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Year : 2018  |  Volume : 4  |  Issue : 3  |  Page : 78

Hyperuricemia: Metabolic impact on kidney

Consultant Nutritionist, Department of Dietetics, Cumballa Hill Hospital, Mumbai, Maharashtra, India

Date of Web Publication23-Apr-2019

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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/jrnm.jrnm_11_19

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How to cite this article:
Desai N. Hyperuricemia: Metabolic impact on kidney. J Renal Nutr Metab 2018;4:78

How to cite this URL:
Desai N. Hyperuricemia: Metabolic impact on kidney. J Renal Nutr Metab [serial online] 2018 [cited 2020 Feb 21];4:78. Available from: http://www.jrnm.in/text.asp?2018/4/3/78/256813

In human beings, uric acid is the poorly soluble circulating end product of the purine nucleotide metabolism. A reduction in the glomerular filtration rate (GFR) contributes to hyperuricemia, which is frequently observed in patients with chronic kidney disease (CKD). Most mammals are endowed with an additional enzyme, urate oxidase, which converts uric acid to more soluble allantoin for excretion, whereas humans have evolutionarily acquired distinct gene mutations that render this latter enzyme inactive, resulting in the inability to produce allantoin. Therefore, the physiologic catabolism of endogenous and dietary purine nucleotides ends with uric acid in humans.

From epidemiological findings, it is clear that an elevated uric acid is strongly associated with the development of CKD but not ubiquitously with the progression of CKD. There is emerging evidence both on experimental and epidemiological bases that hyperuricemia represents a risk factor for the progression of CKD.

It has been demonstrated that the prevalence of hyperuricemia rises in parallel with the GFR decline, which is present in 40%–60% of patients with CKD Stage I to III and 70% of patients with CKD Stage IV or V. In addition, CKD is one of the most common independent risk factors for gout.

If hyperuricemia is symptomatic with presentation of gout, then uric acid-lowering drugs have to be used. However, the role of serum uric acid-lowering treatment in asymptomatic hyperuricemia in CKD is still a matter of serious controversy in the absence of large randomized controlled trials (RCTs). This is true for patients with diabetes mellitus as well. Only adequately powered RCTs would provide definitive answers about efficacy and safety of pharmacological treatment for asymptomatic hyperuricemia in CKD, and at the current level of evidence, it cannot be recommended to prevent or slow down the progression of CKD. The dangers of inappropriately treating asymptomatic hyperuricemia are well documented.

In respect of hyperuricemia, lifestyle and dietary modifications are today the only recommended strategies for reducing the risk of worsening CKD. About two-thirds of uric acid load is derived from internal sources (liver, muscle, and intestine) and one-third from dietary sources, including fructose, alcohol, and purine-rich foods such as certain meats and seafood. High fructose intake (e.g., corn syrup or various soft drinks) can cause intracellular ATP depletion with enhanced nucleotide turnover and uric acid formation. Therefore, uric acid-lowering treatment almost always includes changes in diet and lifestyle, especially in the absence of pharmacological treatment.

The most common risk factors for CKD are obesity and metabolic syndrome, which is strongly associated with hyperuricemia probably as a consequence of insulin resistance and the effects of insulin to reduce the urinary urate excretion. Therefore, additional lifestyle interventions such as exercise and weight reduction become important.

In our population, particular attention needs to be paid to the protein intake, as patients (majority vegetarians) tend to completely eliminate protein-rich foods in view of CKD and/or hyperuricemia, replacing them with dietary carbohydrates. This adds to the carbohydrate and fructose load which only worsens the glycemic control and hyperuricemia leading to worsening of CKD and setting up a vicious cycle.


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