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Results for “KIDNEY TRANSPLANTATION”

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At least 19 recordsLinked to original sources
PubMed1992

Lipid status after combined pancreas-kidney transplantation and kidney transplantation alone in type I diabetes mellitus.

This study was designed to compare changes in lipid status following organ transplantation between type I diabetes mellitus (DM-I) patients receiving combined pancreas-kidney transplantation (PKT) with those receiving kidney transplantation alone (KTA). A retrospective chart review was used to identify pre- and posttransplantation fasting total cholesterol (TC) and triglycerides (TG) in three groups: DM-I patients receiving KTA (DM:KTA; n = 14), DM-I patients receiving PKT (DM:PKT; n = 20), and kidney transplant recipients without DM (NDM; n = 16). The groups were matched for age, gender, weight, duration of dialysis, smoking history, and duration of diabetes mellitus. Linear regression was used to analyze differences in lipid trends over time (up to 24 months posttransplantation) and the effects of prednisone dose, cyclosporine dose, and serum creatinine. Preoperative TC was significantly lower in the DM:KTA group (P < 0.05) compared with DM:PKT or NDM. There were no significant differences in preoperative TG between the three groups. TC and TG decreased over time only in DM:PKT (P = 0.0112, P = 0.0278, respectively). TC increased and TG was unchanged over time in DM:KTA (P = 0.0003, P = 0.1103, respectively). Neither TC nor TG changed over time in NDM. Trends of TC and TG for DM:PKT were significantly different from DM:KTA (P < 0.01 for both). Trend of TC for NDM was also significantly different from DM:PKT (P = 0.0061). Prednisone dose was significantly related to TC in DM:KTA and NDM (P < 0.01) while cyclosporine dose was significantly related to TC for DM:KTA only (P = 0.0013) in the presence of time. None of the variables tested (prednisone dose, cyclosporine dose, and serum creatinine) significantly affected TG in the presence of time. In summary, TC and TG decreased over time only in DM:PKT. In contrast, TC increased while TG was unchanged in DM:KTA over the same interval (0-24 months). If these trends continue, the beneficial change in lipids in the DM:PKT group may translate into a net improvement in atherosclerosis-mediated events for diabetic patients with chronic renal failure who receive PKT compared with those who do not.

Adult↗
PubMed1992

Simultaneous pancreas-kidney transplant versus kidney transplant alone in diabetic patients.

The decision for simultaneous pancreas-kidney (SPK) versus kidney transplant alone (KTA) in diabetic patients with renal failure depends on the potential risks and benefits for each procedure. The purpose of this study was to compare the morbidity, mortality, and renal allograft survival in diabetic patients who underwent SPK versus KTA, and to discern the added risks associated with pancreas transplantation. Between 7/1/86 and 9/30/90, 69 primary cadaver SPK and 59 primary cadaver KTA were performed in type I diabetic patients with chronic renal failure. Antilymphocyte globulin or OKT3 was used for induction therapy, followed by standard triple therapy (prednisone, azathioprine, and cyclosporine). Patient and graft survivals were retrospectively analyzed. In addition, a detailed comparison of morbidity in those patients treated after 7/1/87 was performed (53 SPK, 49 KTA). For those less than 45 years of age (65 SPK, 42 KTA), there were no significant differences (P greater than 0.6) in the actuarial patient survival at one year (SPK 92%, KTA 95%), or two years (SPK 89%, KTA 92%), or actuarial renal allograft survival at one year (SPK 82%, KTA 83%) or two years (SPK 77%, KTA 83%). However, for those greater than 45 years old, actuarial renal allograft survival was significantly higher (P less than 0.03) in the KTA group. The mean serum creatinine levels were similar at one year (SPK 1.8, KTA 1.9 mg/d).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1987

The living donor in kidney transplantation.

