Miss Noha Kamel1,2, A/Prof. RONALD CASTELINO1,3, A/Prof. DANIEL WRIGHT1,4,5, A/Prof. KAMAL SUD6,7, Dr. SURJIT TARAFDAR8,9,10, Dr. Stephen Hughes1, A/Prof. SOPHIE STOCKER1,4,5,11
1School of Pharmacy, Faculty of Medicine & Health, The University of Sydney, Sydney, Australia, 2Department of Clinical Pharmacy and Pharmacy Practice, Faculty of Pharmacy, Mansoura University, Mansoura, Egypt, 3Pharmacy Department, Blacktown Hospital, Blacktown, Sydney, Australia, 4Department of Clinical Pharmacology and Toxicology, St Vincent's Hospital, Sydney, Australia, 5St. Vincent’s Clinical School, Faculty of Medicine, University of New South Wales, Sydney, Australia, 6Nepean Clinical School, The University of Sydney, Sydney, Australia, 7Nepean Kidney Research Centre, Department of Renal Medicine, Nepean Hospital, Kingswood, Sydney, Australia, 8Department of Nephrology, Blacktown Hospital, Blacktown, Sydney, Australia, 9School of Medicine, University of Western Sydney, Sydney, Australia, 10Department of Nephrology, Kasturba Medical College, Manipal, India, 11Sydney Musculoskeletal Health, Faculty of Medicine and Health, The University of Sydney, Sydney, Australia
Biography:
Noha Kamel (https://orcid.org/0000-0002-3299-9555) is a second-year PhD student and casual academic at the School of Pharmacy, University of Sydney. Her PhD research focuses on gout management in patients with kidney failure. She earned her bachelor's degree in clinical pharmacy from Mansoura University, Egypt, in 2017. She then completed her master's degree by research while serving as an assistant lecturer in the Clinical Pharmacy and Pharmacy Department at Mansoura University in 2022. Her master's project investigated sepsis prevention in critically ill trauma patients. Noha has a strong interest in clinical research, particularly in clinical trials and clinical pharmacokinetics.
Background
Acute gout causes significant morbidity in patients receiving dialysis. Although both oxypurinol (allopurinol’s active metabolite) and urate are dialysable, it is unclear if target serum urate concentrations (<0.36 mmol/L) are achieved in these patients.
Aim
To evaluate allopurinol dosing practices and serum urate concentrations in patients with gout on dialysis.
Methods
Adults prescribed allopurinol, receiving dialysis between 1/6/2019 and 30/6/2024, with serum urate documented while on dialysis were included. Data was collected longitudinally one year before dialysis initiation to study entry, including demographics, dialysis modality, allopurinol dosing, and serum urate concentrations. Serum urate concentrations collected during acute inflammation (e.g. sepsis or peritonitis) were excluded.
Results
Forty-eight patients (20 haemodialysis (HD) and 28 peritoneal dialysis (PD)) were included. Most HD patients received thrice-weekly haemodiafiltration (60%) with high flux dialysers (85%) , while 57% of PD patients received automated PD. Allopurinol doses ranged from 50-300 mg daily (mode 100 mg), unchanged from pre-dialysis dose in 94% (45/48) of patients. Serum urate concentrations were collected before HD sessions; interdialytic (18/20 patients) or during continuous PD (16/28 patients). At 8 (0.07-48) months post-dialysis commencement, median serum urate significantly decreased compared to pre-dialysis (0.53 mmol/L versus 0.3 mmol/L, p=0.006 in HD, 0.53 mmol/L versus 0.31 mmol/L, p < 0.001 in PD). More frequent HD and continuous PD were associated with lower serum urate. Most HD (70%, 14/20) and PD (79%, 22/28) patients had ≥ one serum urate concentration within target throughout dialysis vintage.
Conclusion
Serum urate concentrations decreased post-dialysis without altering allopurinol dose, confirming dialysis helps clear serum urate. This supports considering allopurinol deprescribing based on target urate achievement after commencing dialysis.