ABSTRACT
Aim
People with kidney failure are at increased risk of gout‐related hospitalisations and mortality. Whilst dialysis enhances urate removal and reduces circulating oxypurinol (allopurinol's active metabolite), its effect on achieving target serum urate concentrations (< 0.36 mmol/L) and implications for gout management remain unclear. This study aimed to evaluate serum urate concentrations and allopurinol dosing following commencement of dialysis.
Methods
We conducted a retrospective chart review of adults prescribed allopurinol at a dialysis Centre in New South Wales, Australia, between 01/06/2019 and 30/06/2024. Eligible patients had at least one serum urate concentration recorded after commencing dialysis. Data collected included patient demographics, dialysis modality, allopurinol dosing, and serum urate concentrations, spanning from pre‐dialysis to up to 5 years post‐commencing dialysis.
Results
Forty‐five patients (18 haemodialysis [HD], 27 peritoneal dialysis [PD]) were included. Most HD patients (61%) received thrice‐weekly haemodiafiltration with high‐flux dialysers; 59% of PD patients used automated PD. Allopurinol doses (100–300 mg daily, mostly 100 mg) remained unchanged from pre‐dialysis in 93% (42/45). At 4 (0.25–38) months post‐dialysis, median serum urate concentrations declined compared to pre‐commencing dialysis (HD: 0.31 vs. 0.51 mmol/L, p = 0.031; PD: 0.33 vs. 0.53 mmol/L, p < 0.001). Target serum urate concentrations were reached at least once in 60% of HD and 78% of PD patients.
Conclusion
Serum urate concentrations declined after starting dialysis with unchanged allopurinol dosing, suggesting dialysis independently contributes to urate reduction. These findings support re‐evaluating allopurinol dose in patients after commencing dialysis, including de‐prescribing allopurinol in those who consistently achieve target urate concentrations.
Keywords: allopurinol, gout, haemodialysis, peritoneal dialysis, uric acid
Summary at a Glance
A retrospective review of gout patients on dialysis (2019–2024) shows allopurinol doses are rarely adjusted at dialysis initiation. Yet, serum urate concentrations significantly decline, suggesting dialysis independently lowers urate. This highlights the need to reassess allopurinol use, especially in patients with target urate concentrations before commencing dialysis.
The study investigated allopurinol dosing practises and serum urate concentrations in gout patients with kidney failure following commencing dialysis. Results showed allopurinol dose was most commonly 100 mg, unadjusted upon commencing dialysis. However, serum urate concentrations significantly declined as patients commenced dialysis with more than 50% achieving target urate. This suggests dialysis can independently contribute to urate lowering, and allopurinol therapy can be re‐evaluated after commencing dialysis.
1. Introduction
Gout is a common comorbidity in patients with kidney failure, with a prevalence approximately three times higher than in earlier stages of chronic kidney disease [1]. In patients receiving dialysis, gout is associated with higher hospitalisation and mortality compared to those without gout [2], underscoring the importance of optimal management in this population.
Allopurinol is the first line urate lowering therapy for gout [3]. It is metabolised to an active metabolite, oxypurinol, which is predominantly cleared by the kidneys [4], and appears to be effectively removed by dialysis [5, 6]. This has implications for dosing in patients with gout commencing or already receiving dialysis. Furthermore, serum urate is also cleared by the kidneys and appears to be effectively removed by dialysis [5]. Guidelines for gout management now recommend a ‘treat to target’ approach where allopurinol doses are slowly escalated until serum urate targets are achieved (< 0.36 mmol/L (6 mg/dL) or < 0.3 mmol/L (5 mg/dL) for severe tophaceous gout) [3]. However, it remains unclear if these target serum urate concentrations are achieved and sustained in patients with gout receiving dialysis. Current evidence is scant but suggests that only 23% (14/61) of patients with gout receiving dialysis regularly had serum urate within target despite being prescribed allopurinol (116 ± 66.9 mg/day) [7]. Potential reasons for suboptimal target urate achievement are lack of guidance to support allopurinol use in dialysis coupled with variability in oxypurinol and urate handling across dialysis modalities.
