Thyroid hormones associate with risk of incident chronic kidney disease and rapid decline in renal function: a prospective investigation
- Xiaolin Huang†1, 2,
- Lin Ding†1, 2,
- Kui Peng1, 2,
- Lin Lin1, 2,
- Tiange Wang1, 2,
- Zhiyun Zhao1, 2,
- Yu Xu1, 2,
- Jieli Lu1, 2,
- Yuhong Chen1, 2,
- Weiqing Wang1, 2,
- Yufang Bi1, 2,
- Guang Ning1, 2 and
- Min Xu1, 2Email author
© The Author(s) 2016
Received: 14 August 2016
Accepted: 9 November 2016
Published: 3 December 2016
Thyroid hormones have been associated with renal dysfunction in cross-sectional studies. However, prospective studies exploring the effect of thyroid hormones on renal function decline were sparse and got contradictive results. We aimed to prospectively explore the associations of thyroid hormones with incident chronic kidney disease (CKD) and rapid decline in estimated glomerular filtration rate (eGFR) in Chinese adults.
The participants were from a community-based cohort including 2103 individuals aged 40 years or above without CKD at baseline. Thyroid-stimulating hormone (TSH), free triiodothyronine (FT3) and free thyroxin (FT4) were measured by radioimmunoassay at baseline. Serum creatinine, urinary creatinine and albumin were measured at baseline and follow-up. CKD was defined as eGFR <60 ml/min/1.73 m2 or urinary albumin-to-creatinine ratio ≥30 mg/g. Rapid eGFR decline was defined as an annual eGFR decline >3 ml/min/1.73 m2.
During 4 years of follow-up, 198 participants developed CKD and 165 experienced rapid eGFR decline. Compared to tertile 1, tertile 3 of FT4 levels were associated with 1.88-folds (95% confidence interval [CI], 1.27–2.77) increased risk of incident CKD; and 1.64-folds (95% CI, 1.07–2.50) increased risk of rapid eGFR decline (both P for trend ≤0.02), after adjustment for confounders. Each 1-pmol/l of FT4 was associated with 12% increased risk of incident CKD and 10% of rapid eGFR decline. Among the incident CKD individuals, FT4 was significantly associated with higher risk of concurrent complications and further outcomes of CKD. We did not find associations of FT3 or TSH with CKD or rapid eGFR decline.
Higher FT4, but not TSH and FT3, was associated with increased risk of incident CKD and rapid eGFR decline in middle-aged and elderly Chinese.
KeywordsThyroid hormones Chronic kidney disease Renal function Glomerular filtration rate
Chronic kidney disease (CKD) is manifested as the presence of albuminuria, impaired glomerular filtration rate, or both . It has been found to be associated with an increased risk of cardiovascular morbidity and mortality, bringing heavy social and economic burden subsequently [2–4]. Now, CKD is affecting approximately 13.1% of Americans and 10.8% of Chinese adults [5, 6]. Although diabetes, hypertension, and family history of CKD, etc., have been established as risk factors for CKD [7, 8], disclosure of more novel risk factors for CKD or decline in estimated glomerular filtration rate (eGFR), which is a surrogate for development of CKD , may help extensively understand the pathogenesis of CKD and develop new prevention strategies for CKD.
Thyroid hormones, which are crucial for regulation of human body’s physiological actions, were found influencing GFR, renal blood flow, tubular secretory and re-absorptive processes as well [10–12]. Previous studies reported that overt and subclinical hypothyroidism were associated with higher levels of serum creatinine, reduced eGFR and increased risk of CKD [13–16]. Hyperthyroidism, however, can also lead to or accelerate the development of CKD . In fact, most of the evidence was derived from cross-sectional studies [18, 19]. Prospective studies exploring the effect of thyroid hormones on renal function decline were sparse and got contradictive results [20, 21]. One study showed that normal-to-high levels of thyroid-stimulating hormone (TSH) and normal-to-low levels of free triiodothyronine (FT3) were associated with an increased risk of incident CKD in euthyroid individuals . While the other reported non-significant association between thyroid dysfunction and changes in renal function among older adults .
