INFECTIONS IN RENAL TRANSPLANT PATIENTS IN CENTRAL AUSTRALIA

D TRAN1, B PAWAR1, S NAYAR1, S CHERIAN1
1Alice Springs Hospital Renal Department, The Gap, Australia

Aim: To identify the types of infection experienced by renal transplant patients living in Central Australia, and to quantify the incidence of infection and their clinical outcomes
Background: Immunosuppression in patients post renal transplantation increases their risk of common and opportunistic infections. In addition, due to ecological and socio-economic factors, the types and incidence of infections in Central Australia (particularly its Indigenous population) are different to those of urban centres in Australia.
Methods: We performed a retrospective analysis of 39 patients who had received a renal transplant and had been under care of the Alice Springs renal department in the last 15 years. Using electronic medical records, episodes of infection were identified, as well as associated clinical endpoints such as hospitalisation,  admission to the Intensive Care Unit (ICU), documented acute kidney injury (AKI), graft loss or death with functioning graft.
Results: In the study population, the most common infection was urinary tract infection (29 cases per 100 person-years), followed by respiratory tract infection (21 cases per 100 person-years) and skin infection (12 per 100 person-years). Other infections of note included CMV disease, pulmonary mucormycosis, cryptococcal pneumonia, strongyloidiasis, and giardiasis. The rate of hospitalisation due to infection was 66 per 100 person-years. The rate of documented AKI associated with episodes of infection was 19 per 100 person-years.
Conclusions: renal transplant patients in Central Australia experience frequent infections such as urinary tract, respiratory tract and skin infections, leading to frequent hospitalisations and episodes of AKI.


Biography:
First year renal advanced trainee at Alice Springs Hospital

POST KIDNEY TRANSPLANT NEUTROPAENIA IN SOUTHERN TASMANIA

S KUO1, M JOSE1,2, L JEFFS1, G KIRKLAND1, S YEW1, R YU1
1Royal Hobart Hospital, Hobart, Australia, 2School of Medicine, University of Tasmania, Hobart, Australia

Aim: To determine the incidence of post kidney transplant neutropaenia in Southern Tasmania, its effect on outcome and identify factors associated with increased risk of neutropaenia.
Background: Post-transplant neutropaenia is common and has been associated with poor outcomes. Nonetheless, the optimal management strategy and factors associated with neutropaenia remain unclear.
Methods: A retrospective study was performed on patients (>18 years) who received kidney or kidney-pancreas transplant between 2007-2017. Incidence of and clinical parameters surrounding neutropaenia (<1500 cells/microL) were determined. Pre-transplant parameters and outcome at one year post-transplant were compared to those who did not become neutropaenic.
Results: Of the 105 people who received a transplant (54% male, mean age 49), 54 (51%) first became neutropaenic at a mean time of 115 days post-transplantation with 26% experiencing more episodes subsequently. Post-transplant neutropaenia is associated with increased incidence of infection (68% vs 37%, p<0.05) and infection-related hospital admissions (49% vs 6%, p<0.05). There was a non-statistically significant association with more frequent rejection. CMV positive to negative transplant was associated with increased risk of post-transplant neutropaenia (38% vs 14%, p<0.05). Immunosuppression dose, Trimethoprim/Sulfamethoxazole use and Valgancyclovir use the time of neutropaenia was similar in both groups. There was no statistical significant association found in age at transplantation, gender, previous immunosuppression, type of donor, presence of donor specific antibody, human leukocyte antigen mismatch, ABO compatibility or delayed graft function. Clinician response varied often involving adjustment of multiple medications.
Conclusions: Post-transplant neutropaenia is common and is associated with increased rate of infection with the main risk factor identified being CMV positive to negative transplant.