Few evidence‐based resources are currently available to support optimal allopurinol use and dosing in patients receiving dialysis. For example, the renal drug handbook [8] and the UpToDate database [4] rely on case reports [9] or data from older studies using outdated dialyser technology [10]. The heterogeneity in the dialysis modalities used in clinical practise differently impacts oxypurinol and urate clearances, adding complexity to allopurinol dosing in clinical practise.
Understanding treatment and outcomes in patients undergoing dialysis can optimise patient outcomes. We performed a retrospective chart review of allopurinol prescribing and target serum urate concentration in patients receiving haemodialysis or haemodiafiltration (HD) and peritoneal dialysis (PD), including data from before dialysis commencement.
2. Materials and Methods
2.1. Study Design and Setting
This study was conducted at a large metropolitan dialysis Centre in New South Wales, Australia, serving approximately 200 patients on HD, and 322 patients on PD. Ethics approval was obtained from the institutional human research ethics committee (ETH00394), with waiver of consent due to the study's retrospective nature. Methodology reporting followed the Strengthening the Reporting of Observational Studies in Epidemiology (STROBE) statement [11].
2.2. Inclusion/Exclusion Criteria
Adults (≥ 18 years) prescribed allopurinol for gout, who commenced HD or PD between 1 June 2019, and 30 June 2024, with serum urate concentrations documented after commencing dialysis were eligible for inclusion. Patients were excluded if urate concentrations were measured during acute inflammation (e.g., sepsis, peritonitis, acute gout) or intensive care admission, as this may alter serum urate concentrations [12, 13]. Patients who were permanently transitioned from PD to HD were classified as PD patients, and only the data whilst receiving PD was included.
2.3. Data Collection
Clinical data was collected from electronic medical records (EMR), longitudinally starting 1 year before commencing dialysis up to 5 years post‐commencing dialysis. As such, the period of observation during dialysis varied between patients depending on their date of dialysis commencement. The data collected included patient demographics, concomitant medications known to impact serum urate concentrations (e.g., loop diuretics), comorbidities associated with elevated serum urate concentrations (e.g., cardiovascular disease), dialysis modality (type and regimen), allopurinol dosing (dose and dosing frequency), and serum urate concentrations. Comorbidities were defined as per the International Classification of Diseases (ICD)‐10 chapter [14]. For patients lacking serum urate concentrations within 1 year before commencing dialysis, data from up to 5 years prior to commencing dialysis were reviewed.
Dialysis modality characteristics and allopurinol dosing history were collected around the time a serum urate concentration was available. The type of dialysis was classified as center‐based or home HD, and as automated or continuous ambulatory PD. In patients on HD, the timing of urate sampling and allopurinol dosing (pre‐HD or interdialytic) was recorded. For patients on continuous ambulatory peritoneal dialysis (CAPD) or automated peritoneal dialysis (APD) at night with a manual day exchange, allopurinol administration and serum urate sampling were denoted as ‘during dialysis’ unless clearly confirmed otherwise from the time of the day dwell relative to the urate sampling and allopurinol administration times. Dialysis vintage was defined as the time from commencing dialysis to the last recorded serum urate concentration.
2.4. Data Analysis
Patients were grouped by dialysis modality (HD or PD). Patient characteristics were summarised using descriptive statistics. Normality was assessed using the Shapiro–Wilk test and visual inspection. Differences in study variables between dialysis groups were assessed using χ 2 for categorical variables and Mann–Whitney U test for continuous non‐normally distributed data.
The pre‐post dialysis analysis of serum urate concentrations compared the last available serum urate concentration before commencing dialysis to the first concentration after commencing dialysis. If the first serum urate concentration after commencing dialysis was taken < 24 h from the previous HD session, during a session, within 2 weeks of commencing HD, or during acute illness or a gout flare, the value was excluded, and the next available serum urate concentration was used. These scenarios are known to alter serum urate concentrations [15]. Serum urate concentrations pre‐/post‐ dialysis were compared between dialysis modalities using Mann–Whitney U test and within each dialysis modality using Wilcoxon Sign rank test.
