Chronic miliary gout complicated by chronic renal failure: a case report

A 39-year-old Asian male, with a history of gout spanning a decade, developed non-itchy, non-erythematous nodular papules on his joints, abdomen, and lower back over the past 4 years (Figure 1). These nodules were largely asymptomatic, but some ulcerated and intermittently discharged a chalky substance. Despite managing his hyperuricaemia with oral allopurinol and benzbromarone, the patient’s results were suboptimal. His medical history also included chronic kidney failure and hypertension for over 4 years, obesity with a body mass index (BMI) of 31.9 kg/m², and a 20 year high alcohol intake. Laboratory tests indicated abnormal blood urea nitrogen and serum creatinine levels and a high uric acid level of 11.54 mg/dL (normal range 3.36–6.72 6 mg/dL). In addition, his estimated glomerular filtration rate (eGFR) of 22 mL/min pointed towards renal insufficiency. Increased inflammatory markers, including leucocyte count, were observed. Renal ultrasonography confirmed chronic renal failure, and there were no kidney stones. A dermatological consultation recommended a biopsy of the nodular ulcerative tissue, revealing needle-shaped crystals, typical of tophaceous gout pathology. From these findings, the patient was diagnosed with chronic gout, miliary gout, and chronic renal failure.

Figure 1. Cutaneous and subcutaneous manifestations of gout. (A) The skin on the abdomen has numerous partially ruptured soft miliary tophi papules with a gritty texture. (B) Subcutaneous deposits of white tophaceous material triggering swelling on the palmar area of both hands. (C) Tophi-laden papules and plaques affecting the joints and anterior tibial area. (D) Nodular tophaceous rash on the lower back, accompanied by pigmentation.

The patient’s chronic kidney disease progressed to stage 4 (eGFR < 30 mL/min), causing discontinuation of benzbromarone. Allopurinol dosage adjustments from 100 mg to 300 mg failed to achieve target uric acid levels. Consequently, allopurinol was swapped for febuxostat (40 mg/day). While this led to a slight decrease in uric acid levels, it also provoked gout flares, particularly in the patient’s elbows, knees, wrists, ankles, and interphalangeal joints of both hands. Because of these extensive gout flares, we administered oral low-dose glucocorticoids (prednisone, 10 mg daily), which effectively and promptly reduced inflammation. Furthermore, the patient was advised to abstain from alcohol consumption. Ultimately, the febuxostat dosage was increased to 60 mg/day (1), successfully reducing uric acid levels to below 6 mg/dL.

Prolonged periods of high uric acid levels possibly led to the formation of gouty tophi. However, despite the presence of gouty tophi in the patient’s skin and joints, he did not develop kidney stones. Allopurinol’s effectiveness in handling miliary gout is well documented, yet in this case, is the patient’s reaction did not align with the expected outcomes (2). Recent studies have demonstrated that patients receiving febuxostat show a significant increase in eGFR and a reduced risk of renal disease progression compared to those treated with allopurinol (3, 4). Evidence suggests that patients with stage 4–5 chronic kidney disease may tolerate higher doses of febuxostat to achieve enhanced therapeutic outcomes (1, 3). However, safety concerns prevented us from increasing the dosage.

Studies indicate that ongoing oral glucocorticoid therapy could heighten the probability of developing cutaneous gout and the proliferation of subcutaneous tophi in patients (5). In light of the patient’s stage 4 kidney disease, the use of non-steroidal anti-inflammatory drugs (NSAIDs) was contraindicated. As per the American College of Rheumatology guidelines for managing acute gout flares (6), we have begun preventive treatment with low-dose colchicine (0.5 mg every other day) since the containment of the gout attack. Subsequent monitoring has indicated a lack of notable adverse effects. While the safety profile of colchicine in the context of end-stage renal disease remains ambiguous, clinicians should use glucocorticoids, NSAIDs, and colchicine judiciously in cases of miliary gout.

Despite the patient’s extensive history with chronic gout, his cutaneous manifestations posed diagnostic challenges. These manifestations typically appeared as multiple distinct papules, each about 1–5 mm in diameter, in hues of white or cream, closely resembling pustules filled with a similarly coloured pasty material (7). Unlike articular involvement, skin tophi seldom show inflammatory signs such as swelling, tautness, erythema, or warmth, complicating their detection. Nevertheless, these nodules can develop ulceration, which facilitates obtaining biopsy samples. Pathological evaluations of the skin biopsies or the ulcer exudate are instrumental in confirming the diagnosis of tophaceous gout (8). The aetiology of cutaneous tophi deposition is not well understood, but it is known that patients with a long-standing history of hyperuricaemia are more prone to urate crystal accumulation, potentially leading to atypical site involvement. Research has shown that subcutaneous gouty tophi can occur on various body parts, notably the chest, abdomen, back, limbs, and lower extremities (9).

Alcohol intake has been recognized as a significant trigger for gout flare-ups, regardless of the type of alcoholic drink consumed (10). Consequently, alcohol abstinence becomes a vital aspect of gout management. In addition, with the patient having a high BMI, lifestyle modifications are advised to augment disease control. Despite some studies suggesting that obesity may reduce the risk of cutaneous manifestations in gout, weight management is anticipated to provide extensive health advantages (11). The management strategy is further complicated when dealing with concurrent miliary gout and renal dysfunction, as these conditions limit the preventive use of glucocorticoids for gout attacks, and also restricts the options for using NSAIDs and colchicine, thereby challenging the treatment and management of acute gout episodes in the context of kidney disease. Moreover, it is essential to continue to monitor serum urate levels during treatment with allopurinol and febuxostat in order to optimize the therapy.

Ethics approval

This study involves a human participant, but the institutional research ethics board does not require board review for a single case report when the patient’s privacy is protected, and therefore exempted this study. The patient gave informed consent for the publication of this report and associated images.

Authors’ contributions

Zhang and Huang collated the case report, searched the literature, and wrote the first draft. Li and Zhou collected and analysed case data, guided clinical diagnosis and treatment, and critically reviewed and revised the manuscript. All authors approved the final manuscript for publication.

Disclosure statement

No potential conflict of interest was reported by the authors.

Additional information

Funding

This project is supported by the Guizhou Provincial Science and Technology Department [project number 2022518].