scholarly journals Human uraemic serum displays calcific potential in vitro that increases with advancing chronic kidney disease

2013 ◽  
Vol 125 (5) ◽  
pp. 237-245 ◽  
Author(s):  
Ashish Patidar ◽  
Dhruv K. Singh ◽  
Peter Winocour ◽  
Ken Farrington ◽  
Anwar R. Baydoun
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Serum Creatinine ◽  
Filtration Rate ◽  
Estimated Glomerular Filtration Rate ◽  
Therapeutic Strategies ◽  
High Morbidity ◽  
Kidney Impairment

Vascular calcification (VC) strongly correlates with declining renal function and contributes to the high morbidity and mortality of patients with CKD (chronic kidney disease). It is closely regulated by circulating factors but little is known about the capacity of serum from patients to induce calcification outside the disease setting, which we now define as the calcific potential of serum. We have therefore examined the ability of serum from age- and sex-matched subjects with and without advancing CKD to induce calcification of cultured SMCs (smooth muscle cells). Samples from patients with CKD induced significant calcification compared with controls. More importantly, samples from patients on haemodialysis induced significantly higher calcification than those with moderate or advanced CKD. The calcification induced by the latter two but not those on haemodialysis could be enhanced with calcium chloride and β-GP (β-glycerophosphate). A positive correlation was evident between measured serum creatinine, phosphate, PTH (parathyroid hormone), OPG (osteoprotegerin) and the degree of calcification in vitro. eGFR (estimated glomerular filtration rate), DBP (diastolic blood pressure), haemoglobin and serum albumin correlated negatively. Stepwise multivariate analysis of log-transformed calcific potential data highlighted serum creatinine, albumin and OPG as significant predictors, explaining approximately 50% of the variation. Thus, other regulators, either not investigated or as yet unidentified, may contribute to the calcification potential of serum in vitro. Furthermore, uraemic serum can induce graded calcification outside of the disease milieu that reflects the degree of kidney impairment in vivo. These findings could have important clinical relevance in terms of developing novel diagnostic and/or therapeutic strategies for subjects with CKD.

scholarly journals Correlation of Estimated Creatinine Clearance and Glomerular Filtration Rate in Very Elderly Patients and Antibiotic Prescribing Errors: Cohort Study

2020 ◽  
Vol 33 (13) ◽  
Author(s):  
Manuel Alberto Silva ◽  
Gustavo Dias ◽  
Teresa Cardoso
Keyword(s):  
Chronic Kidney Disease ◽  
Glomerular Filtration Rate ◽  
Kidney Disease ◽  
Renal Disease ◽  
Serum Creatinine ◽  
Glomerular Filtration ◽  
Filtration Rate ◽  
Estimated Glomerular Filtration Rate ◽  
Very Elderly ◽  
Disease Epidemiology

Introduction: Determination of renal function is particularly important when prescribing antibiotics to elderly patients. This study aims to determine the correlation between estimated creatinine clearance and the estimated glomerular filtration rate, for a hospitalized population of very elderly patients, and to audit antibiotic prescribing errors.Material and Methods: Retrospective cohort study of all patients ≥ 80 years hospitalized with antibiotic. Creatinine clearance was calculated using Cockcroft-Gault equation and estimated glomerular filtration rate by Modification of Diet in Renal Disease Study and Chronic Kidney Disease Epidemiology Collaboration equations. Dosing errors were determined through adjustment of daily define dose to renal function.Results: The study included 589 patients. The correlation of Cockcroft-Gault with Modification of Diet in Renal Disease and Chronic Kidney Disease Epidemiology Collaboration was r = 0.98 and 0.96 for the minimum serum creatinine, and 0.97 and 0.93 for the maximum serum creatinine. Based on Cockcroft-Gault, there were errors in the daily defined dose in 45% in the minimum serum creatinine, and 52% in the maximum serum creatinine day. There was a discrepancy in the recording of errors of 14% to 16% when Cockcroft-Gault was compared with Modification of Diet in Renal Disease and Chronic Kidney Disease Epidemiology Collaboration.Discussion: There was a good correlation of Cockcroft-Gault with the estimated glomerular filtration rate by Modification of Diet in Renal Disease or Chronic Kidney Disease Epidemiology Collaboration. Regardless of the equation used to estimate renal function there was a high rate of antibiotic dosing errors documented in this population.Conclusion: This study supports the maintenance of the Cockcroft-Gault equation for drug dosing in the very elderly population. Further studies are needed to investigate underlying causes of prescribing errors.

scholarly journals Adipokines as a link between obesity and chronic kidney disease

2013 ◽  
Vol 305 (12) ◽  
pp. F1629-F1636 ◽  
Author(s):  
Jessica F. Briffa ◽  
Andrew J. McAinch ◽  
Philip Poronnik ◽  
Deanne H. Hryciw
Keyword(s):  
Chronic Kidney Disease ◽  
Glomerular Filtration Rate ◽  
Kidney Disease ◽  
Glomerular Filtration ◽  
Filtration Rate ◽  
Cell Types ◽  
Peripheral Tissues ◽  
Increased Risk