Target urate achievement in patients on HD and PD was assessed in two ways. Firstly, whether there was ≥ one serum urate concentration within target throughout the dialysis vintage, and secondly if the last available serum urate concentration was within target. Timing of allopurinol dosing and serum urate sampling relative to dialysis was estimated based on the times recorded in EMR notes and verified with the renal pharmacist (RC) to ensure plausibility with practises. Analyses were performed using Jamovi (version 2.3.28) [16] and R version 4.5.1 [17]. Graphs were created using ‘ggplot2’ package in R and GraphPad Prism 10.6.1 [18]. A spaghetti plot was generated to visualise the longitudinal changes in serum urate concentrations, beginning prior to the commencement of dialysis (stratified by haemodialysis and peritoneal dialysis) until up to 40 months after commencing dialysis.
3. Results
3.1. Patient Characteristics
Of the 734 patients receiving dialysis, 55 were prescribed allopurinol and had at least one serum urate concentration recorded after commencing dialysis. From these, 10 were excluded on predefined exclusion criteria, leaving 45 patients (18 HD and 27 PD patients) for analysis (Figure 1). Patients were predominantly male (73%) and over 60 years of age. No urate‐lowering therapies other than allopurinol were prescribed, though several patients were on medications known to alter serum urate concentrations. In general, patient characteristics were similar in HD and PD (Table 1). Throughout the dialysis vintage, gout flares were recorded for two patients on HD (NK6HD, NK29HD) and two patients on PD (NK28PD, NK38PD).
FIGURE 1.
Identification and screening to include patients receiving dialysis, on allopurinol, and with available serum urate concentrations suitable for analysis after dialysis start in the chart review.
TABLE 1.
Demographics of patients on allopurinol receiving dialysis, with a serum urate concentration recorded after commencing dialysis.
| Haemodialysis (n = 18) | Peritoneal dialysis (n = 27) | p | |
|---|---|---|---|
| Age (years) median (range) | 60 (45–88) | 67 (24–86) | 0.97 a |
| Gender male n (%) | 14 (78%) | 19 (70%) | 0.58 b |
| Height (cm) median (range) | 171 (154–180) | 164 (145–187) | 0.04 a |
| Weight (kg) median (range) | 87 (66–125) | 73 (49–118) | 0.003 a |
| BMI (kg/m2) median (range) | 30 (22–44) | 27 (20–40) | 0.023 a |
| Aboriginal/Torres strait islander n (%) | 0 (0%) | 1 (3.7%) | 0.41 b |
| Baseline serum urate (mmol/L) median (range) c | 0.51 (0.33–0.69) | 0.53 (0.34–0.84) | 0.44 a |
| Comorbidities | |||
| Cardiovascular disease n (%) | 12 (67%) | 13 (48%) | 0.22 b |
| Hypertension n (%) | 14 (78%) | 22 (81%) | 0.76 b |
| Diabetes n (%) | 12 (67%) | 14 (52%) | 0.32 b |
| Concomitant medications increasing serum urate n (%) d | 17 (94%) | 25 (93%) | 0.81 b |
| Concomitant medications decreasing serum urate n (%) d | 15 (83%) | 24 (89%) | 0.59 b |
Mann Whitney U test.
Independent χ 2 test.
Baseline serum urate concentration refers to the last available serum urate in the records before commencing dialysis (n = 8 for HD, n = 12 for PD).
Concomitant medications possibly associated with altered serum urate concentrations such as: loop diuretics, thiazide diuretics, β‐blockers, low‐dose aspirin (75–150 mg/day), insulin, angiotensin converting enzyme inhibitors, angiotensin II receptor blockers, calcium channel blockers, leflunomide, atorvastatin, fenofibrates, or oestrogen [19]. Patients in both dialysis modalities had a median (range) of 2 (1–3) medications potentially increasing serum urate, and 1 (1–3) medication potentially reducing serum urate concentration.