Kidney transplantation using either kidneys from living or nonliving donors is now generally regarded as the primary therapy for most patients with end-stage kidney failure. In 1984, 32% of all kidney transplantations done in the United States involved living donors. Reasons justifying the use of kidneys from living donors are the higher success rate and the inadequate supply of cadaveric kidneys. In addition, with a living donor, it is easier to arrange for kidney transplantation before dialysis therapy needs to be started. An analysis of 2495 donor nephrectomies reported in the literature, and 5698 donor nephrectomies reported from the 12 largest centers that do kidney transplantation with living donors, indicates an approximate incidence of 1 donor death per 1600 nephrectomies. Although long-term follow-up in kidney donors has shown only that mild, nonprogressive proteinuria develops in about 33% and that the frequency of hypertension may increase, we advise that the kidney donor have a careful long-term follow-up and avoid a high protein intake because of its potential to lead to progressive glomerular damage.

Family↗
PubMed2002

Pancreas and kidney transplantation.

Kidney transplantation is preferred over dialysis for management of end-stage renal disease complicating type I or type 2 diabetes, for those who are eligible. Simultaneous pancreas-kidney (SPK) or pancreas after kidney transplantation (PAK) is an important alternative to kidney transplantation alone for type I diabetes patients if the patient is able to withstand the additional risks of these procedures, because of the benefits of glucose control on other diabetic complications. Pancreas transplantation alone (PTA) is most useful for the treatment of debilitating, frequent hypoglycemia complicating type I diabetes, if renal function is adequate. One-year pancreas graft survival is best after SPK (82%) but has significantly improved after both PAK (74%) and PTA (76%). The I-year kidney graft and patient survival rates after SPK are similar to kidney transplantation alone. Pancreas transplantation normalizes glucose beyond what can be achieved with insulin therapy and has been shown to decrease progression of or improve most, if not all, diabetic end-organ complications using current immunosuppression regimens. However, the diabetologist and endocrinologist should remain involved in the care of the pancreas or kidney transplant recipient for treatment of vascular disease risk factors such as dyslipidemia, surveillance of other diabetic complications including foot ulcers, surveillance and treatment of bone loss, and management of hyperglycemia if it recurs.

Diabetic Nephropathies↗
PubMed1978

Kidney transplants in mice. An analysis of the immune status of mice bearing long-term, H-2 incompatible transplants.

Kidney transplants between strains of mice which are incompatible at either the K or the D end of the H-2 complex usually function for prolonged periods supporting the lives of nephrectomized recipients. This occurs with no recipient treatment. With multiple H-2 and non-H-2 determined incompatibilities, transplants may be rejected but more slowly than skin grafts. In the strain combination studied most extensively in these experiments (B10.D2 to B6AF(1)) in which the incompatibility was confined to the K end of the H-2 region, about 70 percent of recipients survived for many weeks with normal blood urea nitrogen levels. Skin grafts between untreated members of these strains were rejected promptly (mean survival time of 13.5 +/- 1.1 days) as were kidney transplants to recipients of prior skin grafts. Donor strain skin grafts to recipients of kidney transplants after kidney transplantation enjoyed greatly prolonged survival whereas skin grafts from a third party (A.SW) were rejected normally. If kidney tissue was transferred in the form of free grafts without primary vascular union, it was rejected promptly leaving its recipient highly immunized. Cellular and humoral immunity to donor antigens declined over the first few weeks after transplantation, and the spleens of long-term recipients contained no "killer cells." Recipient lymphoid cells could mount active graft versus host reactions to donor strain antigens on transfer to neonatal mice. Nevertheless, they were distinctly less able to respond specifically by the production of killer cells to donor strain antigens after sensitization in vitro. No evidence that this defect was associated with the presence of suppressor cells was forthcoming from several types of in vivo and in vitro tests.

Animals↗
PubMed1998

An economic analysis of kidney transplantation.

