Hyperuricemia and Proteinuria : A Population-based Prospective Study
Date Issued
2005
Date
2005
Author(s)
Tsai, Shih-Li
DOI
en-US
Abstract
Background
The sequale of hyperuricemia involve renal disease, metabolic syndrome (MS), hypertension, Type II diabetes, and cardiovascular disease, while the latter three were well documented as the major causes of end stage renal disease (ESRD). Owing to this, the linkage between hyperuricemia and early sign of ESRD like proteinuria is of paramount importance to prevent ESRD. However, the causal relationship between hyperuricemia and proteinuria still remains controversial. This thesis aimed to use a longitudinal cohort to (1) estimate prevalence and incidence rate or cumulative incidence of proteinuria; and to (2) elucidate the causal relationship between hyperuricemia and proteinuria, serum creatinine or glomerular filtration rate after adjusting other significant correlates.
Materials and Methods
A total of 59,840 participants in the prospective cohort attending the Keelung Community-based Integrated Screening (KCIS) program were included. Subjects with proteinuria, abnormal serum creatinine or abnormal glomerular filtration rate at the entry of the KCIS program were excluded. Newly diagnosed proteinuria were ascertained in successive years of screening regime until the end of 2004 and treated as dependent variables. The longitudinal data on anthropometry measures, blood pressure measures, biochemical markers, dipstick spot urine analyses, and lifestyle factors were also collected at each visit. The concept of P/I ratio was applied to approximate the mean duration of proteinuria/severe proteinuria. Time-dependent Poisson regression models were conducted to estimate the effect of covariates (time-varying) on developing of event of interests.
Results
The prevalence rates of proteinuria was 11.8% and 12.3% for male and female (p<.0001), respectively. Both increased with advancing age. By the application of the concept of P/I ratio, the average duration of staying in proteinuria was 3.9 years (P: 12.1%; I: 3.1%) (3.5 years for male and 4.4 years for female). The corresponding figures for severe proteinuria were 3.4 years (P: 3.1%; I: 0.8% ) (3.0 years for male and 3.3 years for female). One-year, two-year, and three-year cumulative rates were 0.4%, 1.4%, and 3.0% for severe proteinuria. The corresponding figures 0.9%, 3.5%, and 7.6% for moderate proteinuria and 2.1%, 9.4%, and 15.6% for mild proteinuria.
High level of serum uric acid (SUA>9) was associated with progression from normal to mild proteinuria (RR=1.43, 95% CI: 1.03-1.98), from normal, mild, and moderate to severe proteinuria (RR=2.41, 95% CI: 1.46-4.00), from moderate to severe proteinuria (RR=4.58, 95% CI: 2.47-8.47), and from mild and moderate to severe proteinuria (RR=4.02, 2.32-6.95). It was also associated with the regression from mild to normal proteinuria (RR=0.87, 95% CI: 0.79-0.96) compared to those with normal SUA after controlling for other significant clinical correlates. Moderate level of SUA (7-9 for male, and 6-9 for female) was a risk factor of progression from moderate to severe proteinuria (RR=2.78, 95% CI: 1.69-4.56), and from mild and moderate to severe proteinuria (RR=2.42, 1.59-3.67). The moderate level of SUA also played a role of a hindering factor from regression (RR=0.90, 95% CI: 0.81-0.99).
When considering the disease progress of abnormal GFR, high level of serum uric acid (RR=1.55, 95% CI: 1.18-2.04) and moderate level (RR=1.32, 95% CI: 1.14-1.51) were significant risk factors compared to those with normal SUA after controlling for other significant clinical correlates. Both were significant preventive factors for regression with relative risks of 0.63 (95% CI: 0.53-0.76) and 0.79 (95% CI: 0.71-0.88) for high and moderate levels of SUA, respectively. The similar results were observed when considering the abnormal level of S-Cr.
Regarding the time-dependent models, serum uric acid was still positively associated with progression of proteinuria and inversely associated with regression of proteinuria. After controlling for other significant risk factors, similar findings were noted for the progression to severe proteinuria. For progression from mild to severe proteinuria or from moderate to severe, SUA was not important. Again, once the progression to severe proteinuria, the change of SUA was not associated with the regression of severe proteinuria. By using GFR and S-Cr, the results of time-dependent Poisson regression model revealed SUA was positively associated with decreased kidney function and increasingly associated with regression.
Conclusion
The causal relationship between serum uric acid and kidney dysfunction measured by proteinuria, elevated serum creatinine and decreased estimated GFR was substantiated in this study. These findings imply lifestyle modification of serum uric acid for the prevention of kidney dysfunction or decreased kidney function is imperative.
Subjects
蛋白尿
Hyperuricemia
Proteinuria
SDGs
Type
thesis
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