3.2. Dialysis Modality Details
The median (range) vintage of dialysis was 12 (1.5–37) months in patients on HD and 19 (0.75–51) months in patients on PD. Most patients undergoing HD received center‐based HD except four patients on home HD. All HD patients were on high flux dialysers, most commonly (8/18; 44%) FX CORIAX 80. Blood flow rates ranged from 200 to 320 mL/min (n = 18), and dialysate flow rates ranged from 212 to 321 mL/min (n = 18), with session lengths of 4–5 h (median 4.5 h) in center‐based HD and 4–8 h (median 4.5 h) in home HD. Around 60% of the patients had thrice weekly sessions (11; 61%), with the remainder having twice weekly sessions (7; 39%). Dialysis adequacy (Kt/V) ranged from 1.01 to 1.27 (n = 16). For patients receiving PD, 16 (59%) used APD, and 11 (41%) used CAPD only. Kt/V ranged from 1.27 to 2.89 (n = 27).
3.3. Allopurinol Dosing Practise in Dialysis
Allopurinol dose information before commencing dialysis was unavailable for 2 (11%) patients receiving HD and 9 (33%) patients receiving PD. For the remainder, the most common (range) allopurinol dose before commencing dialysis was 100 (50–300) mg/day for patients on both HD and PD. After commencing dialysis, the most common allopurinol dose remained 100 mg/day and ranged from 100 to 300 mg in patients on HD (15/18 patients) and PD (24/27 patients). Due to the retrospective study design, the median (range) period between commencing dialysis and the first available allopurinol dose was 5 (0–29) months for patients on HD (n = 15) and 10 (0.03–48) months for patients on PD (n = 24). Generally, the allopurinol dose was not altered after commencing dialysis, except for three PD patients who had their dose increased (NK28PD, NK35PD, NK52PD) by increments of 50–100 mg/day. Allopurinol was typically administered before HD sessions (17/18 patients). Allopurinol doses and dialysis regimens for each patient around the time of serum urate concentrations are presented in Figures S1–S8.
3.4. Serum Urate Concentrations in Dialysis
Patients had a median of one serum urate concentration recorded before commencing dialysis and two concentrations recorded throughout the dialysis vintage. The first serum urate concentration after commencing dialysis was mostly collected before the HD session (11/18).
Serum urate concentrations prior to commencing dialysis were similar in patients receiving HD and PD. For each dialysis modality, serum urate concentrations decreased after commencing dialysis. Serum urate concentrations decreased from a median (range) of 0.51 (0.33–0.69) mmol/L at 12 (0.25–60) months before to 0.31 (0.21–0.51) mmol/L at 9 (3–25) months after commencing HD (p = 0.031, n = 6) and from 0.53 (0.34–0.84) mmol/L at 3.5 (0.6–28) months before to 0.33 (0.2–0.67) mmol/L at 4 (0.25–38) months after commencing PD (p < 0.001, n = 12) (Figure 2). Serum urate concentrations after commencing dialysis were similar in patients on HD and PD (p = 0.44). As time progressed following the initiation of dialysis, a modest increase in serum urate concentration was observed, particularly in patients undergoing peritoneal dialysis 20 months after commencing dialysis (Figure 3).
FIGURE 2.
Serum urate concentrations in patients prescribed allopurinol last before and first after commencing haemodialysis/haemodiafiltration (closed circles) or peritoneal dialysis (open circles). The dotted line indicates target urate concentration (0.36 mmol/L) in absence of tophi. HD: Haemodialysis/haemodiafiltration; PD: Peritoneal dialysis. Before and after dialysis refer to the pre‐post analysis of the last urate concentration in the EMR before commencing dialysis compared to first urate concentration in the records after commencing dialysis, respectively. *p = 0.031, ****p < 0.001.
FIGURE 3.
The change in serum urate concentrations in gout patients both before and after commencing (a) haemodialysis/haemodiafiltration or (b) peritoneal dialysis. Square shape indicates allopurinol dose of 50 mg/day; circle 150 mg/day; circle with cross allopurinol dose not reported; diamond: 100 mg/day; triangle: 200 mg/day; inverted triangle: 300 mg/day. Black filled and open symbols indicate urate concentrations before and after commencing dialysis, respectively. The dotted horizontal line indicates target urate concentration (0.36 mmol/L) in absence of tophi whilst the dashed vertical line indicates the time of commencing dialysis (time 0). Each patient's serum urate concentrations before and after commencing dialysis are connected using a line. For the individual plots for each patient, refer to the Figures S1–S8.
