Intestinal Hyperuricemia as a Driving Mechanism for CKD

Johnson, Richard J.

doi:10.1053/j.ajkd.2022.08.001

Cited by 7 publications

(3 citation statements)

References 26 publications

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“… 70 New studies suggest that individuals carrying these variants are at higher risk for progression of CKD. 69 , 71 Dietary mechanisms may also be operative. Fructose, for example, also blocks adenosine triphosphate-binding cassette subfamily G member 2 in the intestine, reducing intestinal uric acid excretion, 72 while increasing urinary excretion, 73 reducing urinary pH, 74 and reducing urine volume.…”

Section: Gout and Ckdmentioning

confidence: 99%

“… 80 Interestingly, this is associated with dietary measures such as intake of fructose or purine-rich foods; howver, it can also occur with block in intestinal uric acid excretion. 71 Another condition might by polycystic kidney disease, in which the enlarging cysts are likely stimulating local uric acid generation. In autosomal polycystic kidney disease, serum uric acid levels are high and correlate with progression, whereas pilot studies suggest that lowering serum uric acid may be protective.…”

Section: Gout and Ckdmentioning

confidence: 99%

See 1 more Smart Citation

Uric Acid and Chronic Kidney Disease: Still More to Do

Johnson¹,

Sánchez-Lozada²,

Lanaspa³

et al. 2023

Kidney International Reports

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Section: Gout and Ckdmentioning

confidence: 99%

Section: Gout and Ckdmentioning

confidence: 99%

Uric Acid and Chronic Kidney Disease: Still More to Do

Johnson¹,

Sánchez-Lozada²,

Lanaspa³

et al. 2023

Kidney International Reports

Self Cite

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“…Uric acid load to the kidney, rather than hyperuricemia, may be more directly involved in kidney injury 16,17 . For example, a cohort study has reported that hyperuricemia was not associated with a faster decline in kidney function except in individuals with impaired function of ATP-binding cassette subfamily G member 2 (ABCG2), a dominant transporter of intestinal urate excretion, which leads to a compensatory increase in uric acid excretion from the kidney 18 .…”

mentioning

confidence: 99%

Association between urinary uric acid excretion and kidney outcome in patients with CKD

Asahina,

Sakaguchi,

Oka

et al. 2024

Sci Rep

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Inhibiting tubular urate reabsorption may protect the kidney from urate-induced tubular injury. However, this approach may promote intratubular uric acid crystallization, especially in acidified urine, which could be toxic to the kidney. To assess how tubular urate handling affects kidney outcomes, we conducted a retrospective cohort study including 1042 patients with estimated glomerular filtration rates (eGFR) of 15–60 mL/min/1.73 m2. The exposures were fractional excretion of uric acid (FEUA) and urinary uric acid-to-creatinine ratio (UUCR). The kidney outcome was defined as a halving of eGFR from baseline or initiating kidney replacement therapy. The median FEUA and UUCR were 7.2% and 0.33 g/gCre, respectively. During a median follow-up of 1.9 years, 314 kidney outcomes occurred. In a multivariate Cox model, the lowest FEUA quartile exhibited a 1.68-fold higher rate of kidney outcome than the highest FEUA quartile (95% confidence interval, 1.13–2.50; P = 0.01). Similarly, lower UUCR was associated with a higher rate of kidney outcome. Notably, patients in the highest quartile of FEUA and UUCR were at the lowest risk of kidney outcome even among those with aciduria. In conclusion, lower FEUA and UUCR were associated with a higher risk of kidney failure, suggesting that increased urate reabsorption is harmful to the kidney.

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