PREDICTION OF THE OUTCOME OF ACUTE RENAL REPLACEMENT THERAPY

Y WANG1, M GALLAGHER1, Q LI1, R BELLOMO2
1The George Institute For Global Health, Newtown, Australia, 2Austin Health, Heidelberg, Australia

Aim:  To identify the predictors for renal recovery to dialysis independence at day 28 in critically ill patients with severe acute kidney injury (AKI) requiring renal replacement therapy (RRT).
Background: Recovery of kidney function is a fundamental outcome for survivors of critical illness. Different modalities of renal replacement therapy (RRT) may impact renal recovery.
Methods:  The IMPROVE-AKI study was an individual patient data meta-analysis of previous RCTs of RRT dose intensity in severe AKI to assess the effects of RRT dose intensity on RRT independence. Baseline variables including demographic characteristics, disease severity and RRT characteristics were collected. The primary outcome was successful renal recovery to dialysis independence at day 28, defined as no requirement of RRT by day 28. Predictors for renal recovery were analysed using logistic regression analysis.
Results:  The IMPROVE-AKI study included 7 RCTs and 3575 patients. Among them, 1926 patients had data on recovery or failed recovery to RRT independence at day 28. Baseline mechanical ventilation (OR 0.70, 95% CI 0.50-0.99, P=0.047) and low pH (OR 0.18, 95% CI 0.05-0.71, P=0.014) predicted decreased likelihood of recovery, while higher baseline urine output (OR 1.21, 95% CI 1.18-1.24, P=0.000), and use of Continuous RRT instead of intermittent RRT (OR 3.04, 95% CI 2.13-4.35, P=0.000) predicted successful renal recovery at day 28. Initial modality of dialysis (i.e. CRRT vs IRRT) was the strongest predictor for renal recovery. The presence of pre-existing CKD did not affect renal recovery in a sensitivity analysis.
Conclusions:  Initial dialysis with CRRT predicted better renal recovery in patients with severe AKI. Further large RCTs are needed to assess effects of different modalities of dialysis on renal recovery in severe AKI patients.


Biography:
Dr Amanda Wang is a nephrologist and post-doctoral research fellow at the George Institute for Global health, with research interest of acute kidney injury and dialysis.

TENDENCY TO PRESCRIBE EXCESSIVE EFFLUENT DOSES FOR CONTINUOUS RENAL REPLACEMENT THERAPY IN OUR MEDIUM-SIZED INTENSIVE CARE UNIT

F REIMANN1, M ROWLAND1, B SEIDEL1, S KHAN1, M BASTICK1
11Intensive Care Unit, Gosford Hospital, Central Coast Local Health District, New South Wales, Australia,

Aim: To evaluate effluent dose prescriptions of continuous veno-venous haemodiafiltration (CVVHDF) in adult patients with acute kidney injury (AKI) in our 15-bed intensive care unit (ICU).
Background: An effluent dose of 25 to 30 mL/kg/hr is routinely recommended for CVVHDF, although a higher dose may be used to correct severe acidosis or hyperkalaemia.
Methods: Records of all patients who underwent continuous renal replacement therapy (CRRT) over a nine month period in 2017 at Gosford Hospital were retrospectively analysed.
Results: Twenty nine patients received CRRT, performed as CVVHDF, with a mean duration of 64 hours. The mean effluent dose prescribed and delivered was 32.7 mL/kg/hr with a standard deviation of 11.0 mL/kg/hr. Of nine patients (31.0 %) who received a dose above 35 mL/kg/hr, only five patients (55.6 %) had an appropriate indication (serum pH less than 7.1 or serum potassium above 7.0 mmol/L). A dose less than 20 mL/kg/hr was initially prescribed and delivered for two patients (6.9 %). Of the eleven patients with very high or very low dose CRRT prescriptions, appropriate dose adjustments were subsequently made for seven patients (63.6 %).
Conclusions: There was a tendency to prescribe excessive effluent doses for CVVHDF in patients with AKI in our ICU. A small number of patients was under-dialysed. The clinical significance of these aberrations is uncertain. An educational program and decision-making tool has been introduced to guide prescribing practice.


