Chia-Ter Chao

Dr. Chia-Ter Chao

National Taiwan University Hospital Bei-Hu branch
+1
orcid

Research Focus & Metrics

Academic Career Length

17Years (2010-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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1 December 2011 in Kidney International
Verified
Journal Article
Closed access
VWVin-Cent Wu
Vin-Cent Wu
THTao-Min Huang
Tao-Min Huang
CLChun-Fu Lai
Chun-Fu Lai
Chih-Chung ShiaoChih-Chung Shiao
Chih-Chung Shiao
YLYu-Feng Lin
Yu-Feng Lin
OGon behalf of the NSARF Group
on behalf of the NSARF Group

Verified
Journal Article
Open access
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MYMing-Tso Yan
Ming-Tso Yan
CCChia-Ter Chao
Chia-Ter Chao
SLShih-Hua Lin
Shih-Hua Lin
Chronic kidney disease (CKD), defined as the presence of irreversible structural or functional kidney damages, increases the risk of poor outcomes due to its association with multiple complications, including altered mineral metabolism, anemia, metabolic acidosis, and increased cardiovascular events. The mainstay of treatments for CKD lies in the prevention of the development and progression of CKD as well as its complications. Due to the heterogeneous origins and the uncertainty in the pathogenesis of CKD, efficacious therapies for CKD remain challenging. In this review, we focus on the following four themes: first, a summary of the known factors that contribute to CKD development and progression, with an emphasis on avoiding acute kidney injury (AKI); second, an etiology-based treatment strategy for retarding CKD, including the approaches for the common and under-recognized ones; and third, the recommended approaches for ameliorating CKD complications, and the final section discusses the novel agents for counteracting CKD progression.

27 September 2018 in Cardiovascular Diabetology
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Journal Article
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CGCOhort of GEriatric Nephrology in NTUH (COGENT) study group
COhort of GEriatric Nephrology in NTUH (COGENT) study group
CCChia-Ter Chao
Chia-Ter Chao
JWJui Wang
Jui Wang
KCKuo-Liong Chien
Kuo-Liong Chien
Diabetes mellitus (DM) correlates with accelerated aging and earlier appearance of geriatric phenotypes, including frailty. However, whether pre-frailty or frailty predicts greater healthcare utilization in diabetes patients is unclear. From the Longitudinal Cohort of Diabetes Patients in Taiwan (n = 840,000) between 2004 and 2010, we identified 560,795 patients with incident type 2 DM, categorized into patients without frailty, or with 1, 2 (pre-frail) and ≥ 3 frailty components, based on FRAIL scale (Fatigue, Resistance, Ambulation, Illness, and body weight Loss). We examined their long-term mortality, cardiovascular risk, all-cause hospitalization, and intensive care unit (ICU) admission. Among all participants (56.4 ± 13.8 year-old, 46.1% female, and 84.8% community-dwelling), 77.8% (n = 436,521), 19.2% (n = 107,757), 2.7% (n = 15,101), and 0.3% (n = 1416) patients did not have or had 1, 2 (pre-frail), and ≥ 3 frailty components (frail), respectively, with Fatigue and Illness being the most common components. After 3.14 years of follow-up, 7.8% patients died, whereas 36.6% and 9.1% experienced hospitalization and ICU stay, respectively. Cox proportional hazard modeling discovered that patients with 1, 2 (pre-frail), and ≥ 3 frailty components (frail) had an increased risk of mortality (for 1, 2, and ≥ 3 components, hazard ratio [HR] 1.05, 1.13, and 1.25; 95% confidence interval [CI] 1.02–1.07, 1.08–1.17, and 1.15–1.36, respectively), cardiovascular events (HR 1.05, 1.15, and 1.13; 95% CI 1.02–1.07, 1.1–1.2, and 1.01–1.25, respectively), hospitalization (HR 1.06, 1.16, and 1.25; 95% CI 1.05–1.07, 1.14–1.19, and 1.18–1.33, respectively), and ICU admission (HR 1.05, 1.13, and 1.17; 95% CI 1.03–1.07, 1.08–1.14, and 1.06–1.28, respectively) compared to non-frail ones. Approximately 6–7% risk elevation in mortality and healthcare utilization was noted for every frailty component increase. Pre-frailty and frailty increased the risk of mortality and cardiovascular events, and entailed greater healthcare utilization in patients with type 2 DM.