In the present investigation, we aimed to explore prospectively the associations of thyroid hormones with risk of incident CKD and rapid eGFR decline; in addition, we examined the associations with predicted risks for concurrent complications and further outcomes of CKD, among the incident CKD participants.
Study population and design
All participants of the present study were recruited from Songnan Community, Baoshan district, Shanghai, in two stages as reported previously [22, 23]. In stage 1, 10,185 residents aged 40 years old or above were enrolled to the screening examination in June and July 2008. According to different levels of fasting plasma glucose (FPG), all participants were categorized into three groups: normal glucose regulation, impaired glucose regulation and diabetes. In stage 2, from June to August 2009, 4012 participants were randomly selected from the three groups on a ratio of 1.44 (normal glucose regulation) to 1.2 (impaired glucose regulation) to 1.0 (diabetes) because subjects with lower glucose levels were expected to have a lower participation rate than those with higher glucose levels, for a more comprehensive survey.
Written informed consent was obtained by each participant and the study protocol was approved by the Institutional Review Board of Rui-Jin Hospital.
A questionnaire survey and anthropometric measurements were conducted both at the baseline and follow-up visit. Sociodemographics, lifestyle factors and medical history were collected by trained physicians with a standard questionnaire via face-to-face interview. Current drinkers and smokers were defined as those who consumed alcohol at least once a week, and those who smoked a cigarette per day or seven cigarettes per week in the past 6 months, respectively. The information on body weight and height was measured with participants wearing light weight clothing and no shoes. Body mass index (BMI) was calculated as weight in kilograms divided into squared height in meters. Waist circumference was measured at umbilical level in a standing position. After at least 5 min rest, blood pressure was measured three times with 1-min interval using an automated electronic device (OMRON Model HEM-752 FUZZY, Omron Company, Dalian, China), at the non-dominant arm in a seated position. The average of the three readings was used for analysis.
After an at least 10 h overnight fast, the venous sample was collected and a 75-g oral glucose tolerance test (OGTT) was performed for each participant both at the baseline and follow-up visit. Levels of serum triglyceride, high-density lipoprotein cholesterol (HDL-c), low-density lipoprotein cholesterol (LDL-c), total cholesterol (TC), and serum creatinine (Cr) were measured by an autoanalyser (ADVIA-1650 Chemistry System, Bayer Corporation, Germany). FPG and OGTT 2-h plasma glucose were measured with using the glucose oxidase method on an autoanalyser (ADVIA-1650 Chemistry System, Bayer Corporation, Germany), and hemoglobin A1c (HbA1c) was determined by high-performance liquid chromatography (BIO-RAD D-10, USA). eGFR was evaluated using the 2009 chronic kidney disease epidemiology collaboration (CKD-EPI) equation  according to the recommendation in the 2012 kidney disease: improving global outcomes (KDIGO) clinical practice guideline for the evaluation and management of CKD :
(1) Females: Cr ≤ 0.7 mg/dl, eGFR = 144 × (Cr/0.7)−0.329 × (0.993)age; Cr > 0.7 mg/dl, eGFR = 144 × (Cr/0.7)−1.209 × (0.993)age. (2) Males: Cr ≤ 0.9 mg/dl, eGFR = 141 × (Cr/0.9)−0.411 × (0.993)age; Cr > 0.9mg/dl, eGFR = 141 × (Cr/0.9)−1.209 × (0.993)age.
A first-voided, early-morning spot urine was collected to measure the urinary albumin and creatinine using rate nephelometry (Beckman Coulter, Fullerton, CA) and alkaline nitroxanthic acid method, respectively. Urinary ACR was calculated as milligrams of urinary albumin excretion per gram of urinary creatinine.
