Academic literature on the topic 'Chronic kidney disease, CKD, CKD treatment'
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Journal articles on the topic "Chronic kidney disease, CKD, CKD treatment"
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Stolpe, Susanne, Bernd Kowall, Christian Scholz, Andreas Stang, and Cornelia Blume. "High Unawareness of Chronic Kidney Disease in Germany." International Journal of Environmental Research and Public Health 18, no. 22 (November 9, 2021): 11752. http://dx.doi.org/10.3390/ijerph182211752.
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Chronic kidney disease (CKD) is associated with an increased risk for cardiovascular events, hospitalizations, end stage renal disease and mortality. Main risk factors for CKD are diabetes, hypertension, and older age. Although CKD prevalence is about 10%, awareness for CKD is generally low in patients and physicians, hindering early diagnosis and treatment. We analyzed baseline data of 3305 participants with CKD Stages 1–4 from German cohorts and registries collected in 2010. Prevalence of CKD unawareness and prevalence ratios (PR) (each with 95%-confidence intervals) were estimated in categories of age, sex, CKD stages, BMI, hypertension, diabetes and other relevant comorbidities. We used a log-binomial regression model to estimate the PR for CKD unawareness for females compared to males adjusting for CKD stage and CKD risk factors. CKD unawareness was high, reaching 71% (68–73%) in CKD 3a, 49% (45–54%) in CKD 3b and still 30% (24–36%) in CKD4. Prevalence of hypertension, diabetes or cardiovascular comorbidities was not associated with lower CKD unawareness. Independent of CKD stage and other risk factors unawareness was higher in female patients (PR = 1.06 (1.01; 1.10)). Even in patients with CKD related comorbidities, CKD unawareness was high. Female sex was strongly associated with CKD unawareness. Guideline oriented treatment of patients at higher risk for CKD could increase CKD awareness. Patient–physician communication about CKD might be amendable.
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Kodali, Meghana, Sarada CV, Bhanuja B., Kumara P., Rajashekar B., Vennela Kodali, Mohan Gunkunta, et al. "Proteinuria as a Marker for Cardiovascular Disease in Renal (Chronic Kidney Disease) Patients." Indian Journal of Cardiovascular Disease in Women WINCARS 03, no. 04 (December 2018): 221–24. http://dx.doi.org/10.1055/s-0039-1681126.
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Abstract Background For the evaluation of total cardiovascular risk in patients with chronic kidney disease (CKD; renal), the amount of protein in the urine has to be considered an important factor. For reducing proteinuria level and lowering the risk of renal, cardiovascular endpoint, this may become a crucial decision. Materials and Methods This is a case-control study of the stage 5 CKD female patients recruited over 2 months in 2017, based on clinical and laboratory investigation. CKD was diagnosed on serum creatinine levels and stage 5 CKD depending on estimated glomerular filtration rate (eGFR) calculation. Coronary artery disease (CAD) was diagnosed on clinical history, electrocardiogram (ECG), and echocardiogram. Results This study was conducted on 50 patients at the authors’ hospital. Out of these, 25 were cases and 25 constituted controls. Out of 25 controls, 13 had microalbuminuria and 12 had proteinuria and no cardiovascular disease. Out of 25 cases, 2 cases had microalbuminuria and 23 had proteinuria. More number of CKD with CAD group had proteinuria than CKD without CAD, which was statistically highly significant (p < 0.000). CKD patients with CAD had higher degree of proteinuria than those without CAD, which was statistically significant (p < 0.005). Conclusion This study showed that proteinuria and its cardiovascular outcomes in CKD patients are correlated. For detection of CAD in CKD patients, proteinuria levels may be crucial regarding the treatment decision.
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Huang, Huiling, Chunmei Zeng, Yuedong Ma, Yili Chen, Cong Chen, Chen Liu, and Yugang Dong. "Effects of Long-Term Statin Therapy in Coronary Artery Disease Patients with or without Chronic Kidney Disease." Disease Markers 2015 (2015): 1–8. http://dx.doi.org/10.1155/2015/252564.
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Introduction.The effect of long-term statin therapy is essential for secondary prevention of adverse clinical outcomes of coronary artery disease (CAD) patients. No study has compared the effects of long-term statin treatment in CAD patients with or without chronic kidney disease (CKD) and CKD only patients.Methods.We compared the effects of long-term statin therapy (average follow-up time 5.79 years) in terms of major adverse cardiovascular events (MACE), all-cause death, and cardiac death among 570 CAD patients with or without CKD and 147 CKD only patients.Results.The all-cause death and cardiac death of the patients with CAD and CKD (24.4% and 20.4%) doubled those of CAD only patients (10.7% and 9.1%) (P<0.001). Long-term statin therapy dramatically reduced the rates of both MACE and all-cause death/cardiac death (by 20.5% and 28.6%/27.7%, resp.) in CAD and CKD patients. CKD only patients had no significant adverse clinical outcomes and were not responsive to long-term statin therapy.Conclusion.Chinese CAD patients with CKD had dramatically high rates of adverse clinical outcomes; for them, long-term statin therapies were exceptionally effective in improving morbidity and mortality. CKD patients who had no cardiovascular disease initially can prognose good clinical outcomes and do not require statin treatment.