Achievement of target serum urate concentrations (≥ 1 concentration < 0.36 mmol/L) whilst receiving dialysis was observed in 60% (6/10) of patients on HD and 78% (21/27) of patients on PD. For 8 patients on HD, achievement of target urate concentrations after dialysis commencement could not be confirmed because the urate sampling time was during or just after the HD session. Patients on PD receiving CAPD or APD plus manual day exchange (n = 14) were twice as likely to achieve target serum urate concentrations compared to those using intermittent nocturnal APD (n = 7).
Based on the last serum urate concentration recorded throughout the dialysis vintage, 54% (7/13) of patients receiving HD and 71% (19/27) of patients receiving PD achieved target serum urate concentrations. Achievement of target serum urate concentrations could not be determined in 5 patients receiving HD because the urate sampling was during the session or on a non‐dialysis day but < 24 h from the previous session.
4. Discussion
In the absence of strong evidence‐based guidelines, understanding real‐world allopurinol use and serum urate control in dialysis patients with gout is essential to ensure patients remain symptom free. In this retrospective study, allopurinol doses were generally unchanged after commencing dialysis, with 100 mg/day being the most common dose. Despite that, serum urate concentrations significantly decreased upon commencing dialysis, and over half of patients on HD and PD achieved target urate concentrations. These findings suggest dialysis itself plays an important role in lowering serum urate concentrations.
Nearly all patients received allopurinol before an HD session, despite recommendations to administer it after. Since approximately 50% of oxypurinol is removed during an HD session, this practise may result in subtherapeutic concentrations unless a supplementary allopurinol dose (half the original) is given after the session [20], a strategy not observed. Hence, patients on HD are likely to have very little exposure to oxypurinol during the interdialytic period, suggesting that serum urate lowering in HD is likely attributable more to dialysis than to allopurinol. This raises the potential for reducing or de‐prescribing allopurinol in patients with gout after they commence dialysis, particularly if urate targets are met. Polypharmacy is common in people on dialysis, with patients taking on average 12 different medicines each day [21]. Identifying deprescribing strategies to reduce the ‘pill burden’ would therefore be highly beneficial for this patient population. Future prospective interventional trials could monitor serum urate, flare rates, and quality of life following deprescribing to provide an evidence‐base for updated gout management guidelines in patients undergoing dialysis. This would assist clinicians to evaluate the ongoing need for allopurinol after dialysis initiation, particularly in asymptomatic patients with stable urate control, balancing risks, costs, and pill burden with the patient's symptom profile and disease history.
Despite the generally unchanged allopurinol doses seen in the patient charts, serum urate concentrations significantly decreased after commencing dialysis, supporting the suggestion that urate lowering is attributed to the dialysis itself. Although the molecular size of uric acid (138 Da) is larger than urea (60 Da) and creatinine (113 Da), it is still dialyzable [22]. Regular serum urate monitoring would therefore facilitate more effective gout management, particularly when modifying the dialysis regimen [23]. However, best practises for reducing or deprescribing allopurinol in dialysis and which patients are candidates for deprescribing are unclear, especially in patients with tophaceous gout, as observed in two patients (NK6HD, NK52PD) in our cohort. The observed necessity of allopurinol in patients with severe tophaceous gout is consistent with recommendations of recent reviews [24] and findings of an exploratory prospective study [25].
Despite the higher urate clearance by HD as compared to PD [20], a similar proportion of patients (> 50%) achieved target urate concentrations on both dialysis types, consistent with existing literature [7]. This suggests that the continuous nature of PD may offset its lower clearance of urate. However, an accurate assessment of target urate attainment, especially in patients on HD, must account for the timing of serum urate concentrations relative to the dialysis session. It is known that pre‐session samples more accurately reflect urate control as after the session, serum urate concentrations transiently decline before rebounding before the next session [26]. Several patients on HD were excluded in our assessment of target urate achievement because of suboptimal timing (during session or < 24 h from the previous session) of urate sampling.
