Kearkiat Praditpornsilpa

Prof. Dr. Kearkiat Praditpornsilpa

Chulalongkorn University
orcid

Research Focus & Metrics

Academic Career Length

28Years (1999-Present)

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

Representative Publications

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30 September 2022 in Nutrients
Verified
Journal Article
Open access
PDF file
WWWannasit Wathanavasin
Wannasit Wathanavasin
ABAthiphat Banjongjit
Athiphat Banjongjit
YAYingyos Avihingsanon
Yingyos Avihingsanon
KPKearkiat Praditpornsilpa
Kearkiat Praditpornsilpa
KTKriang Tungsanga
Kriang Tungsanga
PSPaweena Susantitaphong
Paweena Susantitaphong
Sarcopenia in end-stage kidney disease patients requiring dialysis is a frequent complication but remains an under-recognized problem. This meta-analysis was conducted to determine the prevalence of sarcopenia and explored its impacts on clinical outcomes, especially cardiovascular events, and mortality in dialysis patients. The eligible studies were searched from PubMed, Scopus, and Cochrane Central Register of Controlled trials up to 31 March 2022. We included studies that reported the interested outcomes, and the random-effects model was used for analysis. Forty-one studies with 7576 patients were included. The pooled prevalence of sarcopenia in dialysis patients was 25.6% (95% CI 22.1 to 29.4%). Sarcopenia was significantly associated with higher mortality risk (adjusted OR 1.83 (95% CI 1.40 to 2.39)) and cardiovascular events (adjusted OR 3.80 (95% CI 1.79 to 8.09)). Additionally, both low muscle mass and low muscle strength were independently related to increased mortality risk in dialysis patients (OR 1.71; 95% CI (1.20 to 2.44), OR 2.15 (95% CI 1.51 to 3.07)), respectively. This meta-analysis revealed that sarcopenia was highly prevalent among dialysis patients and shown to be an important predictor of cardiovascular events and mortality. Future intervention research to alleviate this disease burden in dialysis patients is needed.

19 April 2018 in Critical Care
Verified
Journal Article
Open access
PDF file
NLNuttha Lumlertgul
Nuttha Lumlertgul
SPSadudee Peerapornratana
Sadudee Peerapornratana
TTThananda Trakarnvanich
Thananda Trakarnvanich
WPWanjak Pongsittisak Wanjak Pongsittisak
Wanjak Pongsittisak Wanjak Pongsittisak
KSKajbundit Surasit
Kajbundit Surasit
NSNattachai Srisawat
Nattachai Srisawat
The timing of initiation of renal replacement therapy (RRT) in severe acute kidney injury (AKI) remains controversial, with early initiation resulting in unnecessary therapy for some patients while expectant therapy may delay RRT for other patients. The furosemide stress test (FST) has been shown to predict the need for RRT and therefore could be used to exclude low-risk patients from enrollment in trials of RRT timing. We conducted this multicenter pilot study to determine whether FST could be used to screen patients at high risk for RRT and to determine the feasibility of incorporating FST into a trial of early initiation of RRT. FST was performed using intravenous furosemide (1 mg/kg in furosemide-naive patients or 1.5 mg/kg in previous furosemide users). FST-nonresponsive patients (urine output less than 200 mL in 2 h) were then randomized to early (initiation within 6 h) or standard (initiation by urgent indication) RRT. FST was completed in all patients (100%). Only 6/44 (13.6%) FST-responsive patients ultimately received RRT while 47/60 (78.3%) nonresponders randomized to standard RRT either received RRT or died (P < 0.001). Among 118 FST-nonresponsive patients, 98.3% in the early RRT arm and 75% in the standard RRT arm received RRT. The adherence to the protocol was 94.8% and 100% in the early and standard RRT group, respectively. We observed no differences in 28-day mortality (62.1 versus 58.3%, P = 0.68), 7-day fluid balance, or RRT dependence at day 28. However, hypophosphatemia occurred more frequently in the early RRT arm (P = 0.002). The furosemide stress test appears to be feasible and effective in identifying patients for randomization to different RRT initiation times. Our findings should guide implementation of large-scale randomized controlled trials for the timing of RRT initiation. clinicaltrials.gov, NCT02730117 . Registered 6 April 2016.

