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

PERITONITIS AS A RISK FACTOR FOR CARDIOVASCULAR EVENTS IN PERITONEAL DIALYSIS PATIENTS

K HEPBURN1, K LAMBERT2, J MULLAN2, B MCALISTER2, M LONERGAN1, H HASSAN1
1Department of Renal Medicine, Wollongong Hospital, Wollongong, Australia, 2Centre for Health Research Illawarra Shoalhaven Population (CHRISP), University of Wollongong, Wollongong, Australia

Aim: To examine peritonitis as a risk factor for cardiovascular events (CVE) in patients undertaking peritoneal dialysis (PD).
Background: Cardiovascular disease (CVD) is the leading cause of mortality and morbidity in PD. There is a documented association between infection and an increase in CVE. However, no studies have examined the association between peritonitis and CVE in the PD population.
Methods: All adult patients undertaking PD for more than 3 months in one NSW health district from 2001-2015 were included in this retrospective cohort analysis. Patients, baseline characteristics and peritonitis events were obtained from the ANZDATA Registry. CVE data using ICD10 coding was obtained and data linkage was facilitated by the Centre for Health Research Illawarra Shoalhaven Population (CHRISP). Time-dependent covariate analysis using Cox-proportional models were used to determine hazard ratios.
Results: 212 patients were included; median age was 66 years (IQR 54.3-74.4) and 63.7% were male. Glomerulonephritis was the most common underlying renal disease (29.2%). 128 patients (60%) experienced peritonitis, and 64 (30.2%) experienced CVE. Risk factors for CVE were cerebrovascular disease (HR 2.74, 95%CI 1.37-5.51, p=0.005), diabetes (HR 2.29, 95%CI 1.39-3.77, p=0.001), CVD (HR 1.73, 95%CI 1.04-2.87, p=0.04) and age (HR 1.04, 95%CI 1.02-1.06, p=0.01). Risk of CVE from peritonitis was 1.33 (95%CI 0.79-2.25, p=0.28), even when accounting for covariates (HR 1.33, 95%CI 0.78-2.26, p=0.29).
Conclusions: This is the first study to quantify risk of CVE in PD patients who develop peritonitis. We found that peritonitis increases the risk of CVE by 33%. Statistical significance was not reached in this study, possibly due to a low event rate and relatively small sample size. Larger studies to explore this important association are warranted.


Biography:
Dr Kirsten Hepburn is a second year Nephrology Advanced Trainee in the East Coast Renal Network, Sydney, NSW. Her other degrees include BSc (Psych) and MPH.

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

POST KIDNEY TRANSPLANTATION MEMBRANOPROLIFERATIVE GLOMERULONEPHRITIS ASSOCIATED WITH LIGHT-CHAIN PARAPROTEINAEMIA

A STEINBERG1, N BARRACLOUGH2, P HILL3, K DWYER4, D GOODMAN1, FIERINO1
1Department of Nephrology, St Vincent’s Hospital Melbourne, Fitzroy, Australia, 2Warrnambool Base Hospital, Warrnambool , Australia, 3Department of Anatomical Pathology, St Vincent’s Hospital Melbourne, Fitzroy, Australia, 4School of Medicine, Deakin University, Geelong, Australia

Background: Membranoproliferative glomerulonephritis (MPGN) arising post transplantation can represent de novo disease or recurrence and may be idiopathic or secondary to viral infections, autoimmune disease and malignancy. An accurate diagnosis is critical to guide management and preserve graft function.
Case Report: A forty-five year old male with end-stage renal disease of unknown aetiology received a transplant from his father in 2009 with baseline serum creatinine 150µmol/L, maintained on standard immunosuppression. He developed non-nephrotic range proteinuria (urinary albumin-creatinine ratio [uACR]198mg/mmol) and microscopic haematuria.  A diagnostic transplant renal biopsy demonstrated MPGN; immunofluorescence was positive for IgG kappa and lambda light chains without restriction, C3 and C1q; IgM and IgA were negative. Electron microscopy confirmed immune deposits.   Hepatitis B and C, ANA and ANCA were negative.  C3 was reduced at 0.58 g/L (normal 0.9-1.8); C4 was within normal range.   Serum kappa free light chains were elevated (446 mg/L; normal 3.3-19.4) with an increased ratio (13.4). Bone marrow aspirate revealed a mild plasmacytosis (5-10%). He was treated with high-dose prednisolone and cyclophosphamide but failed to respond with progressive proteinuria and rising creatinine (peak 399µmol/L).  Repeat biopsy again demonstrated MPGN with increasing immune-type deposits.  Targeted B-cell therapy with rituximab (two 1000mg doses) was administered with a clinical response evidenced by an improving creatinine to 198µmol/L, and reduction in proteinuria (uACR 102mg/mmol).
Conclusion: Although the bone marrow aspirate was not diagnostic, the light-chain paraproteinaemia and increasing immune-type deposits on biopsy implicate a primary underlying B-cell clonal disease. The failure to respond to non-specific immunosuppression and the response to rituximab supports this premise.   This case demonstrates the need to better understand mechanisms underlying disease processes to facilitate the delivery of personalised therapy.


Biography:
Adam is a second-year advanced trainee in nephrology.

