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Urinary Melamine Levels and Progression of CKD.

ABSTRACT: BACKGROUND AND OBJECTIVES:CKD is a global public health problem. Some cross-sectional studies have associated environmental melamine exposure with kidney diseases, but evidence is limited. DESIGN, SETTING, PARTICIPANTS, & MEASUREMENTS:We conducted this prospective cohort study to enroll patients with eGFR?30 ml/min per 1.73 m2 in 2006-2010. Urinary corrected melamine levels (ratio of urinary melamine to urinary creatinine) were measured by liquid chromatography/tandem mass spectrometry at enrollment. Kidney outcomes included doubling of serum creatinine levels, eGFR decline >3 ml/min per 1.73 m2 per year, and 30% decline in eGFR in the first 2 years. Subjects were followed until targeted kidney outcomes, cancer, death, last contact, or the end of observation in December 2016. RESULTS:In a total of 293 subjects, the median urinary corrected melamine level was 0.97 (interquartile range, 0.43-2.08) ?g/mmol. Over a median follow-up period of 7.0 years, serum creatinine levels doubled in 80 subjects (27%). Subjects in the highest tertile of urinary melamine level 12.70 ?g/mmol) had a 2.30 (95% confidence interval, 1.25 to 4.23; P<0.01) hazard risk for doubling of serum creatinine compared with those in the lowest tertile (0.02-0.58 ?g/mmol). Similar significant dose-response results were found in eGFR decline >3 ml/min per 1.73 m2 per year and 30% decline in eGFR in the first 2 years. CONCLUSIONS:Urinary melamine level is significantly associated with kidney function deterioration in patients with early-stage CKD.

SUBMITTER: Tsai YC

PROVIDER: S-EPMC6682811 | biostudies-literature | 2019 Aug

REPOSITORIES: biostudies-literature

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Urinary Melamine Levels and Progression of CKD.

Tsai Yi-Chun YC Wu Chia-Fang CF Liu Chia-Chu CC Hsieh Tusty-Jiuan TJ Lin Yu-Ting YT Chiu Yi-Wen YW Hwang Shang-Jyn SJ Chen Hung-Chun HC Wu Ming-Tsang MT

Clinical journal of the American Society of Nephrology : CJASN 20190723 8

<h4>Background and objectives</h4>CKD is a global public health problem. Some cross-sectional studies have associated environmental melamine exposure with kidney diseases, but evidence is limited.<h4>Design, setting, participants, & measurements</h4>We conducted this prospective cohort study to enroll patients with eGFR≥30 ml/min per 1.73 m<sup>2</sup> in 2006-2010. Urinary corrected melamine levels (ratio of urinary melamine to urinary creatinine) were measured by liquid chromatography/tandem m ...[more]

PMID: 31337620

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Project description:Background and objectivesProgressive CKD in Black individuals is strongly associated with polymorphisms in the APOL1 gene, but it is unknown whether dietary risk factors for CKD progression vary in high- versus low-risk APOL1 genotypes. We investigated if APOL1 genotypes modify associations of dietary potassium and sodium with CKD progression and death.Design, setting, participants, & measurementsWe analyzed 1399 self-identified Black participants enrolled in the Chronic Renal Insufficiency Cohort from April 2003 to September 2008. Exposures were calibrated 24-hour urine potassium and sodium excretion. The primary outcome was CKD progression defined as the time to 50% decline in eGFR or kidney failure. The secondary outcome was CKD progression or death. We tested for an interaction between urinary potassium and sodium excretion and APOL1 genotypes.ResultsMedian 24-hour urinary sodium and potassium excretions in Black participants were 150 mmol (interquartile range, 118-188) and 43 mmol (interquartile range, 35-54), respectively. Individuals with high- and low-risk APOL1 genotypes numbered 276 (20%) and 1104 (79%), respectively. After a median follow-up of 5.23 years, CKD progression events equaled 605, and after 7.29 years, CKD progression and death events equaled 868. There was significant interaction between APOL1 genotypes and urinary potassium excretion with CKD progression and CKD progression or death (P=0.003 and P=0.03, respectively). In those with high-risk APOL1 genotypes, higher urinary potassium excretion was associated with a lower risk of CKD progression (quartiles 2-4 versus 1: hazard ratio, 0.83; 95% confidence interval, 0.50 to 1.39; hazard ratio, 0.54; 95% confidence interval, 0.31 to 0.93; and hazard ratio, 0.50; 95% confidence interval, 0.27 to 0.93, respectively). In the low-risk APOL1 genotypes, higher urinary potassium excretion was associated with a higher risk of CKD progression (quartiles 2-4 versus 1: hazard ratio, 1.01; 95% confidence interval, 0.75 to 1.36; hazard ratio, 1.23; 95% confidence interval, 0.91 to 1.66; and hazard ratio, 1.53; 95% confidence interval, 1.12 to 2.09, respectively). We found no interaction between APOL1 genotypes and urinary sodium excretion with CKD outcomes.ConclusionsHigher urinary potassium excretion was associated with lower versus higher risk of CKD progression in APOL1 high-risk and low-risk genotypes, respectively.

Dataset Information

Urinary Melamine Levels and Progression of CKD.

Publications

Urinary Melamine Levels and Progression of CKD.

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