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Cao, Yi-Ling, Ji-Hong Lin, Hans-Peter Hammes, and Chun Zhang. "Flavonoids in Treatment of Chronic Kidney Disease." Molecules 27, no. 7 (April 6, 2022): 2365. http://dx.doi.org/10.3390/molecules27072365.
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Chronic kidney disease (CKD) is a progressive systemic disease, which changes the function and structure of the kidneys irreversibly over months or years. The final common pathological manifestation of chronic kidney disease is renal fibrosis and is characterized by glomerulosclerosis, tubular atrophy, and interstitial fibrosis. In recent years, numerous studies have reported the therapeutic benefits of natural products against modern diseases. Substantial attention has been focused on the biological role of polyphenols, in particular flavonoids, presenting broadly in plants and diets, referring to thousands of plant compounds with a common basic structure. Evidence-based pharmacological data have shown that flavonoids play an important role in preventing and managing CKD and renal fibrosis. These compounds can prevent renal dysfunction and improve renal function by blocking or suppressing deleterious pathways such as oxidative stress and inflammation. In this review, we summarize the function and beneficial properties of common flavonoids for the treatment of CKD and the relative risk factors of CKD.
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Braga, Patrícia C., Marco G. Alves, Anabela S. Rodrigues, and Pedro F. Oliveira. "Mitochondrial Pathophysiology on Chronic Kidney Disease." International Journal of Molecular Sciences 23, no. 3 (February 4, 2022): 1776. http://dx.doi.org/10.3390/ijms23031776.
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In healthy kidneys, interstitial fibroblasts are responsible for the maintenance of renal architecture. Progressive interstitial fibrosis is thought to be a common pathway for chronic kidney diseases (CKD). Diabetes is one of the boosters of CKD. There is no effective treatment to improve kidney function in CKD patients. The kidney is a highly demanding organ, rich in redox reactions occurring in mitochondria, making it particularly vulnerable to oxidative stress (OS). A dysregulation in OS leads to an impairment of the Electron transport chain (ETC). Gene deficiencies in the ETC are closely related to the development of kidney disease, providing evidence that mitochondria integrity is a key player in the early detection of CKD. The development of novel CKD therapies is needed since current methods of treatment are ineffective. Antioxidant targeted therapies and metabolic approaches revealed promising results to delay the progression of some markers associated with kidney disease. Herein, we discuss the role and possible origin of fibroblasts and the possible potentiators of CKD. We will focus on the important features of mitochondria in renal cell function and discuss their role in kidney disease progression. We also discuss the potential of antioxidants and pharmacologic agents to delay kidney disease progression.
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Yan, Ming-Tso, Chia-Ter Chao, and Shih-Hua Lin. "Chronic Kidney Disease: Strategies to Retard Progression." International Journal of Molecular Sciences 22, no. 18 (September 18, 2021): 10084. http://dx.doi.org/10.3390/ijms221810084.
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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.
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Cheung, Wai W., and Robert H. Mak. "Ghrelin in Chronic Kidney Disease." International Journal of Peptides 2010 (March 17, 2010): 1–7. http://dx.doi.org/10.1155/2010/567343.
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Patients with chronic kidney disease (CKD) often exhibit symptoms of anorexia and cachexia, which are associated with decreased quality of life and increased mortality. Chronic inflammation may be an important mechanism for the development of anorexia, cachexia, renal osteodystrophy, and increased cardiovascular risk in CKD. Ghrelin is a gastric hormone. The biological effects of ghrelin are mediated through the growth hormone secretagogue receptor (GHSR). The salutary effects of ghrelin on food intake and meal appreciation suggest that ghrelin could be an effective treatment for anorexic CKD patients. In addition to its appetite-stimulating effects, ghrelin has been shown to possess anti-inflammatory properties. The known metabolic effects of ghrelin and the potential implications in CKD will be discussed in this review. The strength, shortcomings, and unanswered questions related to ghrelin treatment in CKD will be addressed.
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BV, Sumanth. "Chronic Kidney Disease affecting the Characteristics of Blood Pressure: An Observational Study." Journal of Advanced Research in Medicine 08, no. 03 (September 30, 2021): 22–26. http://dx.doi.org/10.24321/2349.7181.202116.
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Background: Chronic kidney disease (CKD) is a global public-health problem that affects millions of individuals. Despite widespread use of medicines to slow the course of CKD, the burden of end-stage renal disease in many affluent nations remains high. Hypertension is far more frequent in persons with CKD than it is in the general population, and it becomes worse as renal function declines. Controlling blood pressure, which is a controllable risk factor for this complication, may reduce the risk of cardiovascular events and decrease the decline of renal function. Objective: To asses the Characteristics of Blood Pressure in Chronic Kidney Disease. Materials and Methods:A cross-sectional Study was conducted at MS Ramaiah Medical College, Bangalore from 1st of January 2018 to 31st of July 2019. A total of 100 Cases were included in the study. Results:In our research, 10% of the participants were under the age of 30. In the research, 33% of the participants had Stage 3 CKD, 35% had Stage 4 CKD, and 32% had Stage 5 CKD. There was a significant difference in mean OSBP and mean ODBP with increasing CKD stage in the research. With rising CKD stage, mean OSBP and ODBP increased. Conclusion: Ambulatory BP measurements revealed a significant degree of overestimation (white coat HTN) and underestimate (masked HTN) of BP among patients with CKD, indicating that adopting ABPM may assist avoid mistakes in BP measurement as well as correct treatment of HTN in CKD.
