ETHYLENE GLYCOL TOXICITY – A RARE CAUSE OF HIGH ANION GAP METABOLIC ACIDOSIS IN AUSTRALIA

GJ WILSON1,2, J ROWLAND1, MR DOWLING1, L FRANCIS3, GT JOHN1,2,AL KARK1,2

1Department of Renal Medicine, Royal Brisbane and Women’s Hospital, Herston, Queensland; 2School of Clinical Medicine, University of Queensland, Herston, Queensland; 3Department of Pathology, Royal Brisbane and Women’s Hospital, Herston, Queensland

Background: Ethylene glycol toxicity is a well-known cause of acute kidney injury (AKI) and high anion gap metabolic acidosis. However, it is a rare presentation in Australia with only 22 cases reported in 2014. The diagnosis of ethylene glycol toxicity is challenging in the absence of a history of ingestion and can be misdiagnosed as lactic acidosis which, due to structural similarities with glycolate, causes falsely elevated lactate levels on some instruments.

Case Report: A 36 year-old female presented to the emergency department with an altered level of consciousness and tachypnoea requiring urgent intubation. She was anuric and had an AKI (creatinine 182 umol/L). An iSTAT venous blood gas demonstrated a high anion gap metabolic acidosis (pH 7.08, HCO3 6, CO2 19, anion gap 34) and an elevated serum lactate (9.4 mmol/L). She was provisionally diagnosed with type B lactic acidosis and transferred to ICU for ventilation and continuous veno-venous haemodiafiltration. Upon extubation, the patient denied any toxic ingestions and renal biopsy was performed demonstrating crystalloid material birefringent under polarised light consistent with oxalate nephropathy. Urinary organic acids were requested and urinary glycolate and oxalate levels were elevated (2200 mmol/mol Cr and 520 mmol/mol Cr). Ethylene glycol levels were requested from admission bloods and demonstrated a toxic level of 8.8 mmol/L confirming a diagnosis of ethylene glycol toxicity. The patient continued to deny any ethylene glycol ingestion even after psychiatric consultation.

Conclusions: Ethylene glycol toxicity is a well-known but rare cause of AKI and high anion gap metabolic acidosis. It should be considered in all patients with AKI and high anion metabolic acidosis even in the absence of a history of ingestion.

RATES AND CHARACTERISTICS OF ACUTE KIDNEY INJURY (AKI) IN THE CHRONIC KIDNEY DISEASE IN QUEENSLAND (CKD.QLD) REGISTRY

GJ WILSON1,2, A MALLETT1,2,3,4, A KARK1,2, AK TAN2,5,A CAMERON1,2,4,  Z WANG2,4, HG HEALY1,2,  WE HOY2,4

1Department of Renal Medicine, Royal Brisbane and Women’s Hospital, Herston, Queensland; 2CKD.QLD & NHMRC CKD.CRE, University of Queensland, Herston, Queensland; 3Centre for Rare Diseases Research, Institute for Molecular Bioscience and School of Medicine, The University of Queensland, St Lucia, QLD; 4Centre for Chronic Disease, University of Queensland, Herston, Queensland; 5Department of Renal Medicine, Logan Hospital, Queensland

Aim: To describe the rates and characteristics of patients with AKI in an Australian CKD population.

Background: AKI is well described as a risk factor for the development and progression of CKD. However, AKI is a diverse clinical syndrome and what factors increase this risk has yet to be fully investigated.

Methods: Patients enrolled in the CKD.QLD registry from Logan Hospital and RBWH (n=2367) were assessed for a diagnosis of AKI either as the cause of CKD or as an acute on chronic kidney injury. The remaining patients were used as a comparator group (CKD only). Patient demographics, co-morbidities, cause of AKI and outcomes between and within these groups were compared.

Results: 159 patients (6.7%) had AKI as the cause of their CKD (primary AKI) and 176 (7.4%) had an acute on chronic kidney injury (AKI on CKD).  There was a male predominance in patients with primary AKI compared to AKI on CKD and CKD only (61.4% vs. 55.1% & 50.3%; p=0.03). Patients with AKI on CKD were older than both primary AKI and CKD only patients (67.3 yrs vs. 62.3 & 64.7 yrs; p<0.01). Patients with primary AKI or with AKI on CKD had lower rates of diabetes mellitus and hypertension compared to CKD only (21.4% & 35.8% vs. 48.9% p<0.01; 52.8% & 73.9 vs. 77.8%; p<0.01). The most common causes of primary AKI and AKI on CKD were obstructive nephropathy (36.5% & 40.9%) and acute tubular necrosis (26.4% & 25.6%).

