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Associations Between Hyperuricemia and Chronic Kidney Disease: A Review.

Prasad Sah OS, Qing YX - Nephrourol Mon (2015)

Bottom Line: The most common risk factors for CKD are obesity and the 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.Although many evidence-based studies have suggested that uric acid itself may harm patients with CKD by increasing inflammation and CKD progression, the issue is still a matter of controversy.Special attention should be paid to specific contraindications to certain drugs and the possibility of infectious arthritis.

View Article: PubMed Central - PubMed

Affiliation: Department of Nephrology, First Affiliated Hospital, Sun Yat-Sen University, Guangzhou, China.

ABSTRACT

Context: 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).

Evidence acquisition: Hyperuricemia is defined as a serum uric acid level > 7.0 mg/dL in males and > 6.0 mg/dL in females, while CKD is defined as kidney damage or a GFR < 60 mL/min/1.73 m(2) for 3 months or more, irrespective of the cause. Hyperuricemia is common in CKD and may occur because of decreased excretion, increased production, or a combination of both mechanisms.

Results: The causes for hyperuricemia in overproducers may be either exogenous or endogenous. CKD has become a global public health problem because of its high prevalence and the accompanying increase in the risk of end-stage renal disease, cardiovascular disease, and premature death. The most common risk factors for CKD are obesity and the 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. For recurring bouts of hyperuricemia or gout, patients should have a blood test and joint fluid test to determine whether the medication taken is effective. Interventional studies are a useful clinical research tool in clarifying the role of hyperuricemia in CKD.

Conclusions: Although many evidence-based studies have suggested that uric acid itself may harm patients with CKD by increasing inflammation and CKD progression, the issue is still a matter of controversy. Special attention should be paid to specific contraindications to certain drugs and the possibility of infectious arthritis.

No MeSH data available.


Related in: MedlinePlus

Schematic Representation of Uric Acid Homeostasis
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fig19862: Schematic Representation of Uric Acid Homeostasis

Mentions: Urate is filtered readily by the glomerulus and subsequently reabsorbed by the proximal tubular cells of the kidney, and the normal fractional excretion of uric acid is approximately 10% (17). Human kidneys reabsorb urate, which may contribute to the higher serum uric acid levels in humans compared with other species. In addition, uricase mutation prevents further uric acid degradation in human beings (18). The human urate transporter, i.e. URAT1 (encoded by the SLC22A12 gene), facilitates uric acid reabsorption in the proximal convoluted tubule (19). A recent study showed that GLUT9 (encoded by SLC2A9), which is a member of the glucose transporter family, could be a major regulator of uric acid homeostasis (20). Uric acid homeostasis and the main factors that lead to increased serum uric acid levels in CKD are schematically depicted in Figure 1.


Associations Between Hyperuricemia and Chronic Kidney Disease: A Review.

Prasad Sah OS, Qing YX - Nephrourol Mon (2015)

Schematic Representation of Uric Acid Homeostasis
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4537598&req=5

fig19862: Schematic Representation of Uric Acid Homeostasis
Mentions: Urate is filtered readily by the glomerulus and subsequently reabsorbed by the proximal tubular cells of the kidney, and the normal fractional excretion of uric acid is approximately 10% (17). Human kidneys reabsorb urate, which may contribute to the higher serum uric acid levels in humans compared with other species. In addition, uricase mutation prevents further uric acid degradation in human beings (18). The human urate transporter, i.e. URAT1 (encoded by the SLC22A12 gene), facilitates uric acid reabsorption in the proximal convoluted tubule (19). A recent study showed that GLUT9 (encoded by SLC2A9), which is a member of the glucose transporter family, could be a major regulator of uric acid homeostasis (20). Uric acid homeostasis and the main factors that lead to increased serum uric acid levels in CKD are schematically depicted in Figure 1.

Bottom Line: The most common risk factors for CKD are obesity and the 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.Although many evidence-based studies have suggested that uric acid itself may harm patients with CKD by increasing inflammation and CKD progression, the issue is still a matter of controversy.Special attention should be paid to specific contraindications to certain drugs and the possibility of infectious arthritis.

View Article: PubMed Central - PubMed

Affiliation: Department of Nephrology, First Affiliated Hospital, Sun Yat-Sen University, Guangzhou, China.

ABSTRACT

Context: 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).

Evidence acquisition: Hyperuricemia is defined as a serum uric acid level > 7.0 mg/dL in males and > 6.0 mg/dL in females, while CKD is defined as kidney damage or a GFR < 60 mL/min/1.73 m(2) for 3 months or more, irrespective of the cause. Hyperuricemia is common in CKD and may occur because of decreased excretion, increased production, or a combination of both mechanisms.

Results: The causes for hyperuricemia in overproducers may be either exogenous or endogenous. CKD has become a global public health problem because of its high prevalence and the accompanying increase in the risk of end-stage renal disease, cardiovascular disease, and premature death. The most common risk factors for CKD are obesity and the 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. For recurring bouts of hyperuricemia or gout, patients should have a blood test and joint fluid test to determine whether the medication taken is effective. Interventional studies are a useful clinical research tool in clarifying the role of hyperuricemia in CKD.

Conclusions: Although many evidence-based studies have suggested that uric acid itself may harm patients with CKD by increasing inflammation and CKD progression, the issue is still a matter of controversy. Special attention should be paid to specific contraindications to certain drugs and the possibility of infectious arthritis.

No MeSH data available.


Related in: MedlinePlus