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Lamprea-Montealegre, Julio Alejandro, Michael G. Shlipak, and Michelle M. Estrella. "Chronic kidney disease detection, staging and treatment in cardiovascular disease prevention." Heart 107, no. 16 (February 10, 2021): 1282–88. http://dx.doi.org/10.1136/heartjnl-2020-318004.
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Globally, nearly 10% of the population has chronic kidney disease (CKD), defined as a glomerular filtration rate less than 60 mL/min/1.73 m2 and/or a urinary albumin to creatinine ratio greater than 30 mg/g (3 mg/mmol). Persons with CKD have a substantially high risk of cardiovascular disease. Indeed, most persons with CKD are far more likely to develop a cardiovascular event than to progress to end-stage kidney disease. Although early detection and staging of CKD could help prevent its cardiovascular consequences, current rates of testing for CKD are very low, even among high-risk populations such as persons with diabetes, hypertension and cardiovascular disease. In this review, we first describe the need to test for both estimated glomerular filtration rate and albuminuria among persons at high risk of CKD in order to properly stage CKD and enhance cardiovascular risk stratification. We then discuss how detection and staging for CKD could help prioritise patients at high risk of atherosclerotic cardiovascular disease and heart failure who could derive the largest benefit from cardiovascular preventive interventions. In addition, we discuss the central role of CKD detection and staging in the initiation of cardiorenal preventive therapies, such as the sodium–glucose cotransporter 2 inhibitors, which have shown overwhelming evidence of cardiorenal protection. We conclude by discussing strategies to overcome historical barriers to CKD detection and treatment.
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Martins, David, Lawrence Agodoa, and Keith Norris. "Chronic Kidney Disease in Disadvantaged Populations." International Journal of Nephrology 2012 (2012): 1–6. http://dx.doi.org/10.1155/2012/469265.
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Disadvantaged populations across the globe exhibit a disproportionate burden of chronic kidney disease (CKD) because of differences in CKD occurrence and outcomes. Although many CKD risk factors can be managed and modified to optimize clinical outcomes, the prevailing socioeconomic and cultural factors in disadvantaged populations, more often than not, militate against optimum clinical outcomes. In addition, disadvantaged populations exhibit a broader spectrum of CKD risk factors and may be genetically predisposed to an earlier onset and a more rapid progression of chronic kidney disease. A basic understanding of the vulnerabilities of the disadvantaged populations will facilitate the adaptation and adoption of the kidney disease treatment and prevention guidelines for these vulnerable populations. The purpose of this paper is to examine recent discoveries and data on CKD occurrence and outcomes in disadvantaged populations and explore strategies for the prevention and treatment of CKD in these populations based on the established guidelines.
Dissertations / Theses on the topic "Chronic kidney disease, CKD, CKD treatment"
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El-Khoury, Joe M. "Chronic Kidney Disease: Vitamin D Treatment Regimens and Novel Assay Development for Kidney and Cardiovascular Function Biomarkers." Cleveland State University / OhioLINK, 2012. http://rave.ohiolink.edu/etdc/view?acc_num=csu1343914060.
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Masconi, Katya. "The occurance of genetic variations in the MYH9 gene and their association with CKD in a mixed South African population." Thesis, Stellenbosch : Stellenbosch University, 2012. http://hdl.handle.net/10019.1/71697.
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Thesis (MScMedSc)--Stellenbosch University, 2012.ENGLISH ABSTRACT: The purpose of this study was to investigate the association of the selected MYH9 single nucleotide polymorphisms (SNPs) with chronic kidney disease (CKD) and its related co-morbidities in the South African mixed ancestry population residing in Bellville South, Cape Town. In 2008, two landmark studies identified SNPs in the MYH9 gene which explained most of the increased risk for non-diabetic CKD in African Americans. These polymorphisms were later found to be weakly associated with diabetic nephropathy. Three SNPs that exhibited independent evidence for association with CKD were selected (rs5756152, rs4821480 and rs12107). These were genotyped using a Taqman genotyping assay on a BioRad MiniOpticon and confirmed by sequencing in 724 subjects from Bellville South, Cape Town, South Africa. Prevalent CKD was defined based on the estimated glomerular filtration rate calculated using the modification of diet in renal disease (MDRD) formula. Chronic kidney disease was present in 214 subjects (29.6%), 96.3% were stage 3 and only 8 subjects were stage 4. In additive allelic models, adjusted for age and gender, rs5756152 demonstrated an association with kidney function whereby each G allele of rs5756152 increased eGFR by 3.67 ml/min/1.73, reduced serum creatinine by 4.5% and increased fasting plasma glucose by 0.51 mmol/L. When an interaction model was used, the effect of rs5756152 on serum creatinine, eGFR and blood glucose levels was retained, and enhanced, but only in diabetic subjects. In addition, rs4821480 T allele increased eGFR while rs12107 A allele decreased glucose levels in diabetic subjects. In contrast to reports that MYH9 SNPs are strongly associated with non-diabetic end stage renal disease, our study demonstrated that rs5756152 and rs4821480 are associated with early kidney function derangements in type 2 diabetes whilst rs12107 is associated with glucose metabolism. Our findings, along with previous reports, suggest that the MYH9 gene may have a broader genetic risk effect on different types of kidney diseases than previously thought.