Conclusions: This is the first description of AKI in an Australian CKD population. Our findings confirm AKI as a significant risk factor for developing CKD even in the absence of other risk factors.

PATIENT-DERIVED ENDOTHELIAL CELL FUNCTION IS PREDICTED BY CONTROLLED BLOOD PRESSURE

HUUSKES BM1, KERR PG2, SAMUEL CS3, RICARDO SD1

1Biomedical Discovery Institute, Department of Anatomy and Developmental Biology, Monash University, Clayton, Victoria; 2Department of Medicine, Monash Medical Center and Monash University, Clayton, Victoria; 3Biomedical Discovery Institute, Department of Pharmacology, Monash University, Clayton, Victoria

Aim: To determine if clinical parameters observed in patients on haemodialysis affected the appearance of patient-derived endothelial cells in culture.

Background: Low circulating endothelial progenitor cell (EPC) numbers have been linked to worsening outcomes for dialysis patients. EPC function can be measured by their ability to form colony forming units (CFU) and late outgrowth endothelial cells (OECs) in vitro. Numerous clinical parameters may affect EPC function, yet their affect on OEC appearance remains unknown.

Methods: Dialysis-dependent patients (n=20) were recruited to this study; and their age, time on dialysis, blood pressure (BP), EPO, statin use and smoking status was collected. Blood (10mls) was obtained prior to a single dialysis session and peripheral blood mononuclear cells isolated and cultured. After 7 days CFU was assessed, and cells were further cultured for 21 days or until OECs appeared (identified by cobblestone morphology). Correlations between patient clinical parameters and OEC appearance were investigated.

Results: Patient age, time on dialysis, statin use, and BP did not correlated with circulating EPC level. However, patients administered EPO had lower circulating EPCs compared to patients who were not (p<0.05). Only 9/20 patient-derived cells formed OECs, which was not correlated to starting %EPC or any other clinical parameter except for BP. OECs were significantly greater in patients who had low systolic (p<0.01) and diastolic (p<0.05) BP.

Conclusions: BP affects dialysis-dependent patient-derived OEC numbers in culture, suggesting that controlling BP may be key to maintaining vascular health in patients on dialysis.

“UNEARTHING” THE CAUSE OF ACUTE KIDNEY INJURY IN A GARDENER

D ARIYARATHNA1, D HSU2, J YONG3, M KILLINGSWORTH3, J RUTLAND4, J WONG1

1Renal unit Liverpool Hospital, Liverpool, New South Wales; 2Haematology Department Liverpool Hospital, Liverpool, New South Wales; 3Anatomical Pathology Liverpool Hospital, Liverpool, New South Wales; 4Respiratory Department Liverpool Hospital, Liverpool, New South Wales. 

Background:  Acute kidney injury (AKI) due to Legionnaires’ disease is attributed to acute interstitial nephritis or acute tubular necrosis.  There exists a single case report of Legionella pneumophila associated with haemolytic uraemic syndrome (aHUS).  To our knowledge, this report is the first of Legionnaires’ disease due to Legionella longbeachae associated AKI due to aHUS.

Case Report:  A 74-year-old avid male gardener with pneumonia presented with initial investigations revealing normal renal function and platelet count, but on day 7he developed oliguric AKI with creatinine 395 µmol/L requiring dialysis. Urine was negative for white cells, red cells or casts. He was proteinuric with 0.99g/day. Vasculitic screen were negative. Renal ultrasound revealed normal sized kidneys and collecting systems.  Subsequently his platelets reduced to 85 x109/L and haemoglobin to 58g/L. Peripheral blood film revealed schistocytes and red cell fragments. Haptoglobin was <0.08g/L and lactate dehydrogenase 1312, consistent with thrombotic microangiopathy (TMA). Shiga toxin was negative, ADAMTS 13 was 54%.  Plasma exchange improved his platelet count to 163×109/L. Eculizumab was commenced on day 11 with no further evidence of microangiopathic haemolysis. Renal biopsy showed protein fibrin thrombi in glomerular capillary lumens consistent with TMA and concomitant interstitial nephritis and ATN.  On 3 months follow up, his creatinine, LDH, haptoglobin and platelets had normalised.  He had reduced membrane cofactor protein (MCP) 0.76. Complement factors I was 36mg/L (NR, 38-58mg/L) and CFH >700mg/L (NR, 350-590mg/L).  Serology confirmed Legionella longbeachae serotype 1, which we believe is the precipitant of his aHUS.