Kidney transplantation is the most cost-effective treatment modality for end-stage renal disease (ESRD). Nonetheless, in keeping with the managed care mandate, expense has become an increasingly significant issue. Over $11 billion is now spent each year on ESRD treatment. Medicare per capita annual payments exceed $36,000 per beneficiary. Transplant procedure charges and outcomes vary dramatically across the United States. The average charge for a kidney transplant is approximately $82,000. Graft and patient survival rates are highly variable, even among the most active programs in the US. Individual transplant programs must implement approaches to contain their costs and assure quality. At the Mayo Clinic, our mean charge for a kidney transplant ($53,510) in 1996 was 27.2% below expected, given national medical inflation over the past decade. Unfortunately, the net operating income associated with our kidney transplant program has been severely eroded in an increasingly brutal economic environment.

Cost Control↗
PubMed1995

Bone mineral density after kidney transplantation. A cross-sectional study in 190 graft recipients up to 20 years after transplantation.

Kidney transplant recipients are exposed to multiple factors that lead to osteoporosis after kidney transplantation. Recent short-term longitudinal studies revealed a strong decline of bone mineral density (BMD) within 1 year after transplantation. The long-term course of BMD after transplantation is still unknown. Therefore, we performed a cross-sectional study to determine BMD in 190 renal graft recipients (mean age 44 years, range 20-71 years) by dual-energy x-ray absorptiometry at various time intervals up to 20 years after transplantation (range 0-237 months). Mean BMD of graft recipients was lower than BMD values of an age- and sex-matched European reference collective at every time of measurement after renal transplantation (P < 0.01). Lowest mean BMD values were measured 12-24 months after transplantation. No loss of BMD occurred after the second posttransplant year beyond the normal age- and sex-dependent decline of BMD. Mean daily prednisone dosage was significantly higher within the first 2 posttransplant years compared with the later posttransplant period (13.1 +/- 6.2 vs. 6.7 +/- 3.4 mg/day). Other drugs or metabolic causes, including daily dosage of CsA, AZA, parathormone level, and graft function, did not show additional important differences before and after the second posttransplant year. Interpreting the results of a cross-sectional study in light of a time-dependent process, we suggest that the preexisting low BMD of kidney transplant recipients at the time of transplantation is further strongly reduced within the initial 2 posttransplant years, probably due mainly to the effect of prednisone therapy. After that time, when prednisone dosage is below a threshold of 7.5 mg/day, only a moderate, normal loss of BMD is apparent, even in patients up to 20 years after transplantation.

Adult↗
PubMed2026

Urine Proteomics as a Source of Biological Information and Outcome Predictor in Living Kidney Transplantation.

Kidney transplantation (KTx) is the preferred treatment for kidney failure. However, post-transplant management is challenging due to the limited lifespan of transplanted organs. Current methods for monitoring post-transplant complications are invasive and have limitations. Therefore, there is an urgent need for novel non-invasive biomarkers. This study investigates the proteomic composition of urine to understand renal biology during the process of transplantation and to identify potential markers for outcome prediction. Urine samples were collected from donors before transplantation and from recipients 4 weeks and 1 year after transplantation. Proteomic analysis was performed using mass spectrometry and label-free quantification. Statistical analyses included principal component analysis (PCA) and enrichment analysis. The resulting key findings were confirmed in an independent validation cohort. In addition, correlative regression models to evaluate the relationship between protein abundance and clinical outcomes in the further course after transplantation were performed. 106 urine samples in the setting of 70 kidney transplantations were analyzed. PCA revealed distinct clustering of donor and recipient samples, indicating significant proteomic changes after transplantation. Hierarchical clustering and gene ontology analysis identified molecular changes as a response to transplantation and showed an over-representation of relevant pathways related to inflammation, cell immune response and coagulation in both the original and validation cohorts. Multivariate regression analysis, including linear and logistic regression, identified 11 potential protein biomarkers, including ORM2, IL1RAP, APP, and FABP4 as predictors of eGFR 12 months after transplantation and 1 HP as a predictor of infections within the first year after transplantation, respectively. This study underscores the potential of non-invasive urine proteomics for identifying biological processes involved in kidney transplantation and for enhancing post-transplant monitoring and outcome prediction. We identified 12 potential biomarkers with added value to standard clinical parameters linked to transplant outcomes, which will be promising candidates for future outcome monitoring after KTx.

Humans↗