AFRIKAANSE OPSOMMING: Hierdie studie het ondersoek ingestel na die verband tussen drie gekose MYH9-enkelnukleotied-polimorfismes (SNP’s) en chroniese niersiekte (hierna ‘niersiekte’), wat verwante ko-morbiditeite insluit, onder ’n Suid-Afrikaanse populasie van gemengde afkoms in Bellville-Suid, Kaapstad. Twee rigpuntstudies het in 2008 op SNP’s in die MYH9-geen afgekom wat verklaar het waarom Afro-Amerikaners ’n hoër risiko vir niediabetiese niersiekte toon. Later is bevind dat hierdie polimorfismes ook ’n swak verband met diabetiese nefropatie het. Drie SNP’s wat elk onafhanklik bewys gelewer het van ’n verband met niersiekte is vervolgens gekies (rs5756152, rs4821480 en rs12107). Die SNP’s is daarná met behulp van die Taqman-toets op ’n BioRad MiniOpticon aan genotipering onderwerp, en is toe deur middel van reeksbepaling by 724 proefpersone van Bellville-Suid, Kaapstad, Suid-Afrika, bevestig. Die voorkoms van niersiekte is bepaal op grond van die geraamde glomerulêre filtrasietempo (eGFR), wat aan die hand van die ‘niersiekte-dieetveranderings’- (MDRD-)formule bereken is. Daar is bevind dat 214 proefpersone (29,6%) aan chroniese niersiekte ly – 96,3% was in fase 3 en slegs agt proefpersone in fase 4. In toegevoegde alleliese modelle wat vir ouderdom en geslag aangepas is, het rs5756152 ’n verband met nierfunksie getoon: Elke G-allel van rs5756152 het eGFR met 3,67 ml/min/1,73 verhoog, serumkreatinien met 4,5% verlaag en vastende plasmaglukose met 0,51 mmol/L verhoog. Toe ’n interaksiemodel gebruik is, is die effek van rs5756152 op serumkreatinien, eGFR en bloedglukosevlakke behou en versterk, hoewel slegs by diabetiese proefpersone. Daarbenewens het die T-allel van rs4821480 eGFR verhoog, terwyl die A-allel van rs12107 ook glukosevlakke by diabetiese proefpersone verlaag het. In teenstelling met bewerings dat MYH9-SNP’s ’n sterk verband met niediabetiese eindstadiumniersiekte toon, het hierdie studie bewys dat rs5756152 en rs4821480 met vroeë nierfunksieversteurings by tipe 2-diabetes verband hou, terwyl rs12107 weer met glukosemetabolisme verbind word. Tesame met vorige studies, doen hierdie navorsingsbevindinge dus aan die hand dat die MYH9-geen dalk ’n groter genetiese risiko-effek op verskillende tipes niersiekte het as wat voorheen vermoed is.
Cape Peninsula University of Technology Research Fund
University of Stellenbosch Merit Bursary
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Amagwu, Anthony C. "Management of Chronic kidney Disease by Advanced Practice Nurses." ScholarWorks, 2018. https://scholarworks.waldenu.edu/dissertations/4832.
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Despite best available care, uncontrolled chronic kidney disease (CKD) - a complex disease that impacts millions in the United States, will eventually progress to end stage renal disease which is associated with high morbidity and mortality. New evidence suggests management of earlier stages of CKD is effective in delaying disease progression. This project evaluated the impact of a CKD class, led by a nephrology nurse practitioner, on preventing disease progression in advanced CKD patients with diabetes and hypertension. The purpose of the class was to validate the need for the advanced practice nurse (APN) in the care continuum of CKD. CKD education is a quality improvement project based on the chronic illness trajectory nursing model by Corbin and Strauss. Using a case-control method and a simple descriptive statistic to compare the mean values, retrospective data from 52 patients were analyzed. Twelve non-participating patients had a mean 7% increase in serum creatinine levels at the 1-year mark. Forty participating patients saw a mean decrease of 30% serum creatinine. With significant evidence suggesting that disease progression is delayed and renal function is improved in all study markers for patients who participated in a CKD education class led by a nephrology nurse practitioner and who received usual care - an argument can be made for updating the APN role in the continuum of care for those with CKD. The results may contribute to social change by providing improved access to quality care that addresses the socioeconomic devastation of end stage renal disease.
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So, Beng Hock. "Chronic kidney disease : determining chronicity, prevalence, variation and survival in a community chronic kidney disease (CKD) cohort." Thesis, University of Glasgow, 2018. http://theses.gla.ac.uk/30671/.