Conclusions:  We present the first aHUS case attributed to legionella longbeachae, with this gentleman expressing reduced MCP.  With early suspicion of aHUS, he responded extremely well to Eculizumab treatment.

A CASE OF ACUTE KIDNEY INJURY AND THROMBOTIC MICROANGIOPATHY SECONDARY TO UROTHELIAL CANCER AND THE IMPACT OF TREATMENT ON THE DISEASE PROCESS

B TALBOT1,2, J OTHMAN2, RCF CHAN2, M KRISHNASWAMY2, K ARCHER2, V CHEN2,3, S SEN2

1The George Institute, Sydney, NSW; 2Concord Repatriation General Hospital, Sydney, NSW; 3The University of Sydney, Sydney, NSW.

Background:

Thrombotic microangiopathy (TMA) describes a pathological process of microvascular thrombosis, consumptive thrombocytopenia and microangiopathic haemolytic anaemia leading to end-organ ischaemia and infarction. Patients may present with acute renal failure and/or cerebral dysfunction. TMA is a feature of several clinical disorders and rarely can be associated with malignancy.

Case Report: A 71 year old gentleman presented with flank pain, fevers and deteriorating renal function. He was known to have unilateral hydronephrosis and a poorly defined hilar soft tissue density in the left kidney.

On arrival he was septic and haemodynamically unstable. Investigations revealed microcytic anaemia, acute kidney injury and raised inflammatory markers. Significant fragmentation was seen on the blood film, reflected in the low mean corpuscular volume (MCV). Iron deficiency was excluded. Repeat imaging did not explain the renal deterioration. Antibiotics were given and haemodialysis initiated due to anuria, fluid overload and hyperkalaemia.

Biopsy of the unobstructed kidney revealed florid TMA without involvement of non-glomerular vessels. Serological markers did not reveal an underlying cause.

Ongoing sepsis required intensive care support and left nephrostomy insertion. Spontaneous bleeding from his left renal artery required angiographic embolisation and subsequent open nephrectomy. Histology showed high grade invasive papillary urothelial carcinoma with evidence of infarction following embolisation. Disseminated disease was later confirmed.

An increase in MCV and haemoglobin paralleled the reduction in fragmentation seen following embolisation and nephrectomy suggesting direct effect of these treatments on the TMA.

Despite these interventions he deteriorated and died with palliative care support.

Conclusion: We present a case of acute kidney injury secondary to TMA associated with urothelial cancer, which is the first described and showed haematological improvement with treatment of the malignancy.

RENAL CONSULT AUDIT AT A TERTIARY REFERRAL HOSPITAL

CM OGILVY1, H GOCK1, L NGUYEN2, F IERINO1, SL FORD1

1St Vincent’s Hospital, Melbourne, Victoria; 2School of Medicine, The University of Melbourne, Victoria

Aim: To characterise inpatients referred to nephrology within a tertiary hospital, analysing patterns of acute kidney injury (AKI), patient outcomes, and identifying areas for quality improvement.

Background: AKI is common, has high morbidity and mortality and predicts adverse outcomes.

Methods: A retrospective review of patients referred to St Vincent’s Hospital nephrology unit over 3-months from July to October 2016. Utilising medical records and results databases, patient demographics, referral characteristics and renal outcomes were assessed.

Results: 55 patients were analysed, 58% were male and two-thirds over 60yo. 50% were admitted under medical units and 75% had >4 comorbidities. 52% were referred within 48 hours of admission. Baseline renal function included CKD Stage 1 in 27%, Stage 2 in 18%, Stage 3 in 31%, Stage 4 in 11%, Stage 5 in 4% and 9% unknown.