Amongst PD regimens, greater reductions in serum urate were observed with CAPD or APD plus manual daytime exchange. PD membrane function declines over time leading to sub‐optimal clearance of solutes [27]. This might explain the modest increase in serum urate concentrations particularly after 20 months of commencing peritoneal dialysis. Guidelines currently offer limited direction on whether allopurinol is needed in patients on PD before peritoneal membrane exhaustion and how to best adjust allopurinol dose to account for peritoneal membrane changes [4]. Regular long‐term monitoring of serum urate concentrations may also be helpful to capture any increase in serum urate concentrations above the target as the efficiency of dialysis decreases.
The study results have some limitations. The retrospective design meant that serum urate concentrations were collected at irregular intervals. To account for this, target urate attainment was evaluated using two different approaches using both single and serial target achievement. In addition, the ability to control for confounders like coexisting medications and variability in dialysis techniques was limited by the study design; however, as each patient is their own control, this reduces the potential impact of confounders. Where possible we have tried to present results stratified by dialysis modality. However, intraindividual variability was noted, especially in peritoneal dialysis, as different modalities (APD, CAPD, APD plus CAPD) were used at different points of time. Estimating gout flare frequency via EMRs is inherently limited by inconsistent documentation and underuse of diagnostic confirmation via joint aspiration, limitations echoed in prior reviews [28]. Results of four patients developing gout flares after commencing dialysis should be considered as a rough estimate, albeit consistent with a previous study [29]. Similarly, we have likely underestimated the proportion of patients with tophaceous gout using the EMR, as tophi can be subclinical and synovial fluid aspiration or ultrasound imaging is required to be detected [30], an infrequent practise at our institution. We did not include a comparator group of patients with gout receiving dialysis not prescribed allopurinol. Given that dialysis lowers serum urate concentrations, this group of patients could be investigated in future studies.
5. Conclusions
This investigation of real‐world use of allopurinol in patients on dialysis showed that dialysis alone may control serum urate for many patients with gout as it reduced serum urate concentrations despite allopurinol doses being unchanged by prescribers. These findings highlight the potential for allopurinol deprescribing in selected patients receiving dialysis based on sustained target urate achievement. Similar target urate achievement was observed in patients on HD and PD, and where patients on HD received their allopurinol dose prior to their dialysis, risking reduced efficacy because of suboptimal exposure to oxypurinol. Adjunct allopurinol treatment may, however, be required in patients with tophaceous gout or those on long‐term PD. Further research is warranted to examine allopurinol deprescribing in patients with gout receiving dialysis to provide evidence for updated gout management guidelines for these patients. Implementation of allopurinol deprescribing can reduce medication burden, healthcare costs, and adverse drug reactions whilst maintaining effective gout management.
Author Contributions
N.K., S.S., R.C., and D.W. contributed to the design of the study. N.K. carried out the data collection and performed the statistical analysis. N.K. and S.S. wrote the first draft. R.C., D.W., K.S., S.T., S.H. reviewed and edited the first draft. All authors approved the manuscript.
Funding
The authors have nothing to report.
Disclosure
K.S. has received speaker's honoraria from Baxter Healthcare and Fresenius Medical Care.
Ethics Statement
Ethics approval was obtained from the institutional human research ethics committee, Western Sydney Local Health District (ETH00394).
Consent
Due to the retrospective nature of the study, a waiver of consent was approved by the ethics committee in accordance with Australia's National Statement on Ethical Conduct in Human Research (NHMRC, 2018) Sect. 2.3.10.
Conflicts of Interest
The authors declare no conflicts of interest.
Supporting information
Figure S1: Serum urate concentrations of Individual haemodialysis patients (NK1HD to NK13HD) before commencing dialysis throughout the dialysis vintage with the corresponding allopurinol doses and dialysis modality characteristics around these urate concentrations.