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Chronic kidney disease (CKD) is insidious and most cases are diagnosed through opportunistic serum creatinine (SCr) testing before symptoms develop. However, efforts to accurately assess prevalence have been hampered by the lack of a universally agreed definition of SCr thresholds for the diagnosis of CKD. At the turn of the millennium, two crucial developments occurred. The first was the description of the Modification of Diet in Renal Disease estimated Glomerular Filtration Rate (eGFR) which closely correlated to cumbersome measured GFR and could be used instead in daily clinical practice. The second was the publication of the Kidney Disease Outcomes Quality Initiative (KDOQI) clinical practice guideline for the evaluation, classification and stratification of CKD detailing a new definition of CKD based on GFR thresholds. Together, these two developments formed the basis of CKD as we know it today. Prevalence of CKD varies, and accurate prevalence estimates are difficult to obtain especially with respect to fulfilling the chronicity criterion (reduced eGFR ≥ 90 days). Traditional risk factors for CKD are well described and non-traditional risk factors such as socio-economic status (SES), health literacy and rurality are gaining interest. SCr sampling patterns in the community mean that most individuals with CKD are tested routinely every year. This information may not be considered in its entirety by primary care providers (PCP) which may explain inaccuracies in PCP CKD registers. Accurate identification is important to direct evidence based clinical interventions to this patient group. In chapter 2, a novel algorithm for detecting CKD and confirming chronicity from a laboratory database was developed to identify a CKD cohort of the population served by NHS Ayrshire & Arran. Data linkage of additional laboratory data, Scottish Morbidity Records for co-morbidity, statin dispensing information from Prescribing Information Scotland, area SES, rurality and deaths from Information Services Division Scotland enriched the cohort. Patients on renal replacement therapy were identified and excluded through the Scottish Renal Registry. Multiple imputations were applied where appropriate to address missing values. There were 21,037 individuals from 2010 to 2012 fulfilling the definition of CKD stage 3 – 5. Prevalence of adults with CKD was 5.6% – 5.8%. Average age (± SD) of the cohort was 75 ± 11 years. 64.6% were female and average eGFR for the cohort was 47.32 ± 11.53 mL/min/1.73m2. In chapter 3, laboratory ascertainment of CKD identified 7% more cases than PCP CKD registers. Furthermore, around 25% of patients on PCP CKD registers may be wrongly coded as having CKD. There was a 3.9-fold variation in CKD prevalence amongst PCPs, ranging from 2.8% - 11.0%. Variation fell to 3-fold with laboratory ascertainment, ranging from 3.0% - 9.1%. This fell further with age and gender stratification. Stratified laboratory CKD prevalence was positively associated with SES and rurality, a novel finding, but in multivariate linear regression, only SES, in addition to age and gender, were significant predictors for CKD prevalence. Chapter 4 explored the association between SES, eGFR and all-cause mortality. One-way ANOVA demonstrates a linear relationship between eGFR and SES (F (4,15078) = 2.52, p = 0.039) with a mean difference in eGFR of 0.83 mL/min/1.73m2 between the lowest and the highest SES quintile. However, linear regression modelling found proteinuria, hypertension, peripheral arterial disease, age, gender and serum albumin to be significant predictors for eGFR, but not SES. After adjustment for age and gender imbalance, survival demonstrated substantial influence by SES, but weakened in effect with full adjustment with only Scottish Index of Multiple Deprivation (SIMD) quintile 3 demonstrating a 13% increased risk (HR 1.13, 95% CI 1.03 to 1.24) with no progressive increase in risk associated with lower levels of SES. As a quality of care marker, the dispensing of statin was examined in chapter 5. Having another diagnosis where statins are indicated, male gender, higher serum albumin, CKD stage 3B and age between 65 – 80 were associated with higher odds ratio for statin dispensing. 64% of the cohort was dispensed a statin in 2010, but the proportion fell by 5% to 58% in 2012. This fall in dispensing disproportionately affected younger and less co-morbid CKD patients who were all eligible for a statin. SES and gender did not appear to be a factor in falling dispensing rates. Average LDL levels were lower in the statin group by (mean difference) 0.78 mmol/L (95% CI 0.74 to 0.81) in 2010 and 0.93 mmol/L (0.90 to 0.97) in 2012. 37.2% of all statin prescriptions was for Simvastatin 40 mg. Statins reduce cardiovascular events and mortality in CKD. However, in older patients typical of CKD, evidence is lacking. Chapter 6 examines survival in those dispensed a statin. Those dispensed a statin were younger, more likely to be male, had higher serum albumin and more co-morbid. After full adjustment, statin dispensing was associated with a 24% lower risk of death (HR 0.76, 95% CI 0.71 to 0.83) overall, 18% benefit for primary prevention (no prior coronary heart disease or cerebrovascular disease) (0.82, 0.74 to 0.91), 32% benefit in secondary prevention (0.68, 0.60 to 0.77), 22% benefit in younger (< 76 years) CKD patients (0.78, 0.67 to 0.92) and 22% benefit in the older (≥ 76 years) CKD patients (0.78, 0.71 to 0.85) over 4.5 years follow-up. To illustrate absolute risk reduction, the number needed to treat to avoid one death for all patients is 15.8 (95% CI 12.3 to 22.2) and 12.4 (9.3 to 18.5) for older CKD patients. This thesis demonstrates that centralised ascertainment of CKD is better at case finding, than existing PCP CKD registers. The linkage of additional, routinely collated healthcare data can develop CKD registers into a powerful tool for monitoring quality of care, efficacy of therapy and hypothesis generation which can, and should be, integrated into clinical IT systems with the appropriate information governance oversight in place.