Biography:
Graduated from Medicine in Germany in 2002. Completed Physician training in 2017 with RACP fellowship in Nephrology. Current post-fellowship training in General and Acute Care Medicine

AN UNUSUAL CASE OF ACUTE KIDNEY INJURY

A XAVIER1, K HUSSAIN1
1Goulburn Valley Health, Shepparton, Australia

Introduction: Acute kidney injury due to acyclovir nephrotoxicity is uncommon. Here we present a case that occurred in a teenager who also went on to get diagnosed with diabetes insipidus.
Case Report: A 17 yr old male patient with history of severe learning disabilities due to Angelman syndrome and epilepsy was admitted with pyrexia. His mother had noticed that he had developed multiple mouth ulcers, with resultant reduced oral intake and had become drowsy. On admission he was noted to be dehydrated, with herpetic mouth ulcers and no other source of sepsis identifiable. Septic work up was done and he was treated with cefipime and vancomycin. In the next 48 hrs he became more drowsy and serum sodium rose up to 157 mmol/L from normal. Concerned about the possibility of herpes encephalitis, intravenous acyclovir was commenced along with appropriate intravenous fluids. Creatinine doubled within 24 hrs of commencement of acyclovir and continued to rise for another 3 days and peaked at 263 umol/L. Urine analysis revealed microhaematuria, pyuria and crystals, which was new. Renal screen was negative and renal imaging was normal. Acyclovir was discontinued after 3 days of administration. There was a gradual improvement in renal function back to baseline within 2 weeks. He remained polyuric throughout the admission and this delayed renal recovery. His mother had noted polyuria even prior to this admission. Thus he was brought back in a few weeks and diabetes insipidus was confirmed.
Conclusion: This case highlights the need to ensure that patients are well hydrated during intravenous acyclovir therapy with close monitoring of renal function. This patient was particularly at increased risk due to undiagnosed Diabetes Insipidus.


Biography:
Dr Hussein graduated from Dubai Medical College and had been training in general medicine prior to moving to Australia in 2017.She is currently a medical registrar in GV Health

STATIN-ASSOCIATED RHABDOMYOLYSIS WITH RENAL FAILURE AS A CONSEQUENCE OF DRUG-DRUG INTERACTION WITH ERYTHROMYCIN

V HERON1, S WILKINSON1, A YOUNG1, M NICHOLSON1, S GOVINDARAJULU1, S VENUTHURUPALLI1
1Renal Service, Darling Downs Hospital and Health Service, Toowoomba, Australia

Background: Statins are amongst the most widely prescribed medications worldwide. Myopathies are a well-recognised adverse effect, including rhabdomyolysis. Simvastatin, along with atorvastatin, are metabolised by cytochrome P450 isoenzyme 3A4 (CYP3A4). The risk of statin-associated rhabdomyolysis is increased in patients receiving concurrent treatment with medications that inhibit CYP3A4, including macrolide antibiotics.
Case Report: A 78 year old male presented with lower back pain and generalised weakness. His past medical history was significant for ischaemic heart disease, type 2 diabetes, dyslipidaemia and chronic kidney disease with a baseline creatinine of 200-220μmol/L. His regular medications included aspirin, insulin, candesartan and long-term high-dose simvastatin. One week prior to hospital presentation he had completed a course of erythromycin for a lower respiratory tract infection. He was initially admitted to the short stay unit for physiotherapy and was subsequently referred for medical admission. Investigations on admission revealed an acute kidney injury (creatinine 377μmol/L; GFR 12), which was managed with intravenous fluids. During the course of admission, his weakness progressed and pain extended to involve his thighs and shoulders and there was concern raised regarding the possibility of rhabdomyolysis. Creatinine kinase was elevated at 11,600U/L, peaking at 229,000U/L, despite aggressive intravenous rehydration. This was associated with a creatinine of 727μmol/L and urine myoglobin of 164,000mcg/L. He subsequently became anuric, necessitating commencement of dialysis. Testing for anti-hydroxymethylglutaryl-coenzyme A reductase (HMGCR) autoantibodies was negative.
Conclusion: In the case of this patient, given long-term statin therapy without previously reported myopathy, the sudden onset of severe rhabdomyolysis was attributed to the concurrent prescription of erythromycin. This case highlights the importance of recognising potential drug interactions amongst commonly prescribed medications, to avoid detrimental adverse effects.