Biography:
Renal registrar at Royal Hobart Hospital

THE ASSOCIATION OF BODY MASS INDEX CHANGE ONE YEAR POST KIDNEY TRANSPLANTATION WITH GRAFT AND PATIENT SURVIVAL: A COMPARATIVE STUDY BETWEEN INDIGENOUS AND NON-INDIGENOUS AUSTRALIANS

P SUBRAMANI1, S ULLAH2,3,4, W MAJONI5,6,7, J HUGHES2,5,6,7, S MCDONALD1,2,3
1Central Northern Adelaide Renal and Transplantation Services, Royal Adelaide Hospital, Adelaide, Australia, 2Australia and New Zealand Dialysis and Transplant (ANZDATA) Registry, Adelaide, Australia, 3University of Adelaide School of Medicine, Faculty of Health and Medical Sciences, Adelaide, Australia, 4South Australian Health and Medical Research Institute (SAHMRI), Adelaide, Australia, 5Department of Nephrology, Royal Darwin Hospital, Darwin, Australia, 6Menzies School of Health Research, Wellbeing and Preventable Chronic Diseases, Darwin, NT, Darwin, Australia, 7Flinders University Faculty of Medicine, Nursing and Health Sciences, Northern Territory Medical Program, Darwin, Australia

Aim: To compare the association of body mass index (BMI) change in the first year post kidney transplantation with graft and patient survival in Indigenous and non-Indigenous Australians.
Background: Significant post-transplant weight loss or gain is associated with poorer transplant outcomes in non-Indigenous Australians. There is little data comparing early weight change with outcomes between Indigenous and non-Indigenous recipients.
Method: ANZDATA Registry data was used to examine these issues. All adult patients (aged 18+) who received a deceased donor primary kidney-only transplant from 1997-2016 were included. Percentage BMI change at 1-year post transplant was calculated. Outcomes were death censored graft loss and death with functioning graft. The associations were analysed using multivariate Cox proportional hazard models with confounder adjustments.
Results: A total of n=6776 non-Indigenous and n=387 Indigenous recipients were included in this study. Over half the recipients in both groups gained BMI in the first year; 23.1% non-Indigenous and 22.3% Indigenous lost BMI. The risk of graft loss and death were increased in the >10% and 5-10% BMI loss categories (adjusted HR 1.9 (1.6-2.4) and 1.5 (1.2-1.8)  respectively (p <0.001) for graft loss and 1.8 (1.4-2.3) and 1.4 (1.1-1.8) respectively (p <0.01) for death) in the non-Indigenous group. These risks were greater (HR 3.0 (1.4-6.5) and 2.6 (1.3-5.3) (p<0.01) for graft loss and 2.1 (0.9-5.1) (p = 0.10) and 3.0 (1.4-6.6) (p<0.01)) in the Indigenous group. There was no increase risk in graft loss or death associated with BMI gain.Conclusion: BMI loss following kidney transplantation is associated with poor survival outcomes with a greater effect amongst Indigenous recipients. BMI loss can therefore be used as a risk marker of outcome in clinical practice.
Conclusion: BMI loss following kidney transplantation is associated with poor survival outcomes with a greater effect amongst Indigenous recipients. BMI loss can therefore be used as a risk marker of outcome in clinical practice


Biography: Priyanka Subramani is currently a final year nephrology trainee at Royal Adelaide Hospital, having spent two years in the Northern Territory, prior to that. Having completed her undergradate medical degree at The University of Adelaide in 2010, she went on to pursue a career as a physician at Monash Health. She has a keen interest in Indigenous health and developing world medicine and is looking to further her experience abroad next year.

KIDNEY TRANSPLANT AND RECIPIENT OUTCOMES IN HYPEROXALURIA.