Measurements of thyroid function
Levels of serum free thyroxin (FT4), FT3, TSH, thyroid peroxidase antibody (TPOAb) and thyroglobulin antibody (TGAb) were measured at the baseline by the Clinical Laboratory for Endocrinology, Shanghai Institution of Endocrine and Metabolic Disease, which was certified by College of American Pathologists, and assessed using chemiluminescent microparticle immunoassay method by Architect system (Abbott Laboratories, Abbott Park, IL). The reference ranges of FT4, FT3 and TSH were 9.01–19.04 pmol/l, 2.62–6.49 pmol/l and 0.35–4.94 μIU/ml, respectively, with the corresponding inter-assay coefficients of variations (CV) of 2.6–5.3%, 4.7–8.0%, and 3.1–3.4%. The reference range was <5.61 IU/ml for TPOAb with an inter-assay CV of 4.3–6.8% and <4.11 IU/ml for TGAb with an inter-assay CV of 3.2–5.2% [23, 25].
In present study, the primary outcome was incident CKD which was defined as the presence of eGFR <60 ml/min/1.73 m2 or urinary ACR ≥30 mg/g at the follow-up visit . The secondary outcome was rapid eGFR decline which was defined as an annual decline [(eGFR at follow up—eGFR at baseline)/follow-up period (years)] in eGFR >3 ml/min/1.73 m2 .
Furthermore, among the participants who developed CKD, we predicted the risks of concurrent complications and further outcomes of CKD by combining eGFR with albuminuria in the 2012 KDIGO clinical practice guideline for the evaluation and management of CKD . It was classified into four colored risk zones for prognosis: low risk, green; moderately increased risk, yellow; high risk, orange; and very high risk, red.
All statistical analyses were performed by using SAS version 9.3 (SAS Institute Inc, Cary, NC, USA). The values of serum TSH, TPOAb, TGAb, triglyceride, FPG and HbA1c, and urinary ACR were normalized by logarithmic transformation because of skewed distributions. Continuous variables were shown as means ± standard deviations (SDs) for those with normal distribution and were shown as medians (interquartile ranges) for those with skewed distribution. All categorical variables were presented as numbers (proportions). Thyroid function measurements were treated as continuous variables with one-unit increase or categorical variables by tertiles: <13.60, 13.60–14.83 and ≥14.84 pmol/l for serum FT4; <4.43, 4.43–4.83 and ≥4.84 pmol/l for serum FT3; <1.151, 1.151–1.860 and ≥1.861 μIU/ml for serum TSH.
Comparisons of baseline characteristics between non-CKD and incident CKD individuals were performed by using t test for continuous variables and Chi-square test for categorical variables. P values for trend for percentages of incident CKD and rapid eGFR decline were tested by using Cochran–Mantel–Haenszel (CMH) method among tertiles of serum FT4.
Multivariable logistic regression analysis was used to evaluate the associations of serum FT4, as well as serum FT3 and TSH, with the development of CKD and rapid eGFR decline. In model 1, age, sex and BMI at baseline were adjusted; in model 2, triglyceride, HDL-c, urinary ACR (for incident CKD only) and eGFR, current smoking and drinking, diabetes and hypertension status, and usage of antidiabetic or antihypertensive drugs at baseline were further adjusted based on model 1; in model 3, serum TPOAb and TGAb levels at baseline were further adjusted based on model 2. Additionally, we used the multinomial logit regression analysis to evaluate the associations of baseline serum FT4 levels with the predicted risks for future outcomes of CKD, among incident CKD individuals.
Significance tests were two-tailed and a P value less than 0.05 was considered to be statistically significant.
