Urine S-Adenosylmethionine are Related to Degree of Renal Insufficiency in Patients with Chronic Kidney Disease

2020 ◽  
Vol 52 (1) ◽  
pp. 47-56
Author(s):  
Maria Petrovna Kruglova ◽  
Alexander Vladimirovich Ivanov ◽  
Edward Danielevich Virus ◽  
Polina Olegovna Bulgakova ◽  
Andrey Segeevich Samokhin ◽  
...  

Abstract Objective To determine whether urine S-adenosylmethionine (SAM) might be an indicator of chronic kidney disease (CKD). Methods We investigated urine levels of SAM and related metabolites (S-adenosylhomocysteine and homocysteine cysteine) in 62 patients (average age, 65.9 years) with CKD (stages II–V). Results Patients with stages III–V CKD stages have significantly decreased urine levels and SAM/S-adenosylhomocysteine ratio and also cysteine/homocysteine ratio in blood plasma (P <.05), compared with patients with stage II CKD. Urine SAM levels allowed us to distinguish patients with mildly decreased kidney function from those with moderate to severe renal impairment (AUC, 0.791; sensitivity, 85%; specificity, 78.6%). Conclusions Our study results demonstrate that urine SAM is a potent biomarker for monitoring renal function decline at early CKD stages. Urine SAM testing confers an additional advantage to healthcare professionals in that it is noninvasive.

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
M Schiavone ◽  
C Gobbi ◽  
A Ratti ◽  
G Ferrari ◽  
A Villarini ◽  
...  

Abstract Introduction Moderate or severe chronic kidney disease (CKD) is regarded as high or very high risk factor in the Systematic COronary Risk Evaluation (SCORE) system, as stated in the ESC guidelines on arterial hypertension. Assessment of cardiovascular (CV) risk should be completed evaluating hypertension-mediated organ damage (HMOD). Purpose The aim of our study was to find out differences in HMOD in patients with or without moderate to severe chronic kidney disease (CKD). Methods We enrolled 80 consecutive non-diabetic hypertensive patients, divided into two groups according to the presence of impaired renal function, evaluated by estimated glomerular filtration rate (eGFR): moderate to severe CKD group (n=26 patients, eGFR <60 mL/min/1.73 m2) and mild CKD - normal renal function group (n=54 patients, eGFR ≥60 mL/min/1.73 m2). A transthoracic echocardiogram was performed to evaluate cardiac HMOD. Small and large vessel damage was assessed by means of non-mydriatic digital fundus oculi examination in order to detect arteriolar narrowing using arteriolar-venular ratio (AVr), applanation tonometry to measure carotid-femoral pulse wave velocity (cfPWV) and carotid ultrasound to quantify intima-media tickness (IMT). Results Moderate to severe CKD patients appeared to be older (mean age 75.54±8.06 vs 63.38±9.62, p=0.001) and showed lower level of total and LDL cholesterol. Both groups showed abnormal values of cfPWV, but these were significantly higher in the presence of moderate to severe CKD (14.12±7.93 m/s vs 10.94±5.81 m/s, p=0.03). Abnormal AVr values were found in patients with higher grade of CKD, with statistically significant differences in the two groups (0.75±0.015 vs 0.81±0.06, p=0.00001). Carotid IMT resulted to be at the upper limit of normality in both groups (0.95±0.15 vs 0.90±0.18, p=0.35). With regard to echocardiography evaluation, left ventricular mass index (LVMi: 105.04±0.4 vs 96.35±1.7, p=0.06) and relative wall thickness (RWT: 0.43±0.02 vs 0.42±0.05, p=0.41) did not differ significantly in the two groups, with a mild trend for LVMi. Both groups showed abnormal diastolic dysfunction on average, but no differences emerged in the presence of more severe renal impairment (deceleration time 281.74±0.37 vs 256.30±0.54, p=0.08; E/A 0.86±0.03 vs 0.95±0.25, p=0.20; E/e' 7.89±2.93 vs 7.60±2.46, p=0.66). Conclusions Our study showed significant differences in HMOD in presence of moderate to severe renal impairment. Moderate to severe CKD seemed to be associated to vascular damage (hypertensive retinopathy and arterial stiffness), while no significant differences in echocardiographic markers of cardiac remodeling were found, suggesting that systemic vascular damage is more closely linked to CKD than cardiac damage. Therefore, the use of fundus oculi examination and PWV should always be considered to properly assess the target organ damage in hypertensive patients with CKD. Funding Acknowledgement Type of funding source: None