V HERON1,2, P KERR2, J KANELLIS2, K POLKINGHORNE2, N ISBEL3, E SEE2
1Renal Service, Darling Downs Hospital And Health Service, Toowoomba, Australia, 2Department of Nephrology, Monash Health, Clayton, Australia, 3Department of Nephrology, Princess Alexandra Hospital, Brisbane, Australia

Aim: To evaluate graft and patient outcomes following kidney transplantation in end stage kidney disease (ESKD) secondary to hyperoxaluria using the Australia and New Zealand Dialysis and Transplant (ANZDATA) Registry.
Background: Hyperoxaluria has presented a challenge for transplant physicians given the risk of disease recurrence in the graft. There has been no analysis of transplant and patient outcomes using the ANZDATA registry.
Methods: This cohort study compared the outcomes of all patients with ESKD secondary to hyperoxaluria who received a kidney transplant in Australia and New Zealand between 1965 and 2015 to propensity score matched controls with ESKD secondary to reflux nephropathy. The primary outcome measure was graft survival. Secondary outcomes included estimated glomerular filtration rate (eGFR), acute rejection and patient survival.
Results: Nineteen kidney transplants were performed in 16 patients with hyperoxaluria between September 1965 and December 2015. Median graft survival was 1.8 years (IQR 0.4–10.6) in hyperoxaluria recipients compared to 6.8 years (IQR 2.7–13.0) in reflux nephropathy controls. Compared to reflux nephropathy, hyperoxaluria was not associated with an increased risk of graft failure (SHR 2.43, 95% CI 0.94—6.22, p=0.07). The most common cause of graft failure in the hyperoxaluria cohort was recurrent disease in contrast to chronic allograft nephropathy for reflux nephropathy recipients. Hyperoxaluria was associated with a higher post-transplant serum creatinine, but not with an increased risk of acute rejection or death.
Conclusion: Compared to reflux nephropathy, ESKD secondary to hyperoxaluria was not associated with inferior graft survival, patient survival, or acute rejection risk. However, post-transplant serum creatinine was higher and there was a shorter time to graft failure.


Biography:
Vanessa Heron is an advanced trainee in nephrology currently working at Toowoomba Hospital, Queensland.

ALLOCATION OF LOW-RISK KIDNEYS: CAN WE OPTIMISE UTILISATION?

P CLAYTON1,2,3, M SYPEK1,4, A GULYANI1,3, J KANELLIS5, S MCDONALD1,2,3
1Australia and New Zealand Dialysis And Transplant (ANZDATA) Registry, Adelaide, Australia, 2Central Northern Adelaide Renal and Transplantation Service, Royal Adelaide Hospital, Adelaide, Australia, 3University of Adelaide, Adelaide, Australia, 4University of Melbourne, Melbourne, Australia, 5Renal Unit, Monash Medical Centre, Clayton, Australia

Aim: To simulate restricting the allocation of low-risk kidneys to recipients with favourable prognoses.
Background: The Australian deceased donor kidney allocation system does not attempt to match the prognosis of kidneys and recipients, leading in some instances to low-risk kidneys (with a high projected graft survival) being allocated to high-risk recipients (with a limited life expectancy).
Methods: We constructed an event-based simulation model by adapting the US Kidney-Pancreas Simulated Allocation Model software to the Australian context. We simulated the current allocation system over 2010-2014 (5,362 patients, 2,833 kidneys), and two alternative models: (1) low-risk kidneys (lowest 20% kidney donor risk index) restricted to non-high-risk recipients (lowest 80% estimated post-transplant survival score [EPTS]), (2) low-risk kidneys restricted to low-risk recipients (lowest 20% EPTS). In each alternative model national sharing for immunological advantage was preserved, and simulations used either the Australian EPTS (incorporating age, waiting time and prior transplantation) or the original US EPTS (additionally incorporating diabetes). Outcomes were the distribution of low-risk kidneys and overall projected life-years.
Results: The characteristics of low-risk kidney recipients were similar when comparing model 1 and the current allocation system, with the exception of less waiting time. In model 2, these kidneys were allocated to younger patients with less waiting time and fewer comorbidities. Overall projected life-years were 86,735 in the current system; 86,842 in model 1 and 87,411 in model 2 using the Australian EPTS; and 87,078 in model 1 and 87,732 in model 2 using the US EPTS.
Conclusions: Avoiding allocating low-risk kidneys to high-risk recipients made only a negligible difference; restricting their allocation to low-risk recipients made more difference to organ distribution but overall life-years gained remained modest.