Characteristics of the participants at baseline
Baseline characteristics of the participants according to incident CKD status
58.9 ± 8.9
63.1 ± 10.1
Male (n, %)
24.7 ± 3.4
25.5 ± 3.8
Waist circumference (cm)
86.3 ± 9.4
89.5 ± 9.7
Current drinker (n, %)
Current smoker (n, %)
134 ± 24
144 ± 27
78 ± 10
81 ± 10
2.40 ± 0.68
2.35 ± 0.68
1.37 ± 0.30
1.34 ± 0.31
Total cholesterol (mmol/l)
5.15 ± 0.96
5.11 ± 1.05
4.65 ± 0.55
4.72 ± 1.11
14.27 ± 1.80
14.85 ± 2.36
eGFR (ml/min/1.73 m2)
92.4 ± 12.2
88.9 ± 14.4
Urinary ACR (mg/g)
Use of antidiabetic drugs (n, %)
Use of antihypertensive drugs (n, %)
Association of thyroid hormones with incident CKD
Association of thyroid hormone levels with incident CKD
P for trend
Each 1-pmol/l increase in FT4
P for trend
Each 1-pmol/l increase in FT3
P for trend
Each 1-μIU/ml increase in TSH
Association of thyroid hormones with rapid eGFR decline during follow-up
Association of thyroid hormones with rapid eGFR decline during follow-up
P for trend
Each 1-pmol/l increase in FT4
P for trend
Each 1-pmol/l increase in FT3
P for trend
Each 1-μIU/ml increase in TSH
Association of baseline serum FT4 levels with the predicted risks for future outcomes of CKD
According to the recommendations in the 2012 KDIGO clinical practice guideline for the evaluation and management of CKD , among the 198 participants who developed CKD during follow-up, 177 participants were at moderately increased risk of concurrent complications and further outcomes of CKD, 17 and 4 were at high risk and very high risk, respectively.
Association of baseline FT4 with predicted risks for future outcomes of incident CKD
Predicted risks for future outcomes of incident CKD
Moderately increased risk
Combined high and very high increased risk
Each 1-pmol/l increase in FT4
Each 1-tertile increase in FT4
In this community-based prospective investigation, we found that high levels of serum FT4 significantly associated with renal function decline in middle-aged and elderly Chinese. Major findings in our study were: (1) elevated levels of serum FT4 at baseline associated with increased risk of incident CKD and rapid eGFR decline; (2) serum FT4 positively associated with the increased risk for concurrent complications and further outcomes of CKD; (3) no significant associations of serum FT3, TSH with incident CKD or rapid eGFR decline were found in the present analysis.
In our study, we reported significant associations of FT4 with both incident CKD and rapid eGFR decline in a large general Chinese population, suggesting that when a higher FT4 level was found in clinical practice, a screening for kidney disease is warranted beyond hyperthyroidism treatments and the thyroid function monitoring. Our results were consistent with several previous findings. A prospective study focusing on thyroid function status and renal function in older persons found that overt hypothyroidism provided a protective effect on changes in renal function over time, whereas hyperthyroidism conveyed a harmful effect . In addition, other perspective studies also demonstrated that overt and subclinical hypothyroidism in older age (>85 years old) might even have a protective effect, particularly on span of life [28, 29]. However, our findings were conflicted with the results from the Kangbuk Samsung Health Study (KSHS), which was performed among 104,633 Korean participants with an average age of 38.0 years old and normal thyroid function at baseline. It reported that high-normal levels of TSH and low-normal FT3 levels below 3 pg/ml, but not FT4 levels, were associated with increased risk of incident CKD, defined as eGFR <60 mL/min/1.73 m2 . The disparate definitions of CKD might be a possible attributor for this discrepancy. In our study, we defined CKD not only on basis of eGFR but also on the presence of albuminuria. Albuminuria would be induced by high thyroid function and then could deteriorate renal function gradually [17, 30]. In addition, it might be due to the relatively older participants in our study than those in KSHS. With the increasing age, renal function declined  and thyroid function changed including increase of serum TSH and FT4, and decrease of total triiodothyronine .