Author(s):  
Qiao Qin ◽  
Fangfang Fan ◽  
Jia Jia ◽  
Yan Zhang ◽  
Bo Zheng

Abstract Purpose An increase in arterial stiffness is associated with rapid renal function decline (RFD) in patients with chronic kidney disease (CKD). The aim of this study was to investigate whether the radial augmentation index (rAI), a surrogate marker of arterial stiffness, affects RFD in individuals without CKD. Methods A total of 3165 Chinese participants from an atherosclerosis cohort with estimated glomerular filtration rates (eGFR) of ≥ 60 mL/min/1.73 m2 were included in this study. The baseline rAI normalized to a heart rate of 75 beats/min (rAIp75) was obtained using an arterial applanation tonometry probe. The eGFRs at both baseline and follow-up were calculated using the equation derived from the Chronic Kidney Disease Epidemiology Collaboration. The association of the rAIp75 with RFD (defined as a drop in the eGFR category accompanied by a ≥ 25% drop in eGFR from baseline or a sustained decline in eGFR of > 5 mL/min/1.73 m2/year) was evaluated using the multivariate regression model. Results During the 2.35-year follow-up, the incidence of RFD was 7.30%. The rAIp75 had no statistically independent association with RFD after adjustment for possible confounders (adjusted odds ratio = 1.12, 95% confidence interval: 0.99–1.27, p = 0.074). When stratified according to sex, the rAIp75 was significantly associated with RFD in women, but not in men (adjusted odds ratio and 95% confidence interval: 1.23[1.06–1.43], p = 0.007 for women, 0.94[0.76–1.16], p = 0.542 for men; p for interaction = 0.038). Conclusion The rAI might help screen for those at high risk of early rapid RFD in women without CKD.


2021 ◽  
Vol 22 (12) ◽  
pp. 6270
Author(s):  
Chia-Ter Chao ◽  
Shih-Hua Lin

The accumulation of uremic toxins (UTs) is a prototypical manifestation of uremic milieu that follows renal function decline (chronic kidney disease, CKD). Frailty as a potential outcome-relevant indicator is also prevalent in CKD. The intertwined relationship between uremic toxins, including small/large solutes (phosphate, asymmetric dimethylarginine) and protein-bound ones like indoxyl sulfate (IS) and p-cresyl sulfate (pCS), and frailty pathogenesis has been documented recently. Uremic toxins were shown in vitro and in vivo to induce noxious effects on many organ systems and likely influenced frailty development through their effects on multiple preceding events and companions of frailty, such as sarcopenia/muscle wasting, cognitive impairment/cognitive frailty, osteoporosis/osteodystrophy, vascular calcification, and cardiopulmonary deconditioning. These organ-specific effects may be mediated through different molecular mechanisms or signal pathways such as peroxisome proliferator-activated receptor γ coactivator 1-α (PGC-1α), mitogen-activated protein kinase (MAPK) signaling, aryl hydrocarbon receptor (AhR)/nuclear factor-κB (NF-κB), nuclear factor erythroid 2-related factor 2 (Nrf2), heme oxygenase-1 (HO-1), Runt-related transcription factor 2 (RUNX2), bone morphogenic protein 2 (BMP2), osterix, Notch signaling, autophagy effectors, microRNAs, and reactive oxygen species induction. Anecdotal clinical studies also suggest that frailty may further accelerate renal function decline, thereby augmenting the accumulation of UTs in affected individuals. Judging from these threads of evidence, management strategies aiming for uremic toxin reduction may be a promising approach for frailty amelioration in patients with CKD. Uremic toxin lowering strategies may bear the potential of improving patients’ outcomes and restoring their quality of life, through frailty attenuation. Pathogenic molecule-targeted therapeutics potentially disconnect the association between uremic toxins and frailty, additionally serving as an outcome-modifying approach in the future.


Hypertension ◽  
2010 ◽  
Vol 55 (5) ◽  
pp. 1110-1115 ◽  
Author(s):  
Martin L. Ford ◽  
Laurie A. Tomlinson ◽  
Thomas P.E. Chapman ◽  
Chakravarthi Rajkumar ◽  
Stephen G. Holt

PLoS ONE ◽  
2021 ◽  
Vol 16 (6) ◽  
pp. e0252186
Author(s):  
Hayne Cho Park ◽  
AJin Cho ◽  
Do Hyoung Kim ◽  
Kyu-sang Yun ◽  
Juhee Kim ◽  
...  