Classification of AKI was pre-renal in 24%, renal in 65% and post renal in 11% of patients. Patients with post-renal AKI presented with the highest peak creatinine (post-renal 896+/-245μmol/L vs renal 354+/-33μmol/L, p<0.0001 vs pre-renal 248+/-20μmol/L, p=0.001) and the worst renal function at discharge (post-renal 449+/-103μmol/L vs renal 182+/-21μmol/L, p<0.005 vs pre-renal 173+/-22μmol/L, p<0.001). Upon discharge, more than half had serum creatinine up to 50% higher than baseline. Patients with renal AKI had the highest rate of dialysis (renal 42% vs pre-renal 0% vs post renal 17%) while pre-renal patients had the lowest inpatient mortality (renal 17% vs pre-renal 0% vs post renal 17%).

Conclusions: AKI in referred hospitalised patients is associated with a high level of morbidity and mortality. Patients with post-renal causes of AKI presenting with severe AKI are at significantly higher risk of worsened renal function at discharge.

SOFA COAGULATION SCORE AND PATIENT OUTCOMES IN SEVERE ACUTE KIDNEY INJURY: ANALYSIS FROM THE RANDOMISED EVALUATION OF NORMAL VERSUS AUGMENTED LEVEL (RENAL) STUDY

J LIN1, Y WANG1, 2*, R Bellomo1, ML DUAN3, MP Gallagher1,2*

1The George Institute for Global Health, Camperdown, Australia; 2The University of New South Wales; 3Beijing Friendship Hospital, Capital Medical University, China. *corresponding authors

Aim: To evaluate the prognostic value of SOFA coagulation scores in patients with severe acute kidney injury (AKI) requiring continuous renal replacement therapy (RRT).

Background: A decline in platelet count is common in critically ill patients with severe AKI. However, there is relatively little data assessing the association of SOFA coagulation scores and clinical outcomes in severe AKI patients receiving continuous RRT.

Methods: We performed a secondary analysis from the Randomised Evaluation of Normal versus Augmented Level of RRT (RENAL) study. The primary endpoint was all-cause mortality at 90 days after randomisation. The secondary outcomes were the length of intensive care unit (ICU) and hospital stay. The association between the SOFA coagulation scores and these outcomes were analysed using multivariate Cox model adjusted for baseline variables.

Results: Among 1465 patients in the RENAL study, the complete SOFA coagulation score data were available in 1280 patients. Among them, 579 patients had high SOFA coagulation scores (defined as ≥1), while 701 patients had normal SOFA coagulation scores (<1). The univariate analysis showed that high SOFA coagulation scores were associated with higher mortality at day 90 (49% versus 38.5%, p=0.0002). There was no significant difference in the length of ICU and hospital stay between these two groups. In multivariate analysis, the association between high SOFA coagulation scores and increased mortality rate at 90 days remained significant.

Conclusions: In the RENAL study, an approximately 50% of patients had an increase in SOFA coagulation scores during their ICU admission. High SOFA coagulation scores were associated with increased mortality at 90 days.

EPIDEMIOLOGY AND COSTS OF MANAGEMENT OF ACUTE KIDNEY INJURY IN A TERTIARY CARE CENTER IN AUSTRALIA

S HERATH1, S KOTWAL2, Z ENDRE1,3

1University of New South Wales, Sydney, New South Wales; 2The George Institute for Global Health, Sydney, New South Wales; 3Prince of Wales Hospital, Sydney, New South Wales

Aim: To quantify delays in care and identify costs in hospitalized patients with AKI.

Background: Acute kidney injury (AKI) is associated with adverse outcome and increased health care burden, but few studies in Australia have systematically assessed delays in care and costs in hospitalised patients.

Methods: Prospective data was collected on 100 consecutive adult patients with AKI referred to nephrology at an urban tertiary care centre. AKI was defined using KDIGO criteria. Baseline characteristics, treating team, time to nephrology consult and the respective costs for management of AKI were recorded. Length of stay was defined as time from AKI diagnosis to discharge from renal services.

Results: Of 100 patients consulted over the course of 8 months, 64 were male, median age 74 years. 52 patients had Stage 3 CKD or higher; 36 had diabetes, and 45 had systolic heart failure. 16 patients had stage two and 44 stage three AKI.

The median time between AKI development to nephrology consult for 83 patients was 1 (interquartile range 3). For 17/100 patients, the renal team became the caring team during the admission.

The median length of stay and costs for patients admitted under the nephrology team was 9 (13.5) days and 190 (41) dollars respectively while it was 14 (20) days and 212 (149) dollars for patients admitted under non-nephrology teams. There wasn’t a correlation between time to consult and length of stay or costs for patients admitted under non-nephrology teams.