In our study, we found that high levels of FT4, but not low levels of TSH, associated with incident CKD and rapid eGFR decline. Analogously, Ahmed MM reported that high levels of FT4, but not low levels of TSH, significantly associated with increasing severity of renal failure in patients with chronic renal failure and averagely aged 61 years old . It might be partially due to the reduced sensitivity of pituitary with the increasing age; and then high FT4 levels could not generate negative feedback to TSH and suppress secretion of TSH [32, 34]. As shown in our study, serum FT4 was positively associated with age (β = 0.012, P = 0.0086), but TSH was not (β = −0.0021, P = 0.27).
However, the mechanisms of the positive associations of serum FT4 levels with incident CKD and rapid eGFR decline remain unclear. It might be due to the fact that high thyroid hormone levels increased the permeability of the glomerular barrier, and subsequently led to proteinuria . Several studies have reported that overt proteinuria was observed in hyperthyroid rats, as well as in Graves’ disease patients . It may also be possible that the presence of albuminuria could promote renal function deterioration. Previous studies found that the elevated ACR, even within normal range, was associated with a faster decline in eGFR [37, 38].
The major strength of our study is the prospective nature. We also carefully performed adjustments for the potential confounders, including the autoimmune thyroid antibodies. Besides, the CKD was defined based on either eGFR <60 ml/min/1.73 m2 or presence of albuminuria recommended by the 2012 KDIGO clinical practice guideline. The rationales arise from the evidence that decrease eGFR or albuminuria were consistently associated with increased risk of death, end stage renal disease or cardiovascular mortality . However, several limitations should be acknowledged. Firstly, the GFR was estimated by the 2009 CKD-EPI equation, rather than the gold standard of GFR measurement, a technetium 99m diethylene-triaminepentaacetic acid (99mTc-DTPA) renal dynamic imaging method. However, the accuracy of CKD-EPI equation to estimate GFR has already been confirmed and validated in many previous studies [40, 41]. Secondly, urinary albumin and creatinine were measured using a single spot urine sample. However, it was more practicable in large epidemiological studies , and was highly agree with the 24-h urinary albumin excretion [42, 43]. Thirdly, there were only two measurements of eGFR rather than repeated measurements of eGFR during follow-up. Fourthly, the current study was conducted in middle-aged and elderly Chinese adults. Hence, more cautions are needed to generalize the findings to other age and ethnic groups.
In conclusion, the present study indicated that a high level of serum FT4, rather than serum TSH and FT3, was associated with increased risk of incident CKD, rapid eGFR decline and increased risks of concurrent complications and further outcomes of CKD. Further studies aimed to validate our findings in other age and other ethnic groups, to examine the association of developing hyperthyroidism with incident CKD, and to explore related mechanisms are warranted in the future.
body mass index
coefficients of variation
chronic kidney disease
estimated glomerular filtration rate
fasting plasma glucose
high-density lipoprotein cholesterol
low-density lipoprotein cholesterol
oral glucose tolerance test
thyroid peroxidase antibody
XH, MX, and GN contributed to the conception and design of this study. XH, LD, KP and LL were involved in the acquisition of data. XH and LD conducted the statistical analysis and interpretation of data, and drafted the manuscript. TW, ZZ, YX, JL, YC, MX, WW, YB, and GN contributed to the revision of the manuscript for important intellectual content. All authors read and approved the final manuscript.
We thank all the participants for their contribution and participation.
The authors declare that they have no competing interests.
Availability of data and materials
The underlying data in this manuscript arise from a dataset of National Clinical Research Center for Metabolic Diseases, and cannot be released, due to security considerations.
Ethics approval and consent to participate
The study was approved by the Institutional Review Board of Rui-Jin Hospital and in accordance to the Declaration of Helsinki. Written informed consent was obtained by each participant.
This work was supported by Grants 2013BAI09B13 from the National Clinical Research Center for Metabolic Diseases, 2015CB553600 from the 973 Program of China, 81471059, 81471062, 81321001 and 81390350 from the National Natural Science Foundation of China, 2015DFA30560 from the National International Science Cooperation Foundation, 2013ZYJB1002 from the Joint Research Program for Important Diseases of the Shanghai Municipal Commission of Health and Family Planning, and the Gaofeng Clinical Medicine Grant Support from the Shanghai Municipal Education Commission (20152508).