Figure S2: Serum urate concentrations of Individual haemodialysis patients (NK15HD to NK32HD) before commencing dialysis throughout the dialysis vintage with the corresponding allopurinol doses and dialysis modality characteristics around these urate concentrations.
Figure S3: Serum urate concentrations of Individual haemodialysis patients (NK36HD to NK55HD) before commencing dialysis throughout the dialysis vintage with the corresponding allopurinol doses and dialysis modality characteristics around these urate concentrations.
Figure S4: Serum urate concentrations of Individual peritoneal dialysis patients (NK52PD to NK14PD) before commencing dialysis throughout the dialysis vintage with the corresponding allopurinol doses and dialysis modality characteristics around these urate concentrations.
Figure S5: Serum urate concentrations of Individual peritoneal dialysis patients (NK16PD to NK25PD) before commencing dialysis throughout the dialysis vintage with the corresponding allopurinol doses and dialysis modality characteristics around these urate concentrations.
Figure S6: Serum urate concentrations of Individual peritoneal dialysis patients (NK28PD to NK38PD) 1 year before commencing dialysis throughout the dialysis vintage with the corresponding allopurinol doses and dialysis modality characteristics around these urate concentrations.
Figure S7: Serum urate concentrations of Individual peritoneal dialysis patients (NK39PD to NK48PD) before commencing dialysis throughout the dialysis vintage with the corresponding allopurinol doses and dialysis modality characteristics around these urate concentrations.
Figure S8: Serum urate concentrations of Individual peritoneal dialysis patients (NK49PD to NK54PD) before commencing dialysis throughout the dialysis vintage with the corresponding allopurinol doses and dialysis modality characteristics around these urate concentrations.
Acknowledgements
The authors would like to thank Prof. Melanie White‐Koning for her statistical consultation. Open access publishing facilitated by The University of Sydney, as part of the Wiley ‐ The University of Sydney agreement via the Council of Australasian University Librarians.
Data Availability Statement
The data that support the findings of this study are available from the corresponding author upon reasonable request.
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Associated Data
This section collects any data citations, data availability statements, or supplementary materials included in this article.
Supplementary Materials
Figure S1: Serum urate concentrations of Individual haemodialysis patients (NK1HD to NK13HD) before commencing dialysis throughout the dialysis vintage with the corresponding allopurinol doses and dialysis modality characteristics around these urate concentrations.
Figure S2: Serum urate concentrations of Individual haemodialysis patients (NK15HD to NK32HD) before commencing dialysis throughout the dialysis vintage with the corresponding allopurinol doses and dialysis modality characteristics around these urate concentrations.
Figure S3: Serum urate concentrations of Individual haemodialysis patients (NK36HD to NK55HD) before commencing dialysis throughout the dialysis vintage with the corresponding allopurinol doses and dialysis modality characteristics around these urate concentrations.
Figure S4: Serum urate concentrations of Individual peritoneal dialysis patients (NK52PD to NK14PD) before commencing dialysis throughout the dialysis vintage with the corresponding allopurinol doses and dialysis modality characteristics around these urate concentrations.
Figure S5: Serum urate concentrations of Individual peritoneal dialysis patients (NK16PD to NK25PD) before commencing dialysis throughout the dialysis vintage with the corresponding allopurinol doses and dialysis modality characteristics around these urate concentrations.
Figure S6: Serum urate concentrations of Individual peritoneal dialysis patients (NK28PD to NK38PD) 1 year before commencing dialysis throughout the dialysis vintage with the corresponding allopurinol doses and dialysis modality characteristics around these urate concentrations.
Figure S7: Serum urate concentrations of Individual peritoneal dialysis patients (NK39PD to NK48PD) before commencing dialysis throughout the dialysis vintage with the corresponding allopurinol doses and dialysis modality characteristics around these urate concentrations.
Figure S8: Serum urate concentrations of Individual peritoneal dialysis patients (NK49PD to NK54PD) before commencing dialysis throughout the dialysis vintage with the corresponding allopurinol doses and dialysis modality characteristics around these urate concentrations.
Data Availability Statement
The data that support the findings of this study are available from the corresponding author upon reasonable request.