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Tangkiatkumjai, Mayuree. "Herbal and dietary supplement use in Thai patients with chronic kidney disease (CKD) and their association with progression of CKD." Thesis, University of Nottingham, 2014. http://eprints.nottingham.ac.uk/27736/.
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The primary objective of this thesis was to determine any associations between herbal and dietary supplement (HDS) use and the fast progression of chronic kidney disease (CKD) in Thai outpatients with CKD. The secondary objectives were to determine any associations between HDS use and CKD complications, and the prevalence and reasons for HDS use. A survey recruited 421 outpatients with stages 3 to 5 CKD from two kidney clinics in Thailand, from January to June 2012. A prospective cohort study followed up these respondents, in particular noting their serum creatinine, as well as serum levels of potassium and phosphate, for 12 months. Such data were extracted from patients’ medical notes. Three hundred and fifty-seven respondents were followed up. The exposed group was defined as the current and regular users of HDS, and the primary outcome of the cohort study was defined as either a decline in the estimated glomerular filtration rate of at least 5 ml/min/1.73m2/year or the initiation of renal replacement therapy. Sixteen HDS users were recruited from the survey to be interviewed about their reasons for using HDS, using open-ended questions to elicit information in the qualitative study. Exclusion criteria were those with had received renal replacement therapy before recruitment. Univariate and multivariate analyses were performed to determine the associations using Chi-squared tests and multiple logistic regressions. Tests were 2-tailed and a p-value < 0.05 was considered statistically significant. The prevalence of HDS use during the previous year in Thai patients with CKD was 45% (95%CI 40%-50%). The most frequently reported influences on HDS use in the survey and the qualitative study were family members, friends and perception of benefits gained from using HDS. An association between HDS use and CKD progression was not found (adjusted OR 1.16, 95%CI 0.66 – 2.03). Two respondents (0.6%) had acute kidney injury, which may be related to the use of unknown Chinese herbal medicines or river spiderwort combined with diclofenac; issues which were reported by their doctor in their medical note. HDS use was associated with uncontrolled hyperphosphatemia (adjusted OR 3.53, 95%CI 1.20 – 10.43), possibly due to the HDS used in the cohort study which contained phosphate or vitamin D. Health care providers should closely monitor CKD patients using Chinese herbal medicine, river spiderwort or HDS containing phosphorus or vitamin D. Further studies need to examine renal adverse effects of specific herbal medicines, particularly in relation to acute kidney injury.
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Eyre, Heather. "Urotensin II in the development of experimental chronic kidney disease." Thesis, University of Manchester, 2015. https://www.research.manchester.ac.uk/portal/en/theses/urotensin-ii-in-the-development-of-experimental-chronic-kidney-disease(e12bed8b-1bef-4bd1-9b19-5546ce7e1af9).html.
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Urotensin II (UII) is a potent peptide hormone with a complex species and vessel-dependent vascular profile. UII and the homologous UII-related peptide (URP) bind to the g-protein coupled urotensin II receptor (UT) with high affinity. The peptide ligands and receptor have been detected in numerous human and rat tissues including heart, brain and kidney. The kidney is a major source of UII, which appears to act as both an endocrine and paracrine mediator of renal function. UII has been shown to influence renal blood flow, glomerular filtration rate and sodium handling in the renal tubules. More speculative actions of UII as a pro-fibrotic mediator include the activation of fibroblasts and promotion of collagen synthesis. Abnormally elevated UII, URP and UT expression has been highlighted in a number of cardio-renal disease states; particularly end stage renal disease, diabetes and diabetic nephropathy (DN). This work aims to investigate the role of the UII system in the development and progression of CKD using an experimental model of CKD in rodents. The first aim of the current work involved establishing the surgical 5/6th subtotal nephrectomy (SNx) model of chronic kidney disease (CKD) in the laboratory and forming a profile of UII expression in late stage experimental CKD to complement UII clinical data which are exclusively from patients in the later stages of disease. UII/URP and UT were substantially over-expressed in the kidneys of SNx rats in late stage CKD. This novel insight complements the clinical profile of CKD/DN where over expression of the UII system is routinely reported. In a second study the 5/6th SNx rat model was used to explore the effects of chronic UT receptor antagonism on the progression of CKD. Although there were no discernible differences in kidney mass or histological profile between the treatment groups at the end of the study, there was a small delay in the development of albuminuria and in the onset of systolic blood pressure elevation in the UT antagonist treated cohort. The study did not produce clear-cut evidence defining the potential therapeutic value of UT-antagonism in the treatment of CKD. Despite this the results are encouraging and suggest that the role of UT-inhibition in CKD is worth considering further.