Biography:
Dr Clayton is a nephrologist at the Royal Adelaide Hospital and serves on the executive of the Australia and New Zealand Dialysis and Transplant (ANZDATA) Registry.

 

MACHINE LEARNING PREDICTION FOR DE NOVO DONOR SPECIFIC ANTIBODIES (dnDSA), AMR AND GRAFT LOSS IN SIMULTANEOUS KIDNEY PANCREAS (SPK) TRANSPLANT RECIPIENTS

A SHARMA1,2, C COOREY1,2, A TAVERNITI1, B NANKIVELL3, J CHAPMAN3, J CRAIG1,2, P O’CONNELL3, H PLEASS3, W LIM4, J YANG5,6, G WONG1,2,3
1Centre for Kidney Research, Westmead, Australia, 2School of Public Health, University of Sydney, Sydney, Australia, 3Centre for Transplant and Renal Research, Westmead, Australia, 4Department of Renal Medicine, Perth, Australia, 5School of Mathematics and Statistics, University of Sydney, Sydney, Australia, 6Charles Perkins Centre, Sydney, Australia

Aim: To develop a prediction model for dnDSA and allograft loss based on the number and location of eplet mismatches in SPK transplant recipients.
Methods: 170 SPK transplant recipients (2005-2017) were assessed using data from ANZDATA registry and NOMS. Adjusted logistic regression were conducted to determine associations between class specific eplet HLA mismatches, dnDSA production, AMR and graft loss. Machine learning models (random forests) were used to predict dnDSA, AMR and allograft loss based on location of eplet mismatches.
Results: The cohort included 92 (54%) males with mean age 38.5 years (SD 6.9) and median follow up time 6.6 years (IQR: 3.9-11.0). The most common class I and II eplet mismatches were at 156RA (35%) and 70D (55%), respectively, with 33 (19%) and 52 (31%) recipients developing Class I and II dnDSA. An increased risk of dnDSA production was observed per 10 increase in Class I (adjusted odds ratio (aOR) 2.0, 95%CI 1.2-3.3, P=0.01), and Class II eplet mismatches (aOR 1.3, 95%CI 1.1-1.5, P=0.01). The presence of Class II dnDSA was associated with increased risk of AMR (aOR 3.9, 95%CI 1.6-9.5, P<0.01). The top eplet mismatches associated with class II dnDA production were located at 45EV and 46VY, corresponding to HLA DQB1*03:01 and DQB1*02:01. Random forest model with the location of the top 10 class specific eplet mismatches achieved a mean cross-validation accuracy of 63.9% and 61.2% for class I and II dnDSA production.
Conclusions: The number of eplet mismatches was associated with dnDSA production at class I and II, and the location of eplet mismatches at 45EV and 46VY on HLA DQB1*03:01 and DQB1*02:01 may predict Class II dnDSA after SPK transplant.


Biography:
Nephrologist and PhD candidate (University of Sydney)

