Summary Delayed graft function (DGF) in deceased donor kidney transplantation is associated with worse outcomes. DGF has been less well studied in live donor transplantation. We aimed to examine the risk factors for DGF, and associations between DGF and short‐ and long‐term outcomes in live donor kidney transplant recipients. Using data from the Australia and New Zealand Dialysis and Transplant (ANZDATA) Registry, we included live donor kidney transplants performed in Australia and New Zealand over 2004–2015 and excluded pediatric recipients (n = 440), pathological donors (n = 97), grafts that failed in the first week (as a proxy for primary non function; n = 38), and grafts with missing DGF data (n = 46). We used multivariable logistic regression to identify the risk factors for DGF and the association between DGF and rejection at 6 months; Cox proportional hazards models to examine the relationship between DGF and patient and graft survival; and linear regression to examine the association between DGF and eGFR at 1 year. DGF occurred in 77 (2.3%) of 3358 transplants. Risk factors for DGF included right‐sided kidney [odds ratio (OR) 2.00 (95% CI 1.18, 3.40)], donor BMI [OR 1.06 per kg/m2 (95% CI 1.01, 1.12)]; increasing time on dialysis and total ischemic time [OR 1.09 per hour (1.00, 1.17)]. DGF was associated with increased risk of rejection at 6 months [OR 2.37 (95% CI 1.41, 3.97)], worse patient survival [HR 2.14 (95% CI 1.21, 3.80)] and graft survival [HR 1.98 (95% CI 1.27, 3.10)], and worse renal function at 1 year [Coefficient ‐9.57 (95% CI −13.5, −5.64)]. DGF is uncommon after live donor kidney transplantation, but associated with significantly worse outcomes. The only modifiable risk factors identified were kidney side and total ischemic time.
Background Lupus nephritis (LN) is a common feature of systemic lupus erythematosus (SLE) and affects 50% of patients with SLE. Racial differences in incidence and prevalence have been well documented worldwide. In Australia, higher incidence and prevalence of SLE had been previously reported in Aboriginal and Torres Strait Australians compared with non‐Indigenous Australians. Aim To describe the differences in clinical features and lupus biomarkers between Aboriginal and Torres Strait Islander Australian and non‐Indigenous Australian patients with LN. Methods We retrospectively identified all consecutive biopsy‐proven LN patients in our institution and compared the clinical features and lupus biomarkers between Aboriginal and Torres Strait Islander Australians and non‐Indigenous Australians. Results Of the 33 consecutive biopsy‐proven LN patients, 26 self‐identified as of Aboriginal and Torres Strait Islander descent. The estimated incidence of LN in Aboriginal and Torres Strait Islander Australian and non‐Indigenous Australians were 5.08 and 0.47 per 100 000 patient‐years respectively. Neurological manifestations (23.08% vs 0%), haematological manifestations (46.50% vs 16.67) and right‐heart catheter proven pulmonary arterial hypertension (23.08% vs 0%) were more frequently observed among Indigenous Australian patients compared with non‐Indigenous Australian patients. The incidence of positive extractable nuclear antigen was also higher among Indigenous Australian patients (84.62% vs 57.14%). Conclusion The present study further supports the observation that lupus in Aboriginal and Torres Strait Islander Australians were of a ‘distinct phenotype’ compared with non‐Indigenous Australians. Future research should be aimed at delineating the reason for this observed difference.
Background Tacrolimus, a post-transplant immunosuppressive drug with a narrow therapeutic window requires close monitoring of levels to avoid under-immunosuppression or toxicity. Top End Renal Services in the Northern Territory (NT) refer to South Australia (SA) for drug levels as there was no local service. We aimed to evaluate the Abbott ARCHITECTi2000 immunoassay against the liquid chemistry tandem mass spectroscopy (LC-MS/MS) used in SA for measuring tacrolimus levels to provide on-site service in NT. Methods 465 specimens were collected over 5 months and analyzed over several reagent lots. We used Passing-Bablok regression plots and Bland–Altman plots to assess the agreement between tacrolimus levels on both platforms. Results The Passing-Bablok regression plot demonstrated a slope of 1.172 (CI 1.136 to 1.207) with an intercept of 0.262 (CI 0.040 to 0.472). In Deming analysis, the slope was 1.095 (CI 1.074 to 1.116) with an intercept of 0.773 (CI 0.592 to 0.955), correlation coefficient (r) was 0.9782. Bland-Altman plot demonstrated positive bias for Abbott ARCHITECT results. The mean absolute bias was 1.494 ug/L and the mean percentage bias was 18.78%. Within run imprecision, Co-efficient of Variation (%) was 5.1, 2.7, 4.3, 3.4 and 3.5 at tacrolimus concentration levels of 4.2, 6.5, 9.5, 17.2 and 24.4 µg/L. Results turnaround time improved by 80%. Conclusion The results demonstrate that Abbott ARCHITECT i2000 is an acceptable method to monitor levels of tacrolimus. The positive bias could be justifiable if the drug levels are initially based and then monitored on results from the same platform.
Conclusions: OPN levels are significantly elevated in ESRD patients. Furthermore, OPN levels were found to be positively correlated with the bone turnover biomarkers iPTH and alkaline phosphatase. We hypothesize that hyperparathyroidism secondary to ESRD increases circulating iPTH, stimulating osteoblast/osteoclast activation and differentiation that increases alkaline phosphatase and OPN production, ultimately resulting in increased bone turnover. Clinical implications include (1) establishing the practice of monitoring OPN levels with iPTH and alkaline phosphatase to better characterize bone turnover in ESRD patients and (2) targeting OPN expression in ESRD for therapeutic management of iPTH-induced bone resorption.
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