15 April 2015 in Nephrology
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Journal Article
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CCChia-Ter Chao
Chia-Ter Chao
YHYuan-Hsin Hsu
Yuan-Hsin Hsu
PCPei-Yu Chang
Pei-Yu Chang
YHYu-Ting He
Yu-Ting He
RURuey-Shiuan Ueng
Ruey-Shiuan Ueng
SHSheng-Jen Huang
Sheng-Jen Huang

30 April 2013 in Annals of Medicine
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Journal Article
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CCChia-Ter Chao
Chia-Ter Chao
VWVin-Cent Wu
Vin-Cent Wu
CKChin-Chi Kuo
Chin-Chi Kuo
YLYen-Hung Lin
Yen-Hung Lin
CCChin-Chen Chang
Chin-Chen Chang
MSMichael Stowasser
Michael Stowasser
Primary aldosteronism (PA) is the most common secondary form of arterial hypertension, with a particularly high prevalence among patients with resistant hypertension. Aldosterone has been found to be associated with cardiovascular toxicity. Prolonged aldosteronism leads to higher incidence of cardiac events, glomerular hyperfiltration, and potentially bone/metabolic sequels. The wider application of aldosterone/renin ratio as screening test has substantially contributed to increasing diagnosis of PA. Diagnosis of PA consists of two phases: screening and confirmatory testing. Adrenal imaging is often inaccurate for differentiation between an adenoma and hyperplasia, and adrenal venous sampling is essential for selecting the appropriate treatment modality. The etiologies of PA have two main subtypes: unilateral (aldosterone-producing adenoma) and bilateral (micro- or macronodular hyperplasia). Aldosterone-producing adenoma is typically managed with unilateral adrenalectomy, while bilateral adrenal hyperplasia is amenable to pharmacological approaches using mineralocorticoid antagonists. Short-term treatment outcome following surgery is determined by factors such as preoperative blood pressure level and hypertension duration, but evidence regarding long-term treatment outcome is still lacking. However, directed treatments comprising of unilateral adrenalectomy or mineralocorticoid antagonists still potentially reduce the toxicities of aldosterone. Utilizing a physician-centered approach, we intend to provide up-dated information on the etiology, diagnosis, and the management of PA.

8 August 2013 in Journal of Bone and Mineral Research
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Journal Article
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WWWei-Jie Wang
Wei-Jie Wang
CCChia-Ter Chao
Chia-Ter Chao
YHYu-Chin Huang
Yu-Chin Huang
CWCheng-Yi Wang
Cheng-Yi Wang
CCChia-Hsui Chang
Chia-Hsui Chang
TFthe National Taiwan University Study Group on Acute Renal Failure
the National Taiwan University Study Group on Acute Renal Failure
Acute kidney injury (AKI) has a negative impact on long-term renal function and prognosis. However, the association between acute renal dysfunction and long-term effects on bone disorders has not yet been characterized. Using a population-based cohort study, we aimed to evaluate associations between AKI and long-term effects on bone fractures. We identified relevant data of all hospitalized patients aged >18 years with histories of dialysis-requiring AKI, with subsequent recovery and discharge, from the claim records of the Taiwan National Health Insurance database between 2000 and 2008. We determined long-term de novo bone fracture and all-cause mortality after patients' index-hospitalization discharge using propensity score–adjusted Cox proportional hazard model. Varying-time models were used to adjust for long-term effects of end-stage renal disease (ESRD) on main outcomes. Among 448 AKI patients who had dialysis and survived 90 days after index-hospitalization discharge without reentering dialysis, 273 were male (60.9%) with a mean age of 61.4 ± 16.6 years. Controls included 1792 hospitalized patients without AKI, dialysis, or bone fracture history. In the AKI recovery group, bone fracture incidence was 320 per 10,000 person-years and hazard ratio (HR) of long-term bone fracture was 1.25 (p = 0.049) compared with the control group, independent of subsequent ESRD status (HR = 1.55; p = 0.01). Both AKI recovery status (HR = 2.31; p < 0.001) and time varying factor of bone fracture (HR = 1.43; p < 0.001) were independent predictors of mortality compared with controls. In conclusion, AKI requiring temporary dialysis independently increases long-term risk of bone fracture, regardless of subsequent progression to ESRD. Long-term bone fractures may negatively impact patient mortality. © 2014 American Society for Bone and Mineral Research.