Gout is a painful form of inflammatory arthritis that occurs in the setting of hyperuricemic monosodium urate crystals deposited in joints and tissues.1 Almost 40% of patients with gout have chronic kidney disease (CKD).2 Incidence of gout increases as kidney function decreases.
The kidneys excrete uric acid, predisposing CKD patients to hyperuricemia. Unfortunately, these patients have contraindications to a number of agents used in the management of gout.3,4 In addition, thiazide and loop diuretics, medications that elevate serum uric acid levels, are often the first-line treatments for CKD.5 According to guidelines recently published by the American College of Rheumataology (ACR), CKD is an indication for urate-lowering therapy (ULT) in patients with a history of gout attacks or hyperuricemia.5
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Each year there are 3.9 million patient visits for gout, and the majority of cases are managed by a primary-care provider (PCP).2 This article is designed to help guide PCPs in the management of gout in CKD patients while reflecting the 2012 ACR recommendations. Table 1 describes the stages of CKD.
The ACR acknowledges that diet and lifestyle modifications alone are not likely to lower serum uric acid to therapeutic levels or serve as gout prophylaxis.5 The primary goals of diet and lifestyle changes are to promote overall health and better management of comorbidities. For all patients, the ACR task force recommends weight loss if obese, overall healthy diet, exercise, smoking cessation, and good hydration.
While recognizing an improved diet is insufficient monotherapy for most, the panel did recommend specific dietary guidelines. All gout patients are advised limit alcohol intake, particularly beer.5 Regardless of gout activity, alcohol overuse should be avoided in all patients (the ACR defines alcohol overuse as more than one serving per day for women and more than two servings per day for men). Avoidance of food and sodas sweetened with high fructose corn syrup is also recommended.
Table 1. GFR Categories in CKD
|G1||>90||Normal or high|
|G3a||45-59||Mildly to moderately decreased|
|G3b||30-44||Moderately to severely decreased|
|Source: Kidney Disease: Improving Global Outcomes (KDIGO) CKD Work Group. KDIGO clinical practice guideline for the evaluation and management of chronic kidney disease. Kidney Int Suppl. 2013; 3:1-150.|
Both thiazide and loop diuretics promote hyperuricemia.3 The ACR suggests eliminating offending agents if deemed nonessential.5 However, both types of diuretics are often first-line choices for BP management in the CKD patient.7 Given the health-related quality-of-life concerns of many gout patients, substitution of a non-urate-elevating antihypertensive should be considered whenever possible.5 Sufficient BP control is rarely achieved with monotherapy in the CKD patient.10 A diuretic may be required in the future to control BP and reduce extracellular fluid.
This article originally appeared on Clinical Advisor