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

DABIGATRAN TOXICITY ASSOCIATED WITH ACUTE INTERSTITIAL NEPHRITIS REQUIRING HAEMODIALYSIS DESPITE REPEAT IDARUCIZUMAB DOSES

L MCBRIDE1, J WANG1, P HO1,2,3, D LANGSFORD1,2
1Northern Health, 2University of Melbourne, 3Monash University,

Background: Dabigatran can be reversed with a single dose of idarucizumab in patients with normal renal function. We present a case of acute kidney injury with dabigatran toxicity requiring three doses of idarucizumab and daily haemodialysis.
Case Report: A 71-year-old man presented with acute gastrointestinal bleeding (haemoglobin 78g/L) and non-oliguric acute kidney injury (creatinine 1414umol/L) 6 weeks after a stroke and commencement of dabigatran (when he had normal renal function). Renal tract imaging, vasculitis and autoimmune screens were normal. His INR was 8.7 (initial APTT not available). Dabigatran was ceased and idarucizumab administered. Post-dose rebound coagulopathy occurred (APTT 89.7) indicating a further idarucizumab dose. Immediately following this dose a temporary dialysis line was inserted and the patient was commenced on increasingly efficient daily haemodialysis, at which time the dabigatran level was undetectably high. At 72 hours the patient was haemodynamically unstable with haemoglobin 64g/L and had rebound in coagulopathy (APTT 45), indicating a third dose of idarucizumab. We observed significant rebound in dabigatran and APTT both following the administration of idarucizumab and haemodialysis. The dabigatran level gradually declined to non detectable over 14 days of daily haemodialysis, when a renal biopsy revealed severe acute interstitial nephritis. Detailed medication history failed to identify a known causative agent. The patient was commenced on 60mg prednisolone daily and haemodialysis was withdrawn 6 weeks later following renal recovery.
Conclusions: This is the first report of biopsy proven dabigatran associated acute interstitial nephritis and also the first report of dabigatran toxicity requiring three doses of idarucizumab. Importantly, the three doses were not sufficient to reverse dabigatran and efficient daily hemodialysis was required to achieve complete dabigatran clearance.


Biography:
Nephrologist and General Physician at Northern Health

 

ACUTE KIDNEY INJURY – eAlert , IMPROVING RENAL OUTCOMES

A XAVIER1, T JACOBSON1,R GILMORE1, Y LIM1
1Goulburn Valley Health, Shepparton, Australia

Background: Acute Kidney Injury (AKI) is present in 5-20%¹ hospitalized patients. Delay in recognition is one of the main hurdles to appropriate management of AKI. We audited the care of patients that had AKI prior to setting up an AKI e-alert system.
Method: An algorithm² on the hospital reporting system was set up to capture patients who had AKI based on creatinine rise. Those with AKI during February 2018 were audited. We looked at promptness in diagnosis and the early management of AKI. This included addressing their medications, targeting blood pressure of >110 systolic, an input /output chart, urine dipstick and renal imaging if appropriate.
Results: 46 (10% of all acute adult admissions) patients had AKI and were included in this audit. Majority of the patients 36 (78%) had AKI 1, 1(2%) patient had AKI 2 and 9 (20%) had AKI 3. 36 (78%) were over 60 yrs of age. Majority (98%) of the patients with AKI 2 and 3 had early recognition (within 24 hrs) and appropriate care.10 (32%) of those with AKI 1 had inadequate care as per the audit standards but did not lead to progression in AKI. All patients with AKI 2 and 3 were referred to the renal team.
Discussion: This audit showed a third of the patients with AKI 1 had delayed recognition and thus deficiencies in their care. The findings supported setting up of an AKI e-alert system. An alert is now automatically generated against the patients name on the handover sheet. We have now set up training about the alert system and management of AKI based on the ABCDE approach ³ with a re-audit in due course.


Biography:
Dr Jacobson graduated from University of Melbourne 2016.Completed internship at GV health Shepparton and currently working as a HMO in Medicine.He has an interest in Acute kidney Injury.

PAR-1/S1P PATHWAY IN RENAL ISCHAEMIA-REPERFUSION INJURY

J LIU1, K TAYLOR1, A AU1, Z ENDRE1, J ERLICH1
1Renal Research Laboratory, Department of Nephrology, Prince of Wales Hospital and Prince of Wales Clinical School, Faculty of Medicine, UNSW Sydney, Randwick, Australia