28 February 2011 in Nephrology Dialysis Transplantation
Verified
Journal Article
Open access
PDF file
KPKearkiat Praditpornsilpa
Kearkiat Praditpornsilpa
NTNatavudh Townamchai
Natavudh Townamchai
TCTawatchai Chaiwatanarat
Tawatchai Chaiwatanarat
KTKhajohn Tiranathanagul
Khajohn Tiranathanagul
PKPisut Katawatin
Pisut Katawatin
SESomchai Eiam-Ong
Somchai Eiam-Ong
Background. Currently, estimated glomerular filtration rate (eGFR) equations have been validated only in Caucasians and African-Americans and is not applicable to people of other races/ethnicities as shown in studies conducted in two Asian populations: Chinese and Japanese. Because of this, it is important that eGFR equations are validated in its prospective population before applying it in the clinical setting and in epidemiologic studies. Therefore, we examined all eGFR equations available: reexpressed isotope dilution mass spectroscopy (IDMS)-traceable Modification of Diet in Renal Disease (MDRD) equation, Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) equation, Chinese equation and Japanese equation. Methods. A total of 350 adult Thai CKD patients were studied. The 99mTc-DTPA plasma clearance was used as a reference for glomerular filtration rate (GFR). The serum creatinine was determined by IDMS reference enzymatic methods (CrEnz) and Jaffe’s kinetic assay (CrJaffe) as indicated in each equation. Results. The disagreement between the reference GFR and eGFR (reference GFR minus eGFR) was 9.6 mL/min/1.73 m2 for the reexpressed IDMS-traceable MDRD equation, 8.0 mL/min/1.73 m2 for CKD-EPI equation, 1.9 mL/min/1.73 m2 for eGFR equation from the Chinese study and 20.9 mL/min/1.73 m2 for the eGFR equation from the Japanese study. The Thai coefficient for the reexpressed MDRD was 1.129. The reexpressed MDRD equation for Thais is as follows: 175 × CrEnz(−1.154) × Age (−0.203) × 0.742 (if female) × 1.129 (if Thai). When stepwise multiple regression analysis was used, the Thai eGFR formula is: 375.5 × CrEnz(−0.848) × Age (−0.364) × 0.712 (if female). Conclusions. Differences in race/ethnicity can significantly affect the results obtained from MDRD-based eGFR equation. It is highly recommended that each population should validate eGFR equations before applying the equation in epidemiologic studies or clinical use.

1 July 2011 in Kidney International
Verified
Journal Article
Closed access
KPKearkiat Praditpornsilpa
Kearkiat Praditpornsilpa
KTKhajohn Tiranathanagul
Khajohn Tiranathanagul
PKPawinee Kupatawintu
Pawinee Kupatawintu
SJSaengsuree Jootar
Saengsuree Jootar
TITanin Intragumtornchai
Tanin Intragumtornchai
SESomchai Eiam-Ong
Somchai Eiam-Ong

7 November 2019 in Journal Of Nephrology
Verified
Journal Article
Closed access
PDF file
SUSuwasin Udomkarnjananun
Suwasin Udomkarnjananun
KTKullaya Takkavatakarn
Kullaya Takkavatakarn
KPKearkiat Praditpornsilpa
Kearkiat Praditpornsilpa
CNClaudia Nader
Claudia Nader
SESomchai Eiam-Ong
Somchai Eiam-Ong
PSPaweena Susantitaphong
Paweena Susantitaphong
We performed a systematic review and meta-analysis to examine factors associated with HBV immune response in dialysis patients, and the association between the immune response to the HBV vaccine and mortality.

26 October 2018 in Critical Care
Verified
Journal Article
Open access
PDF file
NSNattachai Srisawat
Nattachai Srisawat
STSomkanya Tungsanga
Somkanya Tungsanga
NLNuttha Lumlertgul
Nuttha Lumlertgul
CKChalermchai Komaenthammasophon
Chalermchai Komaenthammasophon
SPSadudee Peerapornratana
Sadudee Peerapornratana
JKJohn A Kellum
John A Kellum
Recent randomized trials have not found that polymyxin B hemoperfusion (PMX-HP) improves outcomes for patients with sepsis. However, it remains unclear whether the therapy could provide benefit for highly selected patients. Monocyte human leukocyte antigen (mHLA-DR) expression, a critical step in the immune response, is decreased during sepsis and leads to worsening sepsis outcomes. One recent study found that PMX-HP increased mHLA-DR expression while another found that the treatment removed HLA-DR-positive cells. We conducted a randomized controlled trial in patients with blood endotoxin activity assay (EAA) level ≥ 0.6. Patients in the PMX-HP group received a 2-h PMX-HP treatment plus standard treatment for 2 consecutive days. Patients in the non-PMX-HP group received only standard treatment. The primary outcome compared the groups on median change in mHLA-DR expression between day 3 and baseline. Secondary outcomes compared the groups on the mean or median change in CD11b expression, neutrophil chemotaxis, presepsin, cardiovascular Sequential Organ Failure Assessment (CVS SOFA) score, vasopressor dose, and EAA level between day 3 and baseline. We further compared the groups on mortality, ICU-free days, ventilator-free days, dialysis dependence status, renal recovery, serum creatinine, vasopressor-free days, and major adverse kidney events (MAKE 28), measured on day 28. Fifty-nine patients were randomized to PMX-HP (n = 29) and non-PMX-HP (n = 30) groups. At baseline, mHLA-DR expression, CD11b, neutrophil chemotaxis, and clinical parameters were comparable between groups. The median change in mHLA-DR expression between day 3 and baseline was higher in PMX-HP patients than in patients receiving standard therapy alone (P = 0.027). The mean change in CD11b between day 3 and baseline was significantly lower in the PMX-HP group than in the non-PMX-HP group (P = 0.002). There were no significant changes from baseline in neutrophil chemotaxis, presepsin, CVS SOFA scores, vasopressor doses, or EAA level between groups. On day 28 after enrollment, mortality, ICU-free days, ventilator-free days, dialysis dependence status, renal recovery, serum creatinine, vasopressor-free days, and MAKE 28 were comparable between groups. PMX-HP improved mHLA-DR expression in severe sepsis patients. Future studies should examine the potential benefit of PMX-HP in patients with low mHLA-DR expression. ClinicalTrials.gov, NCT02413541 . Registered on 3 March 2015.