BackgroundFibroblast growth factor-23 (FGF-23), a novel regulator of mineral metabolism, is markedly elevated in chronic kidney disease and has been associated with poor long-term outcomes. However, whether FGF-23 has an analogous role in acute kidney injury is unknown. The goal of this study was to measure FGF-23 levels in critically ill patients with acute kidney injury to determine whether FGF-23 levels were elevated, as in chronic kidney disease.MethodsPlasma FGF-23 and intact parathyroid hormone (PTH) levels were measured in 12 patients with acute kidney injury and 8 control subjects.ResultsFGF-23 levels were significantly higher in acute kidney injury cases than in critically ill subjects without acute kidney injury, with a median FGF-23 level of 1948 RU/mL (interquartile range (IQR), 437-4369) in cases compared with 252 RU/mL (IQR, 65-533) in controls (p = 0.01). No correlations were observed between FGF-23 and severity of acute kidney injury (defined by the Acute Kidney Injury Network criteria); among patients with acute kidney injury, FGF-23 levels were higher in nonsurvivors than survivors (median levels of 4446 RU/mL (IQR, 3455-5443) versus 544 RU/mL (IQR, 390-1948; p = 0.02). Severe hyperparathyroidism (defined as intact PTH >250 mg/dL) was present in 3 of 12 (25%) of the acute kidney injury subjects versus none of the subjects without acute kidney injury, although this result did not meet statistical significance.ConclusionsWe provide novel data that demonstrate that FGF-23 levels are elevated in acute kidney injury, suggesting that FGF-23 dysregulation occurs in acute kidney injury as well as chronic kidney disease. Further studies are needed to define the short- and long-term clinical effects of dysregulated mineral metabolism in acute kidney injury patients.

Objective To determine the relationship between omega‐3 polyunsaturated fatty acid (n‐3 PUFA) consumption (dietary or supplemental) and risk of gout flares. Methods We used data from the Boston University Online Gout Study, an internet‐based case‐crossover study conducted from February 2003 to January 2012. At the times of gout flares (hazard period) and during gout flare–free periods (control periods), participants completed questionnaires regarding exposures, including supplements and diet, during the preceding 48 hours. We examined the relationship of self‐reported n‐3 PUFA–rich supplements and fish intake with the risk of recurrent gout flares using conditional logistic regression, adjusting for total purine intake, diuretic use, and other urate‐lowering or flare prophylactic medications (allopurinol, nonsteroidal antiinflammatory drugs, or colchicine). Results Of the 724 participants, 85% met the 1977 American College of Rheumatology preliminary criteria for the classification of the acute arthritis of primary gout. Twenty‐two percent of the participants reported some form of n‐3 PUFA consumption (supplements, 4.6%; dietary fatty fish, 19%) in the 48 hours preceding a gout flare or flare‐free period. The adjusted odds ratios were 1.01 (95% confidence interval [95% CI] 0.63–1.60; P = 0.98) for all 3 supplements combined and 0.74 (95% CI 0.54–0.99; P = 0.04) for consumption of ≥2 n‐3 PUFA–rich fish servings. Conclusion Dietary n‐3 PUFA–rich fish consumption, when adjusted for total purine intake, was associated with lower risk of recurrent gout flares, whereas n‐3 PUFA supplementation alone, as taken in a self‐directed manner, was not. Consumption of specific sources and adequate doses of n‐3 PUFA for gout flare prevention warrants further study in an adequately powered clinical trial.

Objective To examine impact of pre‐existing and incident problematic musculoskeletal (MSK) areas after total knee replacement (TKR) on postoperative 60‐month Western Ontario and McMaster Universities Osteoarthritis Index (WOMAC) pain/function scores. Methods Using data from a randomized controlled trial of subjects undergoing TKR for osteoarthritis, we assessed problematic MSK areas in six body regions before TKR and 12, 24, 36, and 48 months after TKR. We defined the following two variables: 1) density count (number of problematic MSK areas occurring after TKR; range 0‐24) and 2) cumulative density count (problematic MSK areas both before and after TKR, categorized into four levels: no preoperative areas and density count of 0‐1 [reference group]; no preoperative areas and density count of 2 or more; one or more preoperative areas and density count of 0‐1; and one or more preoperative areas and density count of 2 or greater). We evaluated the associations between categorized 60‐month WOMAC and cumulative density count by ordinal logistic regression. Results Among 230 subjects, 24% reported one or more preoperative problematic MSK area. After TKR, 75% reported a density count of 0 to 1; 25% reported a density count of 2 or more. Compared with the reference group, each cumulative density count category was associated with an increased odds of having a higher category of 60‐month WOMAC pain score, as follows: 2.97 (95% confidence interval [CI], 1.48‐5.98) for no preoperative problematic areas and density count of 2 or greater, 3.31 (95% CI, 1.64‐6.66) for one or more preoperative problematic areas and density count of 0 to 1, and 2.85 (95% CI, 0.97‐8.39) for one or more preoperative problematic areas and density count of 2 or greater. Similar associations were observed with 60‐month WOMAC function score. Conclusion In TKR recipients, the presence of problematic musculoskeletal areas beyond the index knee—preoperatively and/or postoperatively—was associated with worse 60‐month WOMAC pain/function score.