Aim To investigate factors downstream of protease-activated receptor-1 (PAR-1) that may mediate ischaemia-reperfusion injury (IRI).
Background: IRI is a common cause of acute kidney injury (AKI) and occurs post-kidney transplantation. We have previously reported that post-IRI, PAR-1 deficiency reduces histological injury and loss of glomerular filtration rate (GFR). PAR-1 may regulate a number of inflammatory mediators via regulating the sphingosine 1-phosphate (S1P) pathway. S1P is actively exported from cells to act on external S1P receptors (S1Pr1-5) to have a diverse range of effects. We hypothesise that PAR-1 deficiency attenuates renal IRI in part by reducing the injurious S1Pr3 pathway.
Methods Renal IRI was induced by clamping of the renal pedicles for 25 minutes. Sham-operated mice underwent surgery without clamping of the renal pedicles. Mice were culled at 2, 5 and 24 hours post-reperfusion. Blood, urine and kidney tissue was taken for further analysis. Gene expression was performed by real-time PCR.
Results: We assessed S1Pr3, Spinster 2 (SPNS2) a major S1P membrane channel, and Hes1, a downstream product of S1Pr3 activation. Compared to WT, PAR-1 deficiency resulted in reduced SPNS2 expression in both mice undergoing IRI and sham surgery. PAR-1 deficient mice had reduced S1Pr3 levels compared to WT and S1Pr3 levels were not induced at 5 and 24 hours compared to sham operated mice. This supports a functional effect of reduced S1Pr3 and SPNS2 expression in PAR-1 mice as there was reduced Hes1.
Conclusion: Taken together the data supports a potential role of reduced S1Pr3 signalling contributing to protection of PAR-1 deficient mice following IRI. This may occur via both reduced export of S1P to the cell surface and reduced S1Pr3 expression and signalling.


Biography:
Medical student, Renal Research Laboratory, Prince of Wales Hospital and Faculty of Medicine, UNSW

 

PROGNOSTIC SIGNIFICANCE OF LOW LEVEL OF BLOOD GLUCOSE IN SEVERE ACUTE KIDNEY INJURY: A SECONDARY ANALYSIS FROM THE RENAL STUDY

Y XIE2, J LIN3, M GALLAGHER1, R BELLOMO4, M JARDINE1, A WANG1
1The George Institute for Global Health , Sydney, Australia, 2The Second Affiliated Hospital of Soochow University, suzhou, China, 3Beijing Friendship Hospital, Beijing, China, 4 Austin Hospital, Melbourne, Australia

Aim: To determine associations between baseline blood glucose levels (BGL) and clinical outcomes in patients with severe acute kidney injury (AKI) receiving continuous renal replacement therapy (CRRT).
Background: Uncontrolled hyperglycaemia is associated with high mortality in critically ill patients.
Methods: A secondary analysis from the RENAL study was performed. The primary endpoint was all-cause mortality at 90 days after randomization. The secondary outcomes included duration of hospital and ICU stays. The multivariate Cox regression model adjusted for baseline variables was used to assess associations of baseline BGL (measured prior to patient randomization) and mortality.
Results: Baseline BGL data were available in 1404 out of 1508 patients. The patients were divided into 4 groups using quartiles of baseline BGL (group 1, BGL <5.8mmol/L, group 2, BGL 5.8-7.2mmol/L, group 3, BGL 7.3-9.1mmol/L, and group 4, BGL>9.2mmol/L). A total of 627 patients died in 4 groups (51.7% in group 1, 38.7% in group 2, 44.5% in group 3, and 44.0% in group 4). The Cox regression model showed the baseline BGL in patients in the group 1 (<5.8 mmol/L) was associated with an increased risk of death at 90 days (HR 1.47, 95% CI 1.13–1.90, p=0.0036), compared with the group 2 (BGL 5.8-7.2mmol/L), while BGL in the group 3 and 4 did not show a significant impact on 90 days mortality. Furthermore, there were no significant differences in the duration of hospital and ICU stay among these 4 groups (p=0.55 and p=0.30, respectively).
Conclusion: Baseline BGL of less than 5.8mmol/L appears to be associated with higher mortality. This effect may be due to other unmeasured comorbidities but may warrant further study in the setting of severe AKI.