A CASE OF LIVE RENAL TRANSPLANTATION FOR END STAGE KIDNEY DISEASE SECONDARY TO PAROXYSMAL NOCTURNAL HAEMOGLOBINURIA

A TIKU1, L COYLE1, B COOPER1
1Royal North Shore Hospital, St Leonards, Australia

Background: Paroxysmal Nocturnal Haemoglobinuria (PNH) is a rare acquired blood disorder causing intravascular haemolysis and thrombophilia, and is associated with marrow hypoplasia.  It can cause both acute and chronic kidney damage: respectively, through direct toxicity by free haem, and renal haemosiderosis interfering with proximal tubular function and interstitial scarring.  We report a case of PNH-induced renal failure successfully managed by live kidney transplantation (4/6 HLA mismatch, no donor specific antibodies).
Case Report: Our patient was a 53-year-old man with a 20-year history of PNH.  His initial treatment from diagnosis included regular blood transfusions and high dose steroids, though in more recent years requiring eculizumab every 12-14 days.  Despite these treatments, he developed end stage renal failure due to progressive biopsy-proven chronic tubulo-interstitial nephritis.  At time of transplant he had successfully been on home haemodialysis for five-and-a-half years.  He was initially considered for combined bone marrow and kidney transplant as treatment for both PNH and ESKD, however no suitable donor was found.  Peri-transplant treatments included ongoing eculizumab every 12 days, in addition to immosuppression with basiliximab and methylprednisone at induction, and tacrolimus, mycophenolate and prednisolone as maintenance.  Post-transplant function was immediate, with associated fall of creatinine down to a nadir of 111 umol/L.  Complications post-transplant have included a perigraft haematoma requiring surgical evacuation, an episode of steroid-responsive cellular rejection, biopsy-associated haemorrhage, drug-induced leucopaenia and neutropaenia, and occasional episodes of haemolysis associated with viral respiratory tract infections.
Conclusions: To our knowledge this is the first case of successful live renal transplantation for PNH-induced renal failure in Australia.  The logistics associated with the planning for such a transplant can likely only be done with a directed live donor.


Biography:
Advanced Trainee in Nephrology with the East Coast Renal Network.

OBESITY RELATED RENAL GRAFT COMPRESSION LEADING TO ACUTE KIDNEY INJURY

S HULTIN1, L THEBRIDGE1, C FISHER1, C POLLOCK1
1Royal North Shore Hospital, St Leonards, Australia

Background:  We present the first case of renal graft compression from central adiposity resulting in acute kidney injury.
Case Report: A 61 year old man with a cadaveric transplant presented with hypertension and acute kidney injury with a creatinine rise from 80 to 210 µmol/L. His past medical history included controlled diabetes, hypertension, ischaemic heart disease, and obesity requiring gastric sleeve with subsequent weight gain from 90 to 110kg. Renal biopsy was consistent with acute tubular necrosis without significant interstitial inflammation or signs of rejection. Serial renovascular doppler studies of the transplant graft were abnormal. Initial scanning showed severely reduced diastolic flow normalising towards the upper pole (RI0.78). The renal vein flow had normal phasicity and renal artery velocity was 336cm/s. Repeat scanning showed absence of diastolic flow and reduced perfusion despite a patent renal transplant artery and vein. Raising the fatty apron cephalad normalised renal blood flow with resistive indices between 0.76-0.79 throughout the kidney. Subsequent laparascopy ruled out adhesional obstruction and CO2 angiogram confirmed normal transplant vessels, anastomotic sites and intra-renal branches. Following initial empiric pre-biopsy pulsed steroids for presumed rejection, he was treated with bedrest and his creatinine was130µmol/L on discharge. Whilst advising weight loss, he was treated with an abdominal support belt.
Conclusions: Transplant physicians and surgeons need to be aware of renal graft compression from an enlarged bulky omentum and fatty apron. Diagnosis requires positional prone doppler sonography. Aside from weight loss, optimal treatment is not known.


Biography:
Prior to enrolling in medical school, Sebastian completed a Bachelor of Science in Medical Biochemistry to provide a scientific foundation to a future in academic clinical medicine. After graduating from medical school at King’s College London, he continued his post graduate training in Bristol University Hospital Trust and St George Hospital, Sydney, completing FRACP in 2016. He is currently undertaking advanced training in nephrology and collaborating at QIMR Berghofer Institute in cellular immunology. His main academic focus is renal transplantation and transplant immunology.

