < 30). Immunotherapy for all recipients consisted of a triple therapy regimen of cyclosporine or prograf, azathioprine or cellcept, and prednisone. Patients with delayed graft function (DGF), defined as the need for dialysis within 72 h of the transplant procedure, were treated with anti-thymocyte globulin (ATG) or thymoglobulin (TMG) induction for 5-7 d. The rate of DGF (7.1 versus 10.7%) and acute rejection (39.3 versus 35.7%) were similar in the obese and non-obese recipient groups. Patient survival was similar at 1, 3 and 5 yr in both groups. In addition, graft survival was similar at 1 yr. However, a trend toward decreased medium-term graft survival, which reached significance at 5 yr, was observed in the obese group. Furthermore, mean serum creatinine at 1 yr was higher in the obese group (2.0) compared with the non-obese group (1, 4) (p=0.12). This analysis of paired cadaver kidneys indicated that obesity is not a risk factor for DGF, acute rejection, and 1-yr graft survival. However, a decreased medium- and long-term graft survival trend, which reached statistical significance at 5 yr, was observed in obese recipients.
Prophylaxis with oral ganciclovir following a brief course of intravenous ganciclovir provides useful protection against primary CMV disease.
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