Adipocytes secrete a number of bioactive adipokines that activate a variety of cell signaling pathways in central and peripheral tissues. Obesity is associated with the altered production of many adipokines and is linked to a number of pathologies. As an increase in body weight is directly associated with an increased risk for developing chronic kidney disease (CKD), there is significant interest in the link between obesity and renal dysfunction. Altered levels of the adipokines leptin, adiponectin, resistin, and visfatin can decrease the glomerular filtration rate and increase albuminuria, which are pathophysiological changes typical of CKD. Specifically, exposure of the glomerulus to altered adipokine levels can increase its permeability, fuse the podocytes, and cause mesangial cell hypertrophy, all of which alter the glomerular filtration rate. In addition, the adipokines leptin and adiponectin can act on tubular networks. Thus, adipokines can act on multiple cell types in the development of renal pathophysiology. Importantly, most studies have been performed using in vitro models, with future studies in vivo required to further elucidate the specific roles that adipokines play in the development and progression of CKD.

scholarly journals Prognostic Value of the Estimated Glomerular Filtration Rate Decline in Hypertensive Patients Without Chronic Kidney Disease

2019 ◽  
Vol 32 (9) ◽  
pp. 890-899 ◽  
Author(s):  
Gabriel Coll-de-Tuero ◽  
Marc Comas-Cufí ◽  
Antonio Rodríguez-Poncelas ◽  
Joan Barrot-de-la Puente ◽  
Jordi Blanch ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Glomerular Filtration Rate ◽  
Cardiovascular Risk ◽  
Kidney Disease ◽  
Serum Creatinine ◽  
Glomerular Filtration ◽  
Filtration Rate ◽  
Estimated Glomerular Filtration Rate ◽  
Egfr Decline ◽  
Low Rate

Abstract BACKGROUND Our objective of this study was to determine if rate of estimated glomerular filtration rate (eGFR) decline and its intensity was associated with cardiovascular risk and death in patients with hypertension whose baseline eGFR was higher than 60 ml/minute/1.73 m2. METHODS This study comprised 2,516 patients with hypertension who had had at least 2 serum creatinine measurements over a 4-year period. An eGFR reduction of ≥10% per year has been deemed as high eGFR and a reduction in eGFR of less than 10% per year as a low decline. The end points were coronary artery disease, stroke, transitory ischemic accident, peripheral arterial disease, heart failure, atrial fibrillation, and death from any cause. Cox regression analyses adjusted for potentially confounding factors were conducted. RESULTS A total of 2,354 patients with low rate of eGFR decline and 149 with high rate of eGFR decline were analyzed. The adjusted model shows that a −10% rate of eGFR decline per year is associated with a higher risk of the primary end point (HR 1.9; 95% CI 1.1–3.5; P = 0.02) and arteriosclerotic vascular disease (HR 2.2; 95% CI 1.2–4.2; P < 0.001) in all hypertensive groups. The variables associated to high/low rate of eGFR decline in the logistic regression model were serum creatinine (OR 3.35; P < 0.001), gender, women (OR 15.3; P < 0.001), tobacco user (OR 1.9; P < 0.002), and pulse pressure (OR 0.99; P < 0.05). CONCLUSIONS A rate of eGFR decline equal to or higher than −10% per year is a marker of cardiovascular risk for patients with arterial hypertension without chronic kidney disease at baseline. It may be useful to consider intensifying the global risk approach for these patients.

scholarly journals Soluble Fas affects erythropoiesis in vitro and acts as a potential predictor of erythropoiesis-stimulating agent therapy in patients with chronic kidney disease

2020 ◽  
Vol 318 (4) ◽  
pp. F861-F869
Author(s):  
Daniela Mendes Chiloff ◽  
Danilo Candido de Almeida ◽  
Maria A. Dalboni ◽  
Maria Eugênia Canziani ◽  
Sunil K. George ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Glomerular Filtration Rate ◽  
Kidney Disease ◽  
Glomerular Filtration ◽  
Filtration Rate ◽  
Dependent Manner ◽  
Potential Predictor ◽  
Soluble Fas ◽  
Esa Therapy

Serum soluble Fas (sFas) levels are associated with erythropoietin (Epo) hyporesponsiveness in patients with chronic kidney disease (CKD). Whether sFas could predict the need for erythropoiesis-stimulating agent (ESA) usage and its influence in erythropoiesis remain unclear. We evaluated the relation between sFas and ESA therapy in patients with CKD with anemia and its effect on erythropoiesis in vitro. First, we performed a retrospective cohort study with 77 anemic patients with nondialysis CKD. We performed in vitro experiments to investigate whether sFas could interfere with the behavior of hematopoietic stem cells (HSCs). HSCs were isolated from umbilical cord blood and incubated with recombinant sFas protein in a dose-dependent manner. Serum sFas positively correlated with Epo levels ( r = 0.30, P = 0.001) but negatively with hemoglobin ( r = −0.55, P < 0.001) and glomerular filtration rate ( r = −0.58, P < 0.001) in patients with CKD at baseline. Elevated sFas serum levels (4,316 ± 897 vs. 2,776 ± 749, P < 0.001) with lower estimated glomerular filtration rate (26.2 ± 10.1 vs. 33.5 ± 14.3, P = 0.01) and reduced hemoglobin concentration (11.1 ± 0.9 vs. 12.5 ± 1.2, P < 0.001) were identified in patients who required ESA therapy compared with patients with non-ESA. Afterward, we detected that the sFas level was slight correlated with a necessity of ESA therapy in patients with nondialysis CKD and anemia. In vitro assays demonstrated that the erythroid progenitor cell frequency negatively correlated with sFas concentration ( r = −0.72, P < 0.001). There was decreased erythroid colony formation in vitro when CD34+ HSCs were incubated with a higher concentration of sFas protein (1.56 ± 0.29, 4.33 ± 0.53, P < 0.001). Our findings suggest that sFas is a potential predictor for ESA therapy in patients with nondialysis CKD and that elevated sFas could affect erythropoiesis in vitro.

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