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- Inker LA, Astor BC, Fox CH, Isakova T, Lash JP, Peralta CA, et al. KDOQI US commentary on the 2012 KDIGO clinical practice guideline for the evaluation and management of CKD. Am J Kidney Dis. 2014;63(5):713–35.View ArticlePubMedGoogle Scholar
- Collins AJ, Foley RN, Herzog C, Chavers B, Gilbertson D, Ishani A, et al. US renal data system 2010 annual data report. Am J Kidney Dis. 2011;57(1 Suppl 1):A8-e1–526.Google Scholar
- Foley RN, Murray AM, Li S, Herzog CA, McBean AM, Eggers PW, et al. Chronic kidney disease and the risk for cardiovascular disease, renal replacement, and death in the United States Medicare population, 1998 to 1999. J Am Soc Nephrol. 2005;16(2):489–95.View ArticlePubMedGoogle Scholar
- Hallan SI, Matsushita K, Sang Y, Mahmoodi BK, Black C, Ishani A, et al. Age and association of kidney measures with mortality and end-stage renal disease. JAMA. 2012;308(22):2349–60.View ArticlePubMedPubMed CentralGoogle Scholar
- Coresh J, Selvin E, Stevens LA, Manzi J, Kusek JW, Eggers P, et al. Prevalence of chronic kidney disease in the United States. JAMA. 2007;298(17):2038–47.View ArticlePubMedGoogle Scholar
- Zhang L, Wang F, Wang L, Wang W, Liu B, Liu J, et al. Prevalence of chronic kidney disease in China: a cross-sectional survey. Lancet. 2012;379(9818):815–22.View ArticlePubMedGoogle Scholar
- Levey AS, Coresh J. Chronic kidney disease. Lancet. 2012;379(9811):165–80.View ArticlePubMedGoogle Scholar
- James MT, Hemmelgarn BR, Tonelli M. Early recognition and prevention of chronic kidney disease. Lancet. 2010;375(9722):1296–309.View ArticlePubMedGoogle Scholar
- Tohidi M, Hasheminia M, Mohebi R, Khalili D, Hosseinpanah F, Yazdani B, et al. Incidence of chronic kidney disease and its risk factors, results of over 10 year follow up in an Iranian cohort. PLoS ONE. 2012;7(9):e45304.View ArticlePubMedPubMed CentralGoogle Scholar
- den Hollander JG, Wulkan RW, Mantel MJ, Berghout A. Correlation between severity of thyroid dysfunction and renal function. Clin Endocrinol. 2005;62(4):423–7.View ArticleGoogle Scholar
- Katz AI, Emmanouel DS, Lindheimer MD. Thyroid hormone and the kidney. Nephron. 1975;15(3–5):223–49.View ArticlePubMedGoogle Scholar
- Villabona C, Sahun M, Roca M, Mora J, Gomez N, Gomez JM, et al. Blood volumes and renal function in overt and subclinical primary hypothyroidism. Am J Med Sci. 1999;318(4):277–80.View ArticlePubMedGoogle Scholar
- Asvold BO, Bjoro T, Vatten LJ. Association of thyroid function with estimated glomerular filtration rate in a population-based study: the HUNT study. Eur J Endocrinol. 2011;164(1):101–5.View ArticlePubMedGoogle Scholar
- Gopinath B, Harris DC, Wall JR, Kifley A, Mitchell P. Relationship between thyroid dysfunction and chronic kidney disease in community-dwelling older adults. Maturitas. 2013;75(2):159–64.View ArticlePubMedGoogle Scholar
- Kreisman SH, Hennessey JV. Consistent reversible elevations of serum creatinine levels in severe hypothyroidism. Arch Intern Med. 1999;159(1):79–82.View ArticlePubMedGoogle Scholar