Conclusion: There was a tendency for increased costs and length of stay for patients admitted under non-nephrology teams but this did not reach statistical significance due to the smaller sample nature of our pilot study.

UNUSUAL PRESENTATION OF BILATERAL RENAL ARTERY STENOSIS AS ANURIC RENAL FAILURE WITH SUCCESSFUL STENTING

G HARLEY1, M MATHEW1, R RAJ1

1Launceston General Hospital, Launceston, Tasmania

Background: Atherosclerotic renal artery stenosis represents a common clinical problem with the literature suggesting angioplasty and stenting, usually of bilateral disease, is clinically beneficial only in certain clinic scenarios including refractory hypertension, acute episodes of pulmonary oedema or rapidly declining kidney function clearly attributable to this.

Case report: A 57 year old lady, current smoker on long-term olmesartan for hypertension, presented with a three month history of right flank pain and vomiting associated with an acute creatinine rise to 550micromol/L with proteinuria and quickly progressed to anuric renal failure requiring haemodialysis. A non-contrast CT scan showed 8.9cm and 6.8cm on the right and left respectively without evidence of obstruction. She had persistent refractory hypertension with several episodes of acute hypertension and hypoxia requiring non-invasive respiratory support. A right-sided kidney biopsy showed 3 out of 22 sclerosed glomeruli, some ischaemic glomeruli and evolving widespread tubular atrophy.

A CT renal angiogram showed complete occlusion of bilateral renal artery origins with collateral perfusion of both kidneys. An angioplasty and stenting was successfully performed on day 35 of her admission of her right renal artery. The patient became polyuric quickly and her anti-hypertensives were successfully weaned. Her creatinine over the subsequent weeks reduced to 170micromol/L. Unfortunately she developed hypertension with worsening renal function and was commenced back on haemodialysis approximately 10 weeks after having ceased. A repeat angiogram showed a widely patent right renal artery stent.

Conclusions: Although stenting was initially successful in improving her anuric acute kidney injury, with no further acute pulmonary oedema, ultimately she progressed to dialysis-dependence.

GEMCITABINE INDUCED HEMOLYTIC URAEMIC SYNDROME SUCCESSFULLY TREATED WITH ECULIZUMAB – A CASE REPORT

M GANGADHARAN KOMALA1, E FISCHER1, K SUD1,2, B BOSE1,2

1Department of Renal Medicine, Nepean Hospital, Kingswood, New South Wales; 2University of Sydney – Nepean Clinical School, Sydney, New South Wales

Background: Gemcitabine induced hemolytic uraemic syndrome (GiHUS) is rare and can occur in 0.02 to 2.2% of all patients administered this drug. We report a case of GiHUS resistant to corticosteroids and plasma exchange (PEX) that was successfully treated with Eculizumab.

Case Report: A 55 years old female presented with shortness of breath 3 weeks after her last dose of gemcitabine given for ampullary carcinoma. She was found to have acute kidney injury with a creatinine of 125 umol/L and was anemic with a hemoglobin of 66 g/L. She had evidence of microangiopathic hemolytic anemia (MAHA), and also had 7.54 g/day of proteinuria. A kidney biopsy revealed features consistent with thrombotic microangiopathy. She had normal left ventricular (LV) function on echocardiogram and PET scan did not show evidence of active malignancy.

She was diagnosed with GiHUS and commenced on prednisolone 55 mg daily and received PEX. However her renal functions deteriorated with peak creatinine of 297 umol/L. She developed progressive LV dysfunction with a nadir ejection fraction (EF) of 20% and needed to commence hemodialysis for management diuretic resistant pulmonary edema. PEX was ceased after 5 treatments due to poor clinical improvement, persistent MAHA with a normal ADAMTS13 activity of 99% and she was commenced on Eculizumab, with which the hemolytic markers normalised and renal function improved over two months. She is currently dialysis independent and LV function has improved to an EF of >30%.

Conclusion: GiHUS is a rare entity associated with severe morbidity and mortality. Eculizumab should be considered in patients with persistent HUS after cessation of gemcitabine. LV dysfunction associated with aHUS is an increasingly recognized complication that also improves with Eculizumab.

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 conference.

/wp-content/uploads/2017/08/Conference-Design-400×400.png

© 2015 - 2016 Conference Design Pty Ltd