Biography:
Visiting Fellow, Renal & Metabollic Division of The George Institute for Global Health

IgG-4 RELATED DISEASE PRESENTING WITH ACUTE KIDNEY INJURY AND NEPHROTIC RANGE PROTEINURIA

A SAN1, S CHANDLER1, RMILES1
1Greenslopes Private Hospital, Greenslopes, Australia

Background: IgG-4 related disease is a multisystem sclerosing disorder characterised by elevated IgG-4 levels, eosinophilia and Ig-G4 positive plasmacytic infiltration of various organs including kidneys, pancreas, thyroid, salivary glands and biliary tract. The most common renal manifestation is tubulointerstitial nephritis with sclerosis. Membranous nephropathy and proliferative glomerulonephritides may co-exist.
Case Report: A 54-year-old man was referred to the renal clinic in 2012 for multifocal T2 hyperintensities in the kidneys on PET/CT scan during his work-up for IgG monoclonal gammopathy. Past medical history included type 2 diabetes, hypertension and chronic sinusitis. Renal function was normal with serum creatinine 90 μmol/L without haemoproteinuria. Renal MRI confirmed numerous T2 low signal foci, thought to be lipid poor angiomyolipomata.Over five years he developed asthma, progressive sinusitis, profound lethargy, night sweats and low-grade fevers. In March 2018, he represented with serum creatinine of up to 160 μmol/L with nephrotic range proteinuria (urinary protein-to-creatinine ratio of 582 g/mol), hypoalbuminaemia (22 g/L), intermittent microscopic haematuria, marked eosinophilia (5.3 x 10*9/L), and elevated IgG (51g/L). Renal biopsy showed heavy interstitial infiltrate of a mixture of IgG-4 positive plasma cells and eosinophils with zones of collagenous sclerosis. The two glomeruli contained in the specimen were morphologically normal. The diagnosis of IgG-4 related disease was made and renal function recovered within five days of commencing steroid therapy.
Conclusion: IgG-4 related renal disease should be considered in patients presenting with renal parenchymal abnormalities in the presence of systemic symptoms, eosinophilia and elevated IgG. In this case, the urinary abnormalities were suggestive of co-existing glomerulonephritis. However this was not seen, likely due to sampling error. Excellent response to steroid therapy was achieved.


Biography:
Aye San is a dual Advanced Trainee in Nephrology and General medicine at Greenslopes Private Hospital.  She also hold the position of Chief Medical Registrar and Lecturer in Greenslopes Clinical Unit of University of Queensland.

HIGH DOSE VITAMIN C (ASCORBIC ACID) CAUSING RENAL FAILURE DUE TO OXALATE NEPHROPATHY

B DOUCET1,2, E NOBLE1, N GRAY1,2
1Department of Nephrology, Sunshine Coast University Hospital, Birtinya, Australia, 2School of Medicine, University of Queensland, Brisbane, Australia

Background: Vitamin C (ascorbic acid) is commonly prescribed for complementary and alternative medical indications or used as a personal health choice.  Intravenous vitamin C treatments are gaining popularity in the alternative management of malignant conditions despite the lack of evidence to suggest benefit.  The risks of high dose vitamin C may not be appreciated by prescriber or recipient.  One of the most devastating adverse effects of high dose vitamin C is oxalate nephropathy.
Case Report: We report two cases of vitamin C induced oxalate nephropathy.  A 67 year old male with metastatic oesophageal cancer underwent high dose intravenous vitamin C treatment through a registered Australian medical practitioner for treatment of malignancy.  He presented to hospital with anuric renal failure requiring urgent haemodialysis.  Serological and imaging investigations revealed no cause of renal impairment.  He did not respond to fluid resuscitation and remains dialysis dependant.  An 80 year old female presented to hospital with malaise.  Investigations revealed severe kidney injury on the background of consuming multiple self-initiated alternative medications, several containing vitamin C.  No other cause of renal impairment was identified and vitamin C supplements were ceased.  Renal function has improved close to baseline over a one month period.  Renal biopsy in both cases revealed severe tubular injury and extensive tubular oxalate crystal deposition consistent with oxalate nephropathy.
Conclusions:  High dose vitamin C can cause severe and potentially irreversible renal impairment due to oxalate nephropathy and awareness needs to be raised in conventional and alternative medical communities as well as the general population of the danger associated with this treatment.


Biography:
Brian Doucet is a second year Nephrology advanced trainee from Queensland.  He has previously presented at the ANZSN ASM in 2014 and 2017.

 

About ANZSN

The ASM is hosted by Australian and New Zealand Society of Nephrology.

The aims of the Society are to promote and support the study of the kidney and urinary tract in health and disease, and to ensure the highest professional standards for the practice of nephrology in Australia and New Zealand.

Conference Managers

Please contact the team at Conference Design with any questions regarding the Annual Scientific Meeting

© 2015 - 2016 Conference Design Pty Ltd