Background/Purpose: Sodium-glucose cotransporter type 2 inhibitors (SGLT2I) proved substantial benefits in diabetes mellitus (DM), heart failure (HF) and kidney disease (KD). In pivotal trials, SGLT2Is reduced serum urate (SU) levels, but the evidence in patients with gout under other urate-lowering drugs (ULD) in clinical grounds is scarce.The objective is to evaluate the urate outcomes in patients with gout treated with SGLT2I and ULD in clinical practice.

Methods: Retrospective, single-center observational study, enrolling patients with gout from a crystalarthritis specialised clinic. We selected those receiving combined treatment with ULD and SGLT2I, regardless ofthe indication. Cases with no serum urate levels available in the 6 months before andafter combined treatment or starting renal replacement therapy were excluded. The mainvariable of the study was SU level pre- and post-SGLT2I (mg/dL) statistically analized usingWilcoxon test as a non parametric continuous variable. As secondary variables, we measuredthe percentage achievement of SU target (< 6 mg/dL or < 5 mg/dL), the required allopurinoldose (mg) and pre-estimated dose according to the Easy-Allo tool (mg) [PMID 38359899].

Results: Forty-six patients were included: median age 76 years (IQR 15.25), 82.6% men, with highcomorbidity (91.1% with DM, 58.7% with KD, 45.7% with HF) and 10 years (IQR 20) of goutduration. As ULD, 66.7% (n=30) of patients were treated with allopurinol, 28.9% (n=13) withfebuxostat, and 4.4% (n=2) with benzbromarone. Regarding the SGLT2I, 58.7% (n=27) receiveddapagliflozin, 30.4% (n=14) empagliflozin, and 10.9% (n=5) canagliflozin. ULD were initiallyprescribed in 81.4% (n=35), while SGLT2I in the remaining 18.6% (n=8).The target of SU < 6 mg/dL was achieved in 97.7% (95%CI 88.2-99.6%) of the patients, while81.4% also reached < 5 mg/dL (95%CI 65.5-88.9%). The achievement of the < 5 mg/dL targetwas unrelated to the first prescribed medication (ULD 81.3% vs SGLT2I 87.5%, p=1.000) or thetype of xanthine-oxidase inhibitor (allopurinol 79.3% vs febuxostat 91.7%, p=0.651).The start of SGLT2I showed a median SU reduction of 0.85 mg/dL (IQR 3.02, p=0.001 for thebefore-after comparison) [Image 1]. The SU reduction was observed regardless of beingalready on ULD (median 0.80, IQR 2.90, p=0.021) or not (median 3.00, IQR 6.95, p=0.018) or ofchanges in diuretics use (p=0.692).No significant differences in allopurinol dose were found pre- and post-SGLT2I use but with atrend toward a lower dosage than pre-estimated by the Easy-Allo tool [Image 2].The use of SGLT2I showed significant reductions in fasting glucose, HbA1c, and C-reactiveprotein levels, increased urine glucose excretion, and no differences in urine albumin andglomerular filtration rate. We detected a significant reduction in diuretics use pre- and post-SGLT2I (60.9% vs 54.3%, p < 0.001).

Conclusion: The combination of SGLT2I and ULD in patients with gout in clinical practice achievedsignificant SU level reductions and targets of SU < 6 mg/dL and < 5 mg/dL. A trend towards alower dosage requirement of allopurinol was noted, along with a reduced use of diuretics.These promising results require confirmation by further intervention studies.

Image 1. Serum urate (SU) reduction in mg/dL after the start of SGLT2I.

In brackets, 95%CIs. In the pre-SGLT2I serum urate category, the values are higher, with a

mean close to 5.5 mg/dL and with regard to post-SGLT2I serum urate values these are lower,

with a mean close to 4 mg/dL.

Image 2. Allopurinol dose pre-estimated and after the start of SGLT2I.

Box-and-bar plot of Allopurinol dose comparison. The boxes represent the interquartile range

(Q1 to Q3), the dark lines represent the median, and the brackets indicate the range of the data

excluding outliers. We can observe a higher variability in the dose of allopurinol after the

initiation of treatment with SGLT2I with a tendency towards the use of lower doses.

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ACR Meeting Abstracts - https://acrabstracts.org/abstract/effectiveness-of-sodium-glucose-cotransporter-type-2-inhibitors-and-urate-lowering-agents-in-patients-with-gout-data-from-a-single-center-specialised-clinic/