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The historical association between hyperuricemia and kidney disease has been well-recognized from ancient times [1]; however, uric acid has been regarded as a marker rather than a risk factor for the development of renal disease since a decrease in glomerular filtration rate (GFR) per se induces an elevation in serum uric acid level despite compensatory increases in urinary and gastrointestinal excretions of urate [2]. In the past decade, substantial data from epidemiological and interventional studies has provided evidence that uric acid has a causative role in the development and/or aggravation of renal disease. In this issue of Kidney Research and Clinical Practice, Kim et al. reported that where hyperuricemia was already present at the time of diagnosis of immunoglobulin A (IgA) nephropathy, this was associated with a higher rate of renal progression [3]. Although this observational study did not address whether uric acid per se caused an aggravation of renal disease, hyperuricemia was an independent risk factor for IgA nephropathy on multiple regression analysis adjusted to age, gender, blood pressure, and proteinuria. It has been reported already that uric acid at the time of kidney biopsy is one of the independent risk factors determining renal prognosis in IgA nephropathy [4]. Furthermore, treatment of asymptomatic hyperuricemia with allopurinol delayed the renal progression with a lesser increase in blood pressure in patients with IgA nephropathy [5]. In this editorial, recent understanding regarding the role of uric acid in chronic kidney disease (CKD) will be highlighted, together with a review of potential mechanisms by which renal disease might be induced by uric acid, and a reappraisal of hyperuricemia as a novel risk factor for renal progression in CKD.
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