SPONTANEOUS SUPERIOR MESENTERIC VEIN THROMOBOSIS 13 YEARS AFTER SUCCESSFUL RENAL TRANSPLANTATION

A MAHER1, V HERON1, S GOVINDARAJULU1
1Darling Downs Hospital, South Toowoomba, Australia

We describe a case of a spontaneous superior MVT in a patient 13 years post renal transplant. We will detail the potential underlying conditions and pathogenesis leading to a hypercoagulable state in the post transplant setting including post transplant erythrocytosis and the therapeutic challenges surrounding anticoagulation with numerous pharmacological interactions particularly with immunosuppressive medications. A 55 year old female presented with fevers, vomiting, diarrhoea and abdominal pain. On examination she was febrile to 38.6 degrees, tachycardic to 120 beats per minute and normotensive. Abdominal examination demonstrated mild generalised tenderness without peritonism. Past medical history was significant for a cadaveric renal transplant in 2002 for renal failure secondary to reflux nephropathy with a baseline creatinine of 70umol/L. Other comorbidities included post-transplant polycythaemia and an unprovoked below knee deep vein thrombosis (DVT) 6 years previously. Medications included cyclosporin, everolimus, prednisolone, sulfamethoxazole and trimethoprim and aspirin. Investigations included full blood count, biochemistry, C-reactive protein (CRP) and urine, blood and stool cultures. CRP was 160, otherwise there were no abnormalities. Abdominal ultrasound demonstrated a transplant kidney within normal limits with no other positive findings. Her pain resolved with analgesia and she was managed conservatively with intravenous fluids and analgesia with surgical input.  On day three of admission she developed a diffusely tender abdomen. A CT  revealed a complete superior MVT. A heparin infusion was initiated and her symptoms resolved. She was continued on warfarin indefinitely due to two unprovoked thrombotic events. Follow up was arranged given the potential for multiple interactions of warfarin with cyclosporin, everolimus and sulfamethoxazole/trimethoprim.


Biography:
Vanessa Heron is an advanced trainee in nephrology working at the Toowoomba Hospital. Mesenteric venous thrombosis (MVT) is a rare condition with an overall incidence of two cases in a population of 100 000.

ARE THE BIOMARKERS ACCURATE? A CASE OF COVERT ATYPICAL HAEMOLYTIC URAEMIC SYNDROME IN A RENAL ALLOGRAFT RECIPIENT

L SKEAT1, S DHEDA1
1Cairns Base Hospital, Cairns, Australia

Background: Atypical haemolytic uraemic syndrome (aHUS) represents a subset of thrombotic microangiopathies strongly associated with genetic abnormalities in the alternative complement pathway. Recurrence of aHUS in renal allografts is common, as is de novo disease. Surveillance involves monitoring of peripheral haemolysis markers including thrombocytopenia, LDH, haptoglobin, haemoglobin and fragments on blood film. However, multiple case reports of subclinical aHUS are emerging, calling into question the accuracy of peripheral haemolysis markers. We present a case of recurrent aHUS with normal haemolysis markers, suggesting that aHUS can recur in the allograft in the absence of haematological abnormalities.
Case Reports: A 55-year -old Caucasian women with both native and previous renal graft loss from aHUS, with a confirmed C3 mutation presented with worsening graft function of her second renal transplant. Initial biopsy showed antibody mediated rejected treated with plasma exchange, intravenous immunoglobulin and steroids. Graft function did not improve and two further biopsies were inconclusive. Haemoglobin, platelets, LDH, haptoglobin and blood film remained normal during this time. Given a high index of suspicion and with her genetic propensity, a 3rd biopsy was performed with showed covert renal restricted TMA, confirming recurrent aHUS in her graft. Renal function stabilized with eculizumab and the patient has remained on this therapy while completing a 6-month trip around Australia.
Conclusion: This case highlights that aHUS can recur in renal allografts in the absence of haematological abnormalities. Clinicians should maintain a high level of suspicion for recurrent aHUS and have a low thresh-hold to perform a renal biopsy, particularly in those with a confirmed genetic mutation.


Biography:
Dr Lee Skeat is a current trainee renal registrar who has spent time working in Far North Queenslan

SUCCESSFUL KIDNEY TRANSPLANTATION IN A PATIENT WITH MATERNAL INHERITED DEAFNESS AND DIABETES (MIDD)

E HO1, R JUNEJA2, J BARBARA3, J LI4
1Flinders University , Bedford Park, Australia, 2Flinders Medical Centre, Bedford Park, Australia, 3Flinders Medical Centre, Bedford Park, Australia, 4Flinders Medical Centre, Bedford Park, Australia

Background: Maternal Inherited Deafness and Diabetes (MIDD) and Mitochondrial Encephalopathy, Lactic Acidosis and Stroke-like episodes (MELAS) are maternally inherited mitochondrial disorders that have the same m.3243A>G mutation with different phenotypes. Renal involvement is observed in patients with MIDD or MELAS. These patients can progress to end-stage kidney disease, requiring renal replacement therapy.
Case Report: A 54-year-old man presents with chronic kidney disease on a background of diabetes mellitus, sensorineural hearing loss, hypertension, hyperlipidaemia and cardiomyopathy. His mother had been diagnosed with MELAS syndrome. Genetic analysis showed positive for m.3243A>G mutation with a mutational loading of 13%; this is consistent with MIDD. He received a deceased donor kidney transplant in March 2017. He is now 1 year post-transplantation with stable allograft function (serum creatinine 101 µmol/L) and is well.
Conclusion: Patients with m.3243A>G mutation often exhibit a broad array of phenotypes with renal involvement being observed in both MIDD and MELAS. Their prognosis is variable. Kidney transplantation should be considered in these patients. Careful perioperative management including the use of Coenzyme Q10 can help to prevent potential complications. Kidney transplantation can improve a patient’s prognostic outlook.


Biography:
I am currently a Year 3 medical student doing my advanced studies under Dr Jordan Li at the Flinders Medical Centre with an interest in studying the impact of renal transplantation on patients with mitochondrial diseases and observing their progress post-operation.

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