Renamezin® is a modified capsule-type oral spherical adsorptive carbon which lowers indoxyl sulfate levels in patients with advanced chronic kidney disease (CKD). This 24-week prospective observational cohort study was performed to evaluate the effect of Renamezin® upon attenuation of renal function decline. A total of 1,149 adult patients with baseline serum creatinine 2.0–5.0 mg/dL were enrolled from 22 tertiary hospital in Korea from April 2016 to September 2018. Among them, a total of 686 patients completed the study and were included in the intention-to-treat analysis. A total of 1,061 patients were included in the safety analysis. The mean age was 63.5 years and male patients were predominant (63.6%). Most of the patients (76.8%) demonstrated high compliance with study drug (6g per day). After 24 week of treatment, serum creatinine was increased from 2.86±0.72 mg/dL to 3.06±1.15 mg/dL (p<0.001), but estimated glomerular filtration rate was not changed significantly during observation period (22.3±6.8 mL/min/1.73m2 to 22.1±9.1 mL/min/1.73m2, p = 0.243). Patients with age over 65 years old and those under good systolic blood pressure control <130 mmHg were most likely to get benefit from Renamezin® treatment to preserve renal function. A total of 98 (9.2%) patients out of 1,061 safety population experienced 134 adverse events, of which gastrointestinal disorders were the most common. There were no serious treatment-related adverse events. Renamezin® can be used safely to attenuate renal function decline in moderately advanced CKD patients.


2021 ◽  
Vol 7 (3) ◽  
pp. 147-152
Author(s):  
Nur Syamsi ◽  
Andi Alfia Muthmainnah Tanra ◽  
Mariani Rasjid HS

The chronic kidney disease is a global health problem with increasing prevalence and incidence and a poor prognosis. Therefore, those brought about by risk factors are primarily those which can be modified and controlled for their occurrence.  One of the risk factor is smoking habit. The objective of this study was to determine the associations between smoking and renal function profiles in PT.X employees. The study was conducted by using descriptive analytical study with a cross sectional design based on smoking habits and blood test samples of employees. The sample were 40 employees in PT.X which determined by consecutive sampling. The results showed that there were no associations between smoking with age (p = 0.222) and azotemia (p = 1.00) but there were associations between smoking and blood creatinine levels (p = 0.001), urea (p = 0.023), eGFR (p. = 0.001), and the stages of chronic kidney disease (p = 0.047).  Based on the study results, in can be concluded that there were associations between smoking and renal function profiles among employees of PT. X


2018 ◽  
Vol 23 (2) ◽  
pp. 215-222 ◽  
Author(s):  
Yuichi Maruta ◽  
Takeshi Hasegawa ◽  
Etsuko Yamakoshi ◽  
Hiroki Nishiwaki ◽  
Fumihiko Koiwa ◽  
...  

2017 ◽  
Vol 62 (3) ◽  
Author(s):  
Matthew P. Kosloski ◽  
Weihan Zhao ◽  
Thomas C. Marbury ◽  
Richard A. Preston ◽  
Michael G. Collins ◽  
...  

ABSTRACT Hepatitis C virus (HCV) infection is an independent risk factor for developing chronic renal impairment and end-stage renal disease. Limited treatment options are available for HCV genotype 2, 3, 5, and 6 infections in patients with an estimated glomerular filtration rate (eGFR) of <30 ml/min. Glecaprevir and pibrentasvir are active against all six major HCV genotypes, are primarily excreted in the bile, and have minimal renal elimination. Therefore, combined treatment with these direct-acting antivirals may be useful for patients with HCV infection and chronic kidney disease. A phase 1, multicenter, open-label study evaluated the effects of renal impairment on the pharmacokinetics and safety of glecaprevir-pibrentasvir. In substudy 1, 38 subjects with stage 2 to 5 chronic kidney disease who were not on dialysis or who had normal renal function received single doses of the combination of 300 mg glecaprevir and 120 mg pibrentasvir. In substudy 2, 8 subjects requiring hemodialysis received single doses of the combination of 300 mg glecaprevir and 120 mg pibrentasvir under dialysis and nondialysis conditions. Regression analyses demonstrated increased glecaprevir and pibrentasvir plasma exposures, as determined by the area under the curve, with decreasing renal function, up to 56% and 46%, respectively, in subjects with an eGFR of <15 ml/min/1.73 m 2 . In dialysis-dependent subjects, glecaprevir and pibrentasvir exposures were similar (≤18% difference) when study drugs were administered before hemodialysis or on a nondialysis day. Adverse events were mostly mild, with the most common being self-limited fatigue (3 subjects). The study findings support the clinical evaluation of glecaprevir-pibrentasvir without dose adjustment in HCV-infected subjects with renal impairment. (This study has been registered at ClinicalTrials.gov under registration number NCT02442258.)


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