- Woodward A, McCann S, Al-Jubouri M. The relationship between estimated glomerular filtration rate and thyroid function: an observational study. Ann Clin Biochem. 2008;45(Pt 5):515–7.View ArticlePubMedGoogle Scholar
- Basu G, Mohapatra A. Interactions between thyroid disorders and kidney disease. Indian J Endocrinol Metab. 2012;16(2):204–13.View ArticlePubMedPubMed CentralGoogle Scholar
- Lippi G, Montagnana M, Targher G, Salvagno GL, Guidi GC. Relationship between thyroid status and renal function in a general population of unselected outpatients. Clin Biochem. 2008;41(7–8):625–7.View ArticlePubMedGoogle Scholar
- Chonchol M, Lippi G, Salvagno G, Zoppini G, Muggeo M, Targher G. Prevalence of subclinical hypothyroidism in patients with chronic kidney disease. Clin J Am Soc Nephrol. 2008;3(5):1296–300.View ArticlePubMedPubMed CentralGoogle Scholar
- Zhang Y, Chang Y, Ryu S, Cho J, Lee WY, Rhee EJ, et al. Thyroid hormone levels and incident chronic kidney disease in euthyroid individuals: the Kangbuk Samsung Health Study. Int J Epidemiol. 2014;43(5):1624–32.View ArticlePubMedGoogle Scholar
- Meuwese CL, Gussekloo J, de Craen AJ, Dekker FW, den Elzen WP. Thyroid status and renal function in older persons in the general population. J Clin Endocrinol Metab. 2014;99(8):2689–96.View ArticlePubMedGoogle Scholar
- Ning G, Bi Y, Wang T, Xu M, Xu Y, Huang Y, et al. Relationship of urinary bisphenol A concentration to risk for prevalent type 2 diabetes in Chinese adults: a cross-sectional analysis. Ann Intern Med. 2011;155(6):368–74.View ArticlePubMedGoogle Scholar
- Wang T, Lu J, Xu M, Xu Y, Li M, Liu Y, et al. Urinary bisphenol a concentration and thyroid function in Chinese adults. Epidemiology. 2013;24(2):295–302.View ArticlePubMedGoogle Scholar
- Levey AS, Stevens LA, Schmid CH, Zhang YL, Castro AF 3rd, Feldman HI, et al. A new equation to estimate glomerular filtration rate. Ann Intern Med. 2009;150(9):604–12.View ArticlePubMedPubMed CentralGoogle Scholar
- Zhou Y, Ye L, Wang T, Hong J, Bi Y, Zhang J, et al. Free triiodothyronine concentrations are inversely associated with microalbuminuria. Int J Endocrinol. 2014;2014:959781.View ArticlePubMedPubMed CentralGoogle Scholar
- Zoppini G, Targher G, Chonchol M, Ortalda V, Abaterusso C, Pichiri I, et al. Serum uric acid levels and incident chronic kidney disease in patients with type 2 diabetes and preserved kidney function. Diabetes Care. 2012;35(1):99–104.View ArticlePubMedGoogle Scholar
- Li Y, Qin X, Xie D, Tang G, Xing H, Li Z, et al. Body mass index and annual estimated GFR decline in Chinese adults with normal renal function. Eur J Clin Nutr. 2015;69(8):922–6.View ArticlePubMedGoogle Scholar
- Gussekloo J, van Exel E, de Craen AJ, Meinders AE, Frolich M, Westendorp RG. Thyroid status, disability and cognitive function, and survival in old age. JAMA. 2004;292(21):2591–9.View ArticlePubMedGoogle Scholar
- Atzmon G, Barzilai N, Hollowell JG, Surks MI, Gabriely I. Extreme longevity is associated with increased serum thyrotropin. J Clin Endocrinol Metab. 2009;94(4):1251–4.View ArticlePubMedPubMed CentralGoogle Scholar
- Iglesias P, Diez JJ. Thyroid dysfunction and kidney disease. Eur J Endocrinol. 2009;160(4):503–15.View ArticlePubMedGoogle Scholar