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Ferrer, Lucas Manuel. "ROLE OF CKD AND CASPASE-1 IN NEOINTIMAL HYPERPLASIA DEVELOPMENT." Master's thesis, Temple University Libraries, 2014. http://cdm16002.contentdm.oclc.org/cdm/ref/collection/p245801coll10/id/300901.
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Public HealthM.S.
Vascular access dysfunction is a cause of morbidity and mortality in chronic kidney disease (CKD) patients that require hemodialysis. The major cause of vascular access failure is venous stenosis due to neointimal hyperplasia (NH). Vascular smooth muscle cells (VSMC) are critical for the development of NH lesions, as they have the ability to modulate their phenotype from a "contractile" to a "synthetic" phenotype in the presence of uremia, through the regulation of sensor genes for uremia danger signals and VSMC-specific differentiation genes. Recent research indicates that Caspase-1 (casp-1) activation plays an essential role in sensing metabolic danger signal-associated molecular patterns and initiating vascular inflammation. Carbamylated LDL, a uremic toxin that has been shown to be found in higher levels in patients with CKD and in CKD murine models when compared to controls, and could play a role in casp-1 activation. Therefore, the goal of this project is to examine the role of cLDL/CKD-driven casp-1 activation in VSMC and CKD-related NH. We have established a CKD mouse model and published on CKD-associated vascular remodeling. We exposed wild type and caspase-1 knockout mice to our CKD model, analyzed and quantified the NH lesion formed. We also examined in vitro and ex-vivo changes in VSMC-specific differentiation genes when exposed to uremic serum and cLDL, in the presence or absence of caspase-1 inhibitor. We found that CKD serum induces with casp-1 activation and phenotypic changes in VSMCs from a "contractile" to a "synthetic" phenotype, which are reversed with casp-1 inhibition. In an ex-vivo model using relative quantification we found that VSMC contractile markers α -Actin, Calponin, SM-22, and Smoothelin gene expression of CKD mouse carotid VSMC were higher in casp-1 knockout mice when compared to wild-type (1.40, 1.28, 1.22, 1.41 respectively). Also using an in-vivo model, relative quantification of α-actin decreased from 1.0 to 0.329 when VSMCs were exposed to uremic serum and but increased back to 0.588 when Caspase-1 inhibitor is added. The relative quantification of Calponin also decreased from 1.0 to 0.394 when exposed to uremic serum and increased back to 0.601 with caspase-1 inhibitor. We also found that caspase-1 deficiency significantly reversed CKD-related vascular remodeling in casp-1 knockout mice and reduced NH volume by 50% from 1,440,023in wild-type mice to 71,069 µm2 in casp-1 knockouts (p-value 0.002). This evidence provides evidence that casp-1 plays a critical role in NH formation. Furthermore our results provide a novel insight over the therapeutic potential of casp-1 inhibitors for CKD induced NH and other inflammation induced vascular remodeling.
Temple University--Theses
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Lim, Kenneth Jia-En. "Role of Klotho in the development of vascular calcification in patients with chronic kidney disease (CKD)." Thesis, University of Warwick, 2012. http://wrap.warwick.ac.uk/50202/.
Full textAbstract:
Background: Cardiovascular disease is the leading cause of mortality in patients with Chronic Kidney Disease (CKD). Vascular calcification is a significant contributor to cardiovascular mortality in CKD. Klotho is a 130kDa transmembrane protein with cardiovasculo-protective properties and also functions as a co-factor for the phosphatonin, fibroblast growth factor (FGF)-23 at the kidney. FGF-23 levels rise in CKD despite progression of accelerated vascular calcification (VC). There are currently conflicting data on whether FGF-23 may exhibit direct vasculo-protective effects in CKD. Methods and results: In this study, we describe for the first time endogenous Klotho expression in human arteries and human aortic smooth muscle cells (HASMCs). We show that CKD is a state of vascular Klotho deficiency promoted by chronic circulating stress factors, including pro-inflammatory, uremic and disordered metabolic conditions. Mechanistic studies demonstrated that Klotho knockdown potentiated the development of accelerated calcification through a Runx2 and myocardin-SRF dependent pathway. Klotho knockdown studies further revealed that vascular cells are a Klotho-dependent target tissue for FGF-23. FGF-23 mediated cellular activation of p-ERK, p-AKT and cellular proliferative effects, which were abrogated following Klotho knockdown. We next showed that vascular Klotho deficiency driven by pro-calcific stressors could be restored by vitamin D receptor (VDR) activators, in vitro and further confirmed using human arterial organ cultures from CKD patients, in vivo. Furthermore, restoration of Klotho by vitamin D receptor (VDR) activators conferred HA-SMCs FGF-23 responsive and unmasked its anticalcific effects. Conclusions: Chronic metabolic stress factors found in CKD promote vascular Klotho deficiency. Mechanistic studies revealed a bi-functional role for local vascular Klotho, first as an endogenous inhibitor of VC and second, as a co-factor required for vascular FGF-23 signalling. Furthermore, VDR activators can restore Klotho expression and unmask FGF-23 anti-calcific effects.