RITUXIMAB INDUCTION SUCCESSFULLY PREVENTING MESANGIOCAPILLARY GLOMERULONEPHRITIS RECURRENCE IN TRANSPLANTATION

L MCMICHAEL1, S MURTHY1, G IRISH1, S CHANG2, P COATES1, S MCDONALD1
1Central and Northern Adelaide Renal and Transplantation Service, Adelaide, Australia, 2SA Pathology, Adelaide, Australia

Background: Recurrent mesangiocapillary glomerulonephritis (MCGN) post transplantation is a common cause of graft loss with rates of recurrence from 19 to 48% with up to 88% of grafts failing following recurrence. Various strategies have been employed to manage recurrent disease post-transplantation, however there is limited data on pre-emptive management of patients at transplantation.
Case Report: We report a case of a 63-year-old woman with immune-complex-mediated MCGN receiving a second renal transplant following recurrence in her 2/6 HLA mismatched primary transplant.  Primary transplant recurrence was identified on biopsy day 76 following development of proteinuria and increasing creatinine. This was managed with cyclophosphamide and plasma exchange with return to long term haemodialysis at day 86. After 10 years on haemodialysis the patient received a second well matched deceased donor transplant with 0/6 HLA mismatches. Induction immunosuppression included anti-thymocyte globulin at day 0,1,2, plasma exchange at day 3 and rituximab 1g at day 5 and 18. Routine protocol biopsy at day 79 demonstrated minimal tubulitis and no recurrent primary disease. A subsequent biopsy was performed at day 197 due to elevated creatinine following clostridium difficile infection which demonstrated no recurrent disease. She has been maintained on prednisolone, mycophenolate mofetil and tacrolimus with stable graft function at 7 months.
Conclusions: The optimal therapy for managing patients with idiopathic MCGN at the time of transplantation is unknown. We demonstrate a novel protocol utilising planned rituximab and plasma exchange for pre-emptive management of patients with idiopathic MCGN with no sign of recurrence at 7 months post transplantation.


Biography:
Nephrology Registrar at Central Northern Adelaide Renal and Transplantation Service.

PRETRANSPLANT PLASMAPHARESIS IN HLA ANTIBODIES POSITIVE KIDNEY TRANSPLANTATION RECIPIENT

T WIDODO1, I KUSWADI2, H PRASANTO3, I PUSPITAWATI4
1Sardjito Hospital, Yogyakarta, Indonesia, 2Sardjito Hospital, Yogyakarta, Indonesia, 3Sardjito Hospital, Yogyakarta, Indonesia, 4Sardjito Hospital, Yogyakarta, Indonesia

Background: Acute kidney graft rejection caused by antibody mediated is common problem in kidney transplantation. Antibody mediated rejection is B cell mediated rejection directed againts human leucocyte antigen (HLA). Plasmapharesis is one of desenzitation procedure  for kidney transplants recipient who have high level HLA antibodies positive crossmatch. Plasmapharesis can reduced HLA antibodies level and diminished antibody mediated rejection. Plasmapharesis sometimes was combined with immunospressive agents and intravenous immunoglobulin (IVIG) as desenzitation procedure for transplantation patients.
Case: A male 42 years old diagnosed end state renal diseases, routine hemodialysis, undergoing kidney transplantation with unrelated donor with HLA matching results 7/16. Plasmapharesis combine with immunosuppressive monoclonal antibodies and IVIG was taken as desensitization procedure pretransplantation. Post desensitization, renal transplantation was done with good physical and laboratory examination results, no signs of acute rejection were found.
Discussion: Plasmapharesis is a mechanical procedure for high level HLA antibody positive recipients. Plasmapharesis requiring adequate equipment which is not always available in Indonesian hospital. Plasmapharesis would decreased HLA antibodies level in kidney transplant recipients and proposed as one of desensitisation procedure. Plasmapharesis combined with immunosupressive agents and  IVIG would decreased antibody mediated rejection risk. In this case, plasmapharesis proved to be beneficial in lowering HLA antibodies level and clinically useful.
Keyword: Plasmapharesis, HLA antibodies, kidney transplantation.


Biography:
I’m a fellowship program in Renal and Hypertension Division, Internal Medicine, Sarjito Hospital

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