- Hemmelgarn BR, Zhang J, Manns BJ, Tonelli M, Larsen E, Ghali WA, et al. Progression of kidney dysfunction in the community-dwelling elderly. Kidney Int. 2006;69(12):2155–61.View ArticlePubMedGoogle Scholar
- Waring AC, Arnold AM, Newman AB, Buzkova P, Hirsch C, Cappola AR. Longitudinal changes in thyroid function in the oldest old and survival: the cardiovascular health study all-stars study. J Clin Endocrinol Metab. 2012;97(11):3944–50.View ArticlePubMedPubMed CentralGoogle Scholar
- Ahmed MM. Association of renal failure with thyroid dysfunction: a retrospective cohort study. Saudi J Kidney Dis Transpl. 2014;25(5):1017–25.View ArticlePubMedGoogle Scholar
- Bremner AP, Feddema P, Leedman PJ, Brown SJ, Beilby JP, Lim EM, et al. Age-related changes in thyroid function: a longitudinal study of a community-based cohort. J Clin Endocrinol Metab. 2012;97(5):1554–62.View ArticlePubMedGoogle Scholar
- Vargas F, Moreno JM, Rodriguez-Gomez I, Wangensteen R, Osuna A, Alvarez-Guerra M, et al. Vascular and renal function in experimental thyroid disorders. Eur J Endocrinol. 2006;154(2):197–212.View ArticlePubMedGoogle Scholar
- Weetman AP, Tomlinson K, Amos N, Lazarus JH, Hall R, McGregor AM. Proteinuria in autoimmune thyroid disease. Acta Endocrinol. 1985;109(3):341–7.PubMedGoogle Scholar
- Perkins BA, Ficociello LH, Ostrander BE, Silva KH, Weinberg J, Warram JH, et al. Microalbuminuria and the risk for early progressive renal function decline in type 1 diabetes. J Am Soc Nephrol. 2007;18(4):1353–61.View ArticlePubMedGoogle Scholar
- Babazono T, Nyumura I, Toya K, Hayashi T, Ohta M, Suzuki K, et al. Higher levels of urinary albumin excretion within the normal range predict faster decline in glomerular filtration rate in diabetic patients. Diabetes Care. 2009;32(8):1518–20.View ArticlePubMedPubMed CentralGoogle Scholar
- Moynihan R, Glassock R, Doust J. Chronic kidney disease controversy: how expanding definitions are unnecessarily labelling many people as diseased. BMJ. 2013;347:f4298.View ArticlePubMedGoogle Scholar
- Stevens LA, Schmid CH, Greene T, Zhang YL, Beck GJ, Froissart M, et al. Comparative performance of the CKD epidemiology collaboration (CKD-EPI) and the modification of diet in renal disease (MDRD) study equations for estimating GFR levels above 60 ml/min/1.73 m2. Am J Kidney Dis. 2010;56(3):486–95.View ArticlePubMedPubMed CentralGoogle Scholar
- Stevens LA, Schmid CH, Zhang YL, Coresh J, Manzi J, Landis R, et al. Development and validation of GFR-estimating equations using diabetes, transplant and weight. Nephrol Dial Transplant. 2010;25(2):449–57.View ArticlePubMedGoogle Scholar
- Eknoyan G, Hostetter T, Bakris GL, Hebert L, Levey AS, Parving HH, et al. Proteinuria and other markers of chronic kidney disease: a position statement of the national kidney foundation (NKF) and the national institute of diabetes and digestive and kidney diseases (NIDDK). Am J Kidney Dis. 2003;42(4):617–22.View ArticlePubMedGoogle Scholar
- Bakker AJ. Detection of microalbuminuria. Receiver operating characteristic curve analysis favors albumin-to-creatinine ratio over albumin concentration. Diabetes Care. 1999;22(2):307–13.View ArticlePubMedGoogle Scholar