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Lomas, Amy. "The renal effects of nonsteroidal anti-inflammatory drugs (NSAIDS) in dogs with chronic kidney disease (CKD)." Thesis, Kansas State University, 2013. http://hdl.handle.net/2097/20475.
Full textAbstract:
Master of ScienceDepartment of Clinical Sciences
Gregory F. Grauer
Prostaglandins play many important roles in the kidney including regulation of renal blood flow, glomerular filtration, renin release, and sodium excretion. Upon activation of the renin angiotensin aldosterone system (RAAS), prostaglandin upregulation becomes critical to offset the vasoconstrictive effects of norephinephrine, angiotensin II, and vasopressin. Nonsteroidal anti-inflammatory drugs (NSAIDs) produce both their beneficial and detrimental effects through inhibition of the cyclooxygenase enzyme and subsequent interference with prostaglandin production. Healthy canine kidneys express both COX-1 and COX-2, although basal COX-2 expression in dogs is significantly higher than in other species. Nonsteroidal anti-inflammatory drugs that spare COX-1 have exhibited less gastrointestinal toxicity, but no NSAID has been proven safe for the kidney. The kidney is the organ with the second highest reports of adverse drug events, which is usually manifested as functional changes. However, structural changes including renal papillary necrosis, can occasionally be observed. Dogs with chronic kidney disease could be expected to be at increased risk for NSAID-related adverse drug effects. As nephrons and renal reserve are lost in chronic kidney disease, the canine kidney becomes more dependent on COX-2 for production of prostaglandins. Inasmuch as the prevalence of both CKD and OA increases with age, it is expected that many dogs being treated with NSAIDs for OA will have loss of renal reserve and/or early stage CKD. If administration of an NSAID is required for long term treatment of osteoarthritis, frequent monitoring of blood pressure and renal parameters, as well as hepatic enzymes are recommended.
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Miller, Matthew Scott. "The effect of calcifediol supplementation on renin-angiotensin-aldosterone system mediators in dogs with chronic kidney disease." The Ohio State University, 2021. http://rave.ohiolink.edu/etdc/view?acc_num=osu1618829782648424.
Full textBooks on the topic "Chronic kidney disease, CKD, CKD treatment"
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Sprague, Stuart M., and Menaka Sarav. Chronic kidney disease-mineral and bone disorder. Edited by David J. Goldsmith. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0115_update_001.
Full textAbstract:
The kidneys play a critical role in maintaining normal serum calcium and phosphorus concentrations, under the regulation of three main hormones: parathyroid hormone, calcitriol, and fibroblast growth factor 23. With the progression of chronic kidney disease (CKD), most patients develop CKD–mineral and bone disorder (CKD-MBD), which is a systemic disorder involving derangement in mineral metabolism, renal osteodystrophy, and extraskeletal calcification. Disturbances in mineral metabolism develop early in CKD and include phosphate retention, hypocalcaemia, vitamin D deficiency, and hyperparathyroidism. Renal osteodystrophy involves pathologic changes of bone morphology related to progressive CKD and is quantifiable by histomorphometry, based on bone biopsy. CKD-MBD is associated with significant morbidity, including bone loss, fractures, cardiovascular disease, immune suppression, as well as increased mortality. As the disorder begins early in the course of CKD, a proactive approach with intervention is important. Therapeutic strategies could then be employed to prevent and correct these disturbances, aiming to improve cardiovascular outcomes and survival. Current practice guidelines for CKD-MBD are based on insufficient data and high-quality studies are required before specific treatment can be advocated strongly.
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Christensen, Alan J., Julia R. Van Liew, and Quinn D. Kellerman. Depression in Chronic Kidney Disease. Edited by C. Steven Richards and Michael W. O'Hara. Oxford University Press, 2014. http://dx.doi.org/10.1093/oxfordhb/9780199797004.013.013.
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Chronic kidney disease (CKD) is a prevalent medical condition posing a range of unique physical and self-management demands for patients and presenting a variety of patient management challenges for clinicians. Co-morbid depression and other psychiatric disorders represent a significant detriment to the quality of life and clinical outcomes of CKD patients. Evidence suggests that 12% to 40% of individuals in the later stages of CKD meet DSM (III, IV, or IV-TR) diagnostic criteria for a mood disorder. Moreover, the existence of comorbid depression has been associated with earlier patient mortality. Depression assessment is itself complicated by the physiologic and medical treatment status of the patient, and depression is believed to be both underdiagnosed and undertreated in this population. Rigorous empirical demonstrations of the safety and/or efficacy of both pharmacologic and nonpharmacologic treatments for depression are limited for this population. However, a number of important factors that should be considered in treating depression in kidney disease patients have been identified. This chapter summarizes these and other key clinical recommendations relevant to the evaluation and treatment of co-morbidity of depression in this population.
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Hutchison, Alastair J., and Michael L. Picton. Fractures in patients with chronic kidney disease. Edited by David J. Goldsmith. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0121.
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Patients with any degree of chronic kidney disease (CKD) have a much higher risk of fractures than the general population, and the risk of death at 1 year post hip fracture in a dialysis patient is over 60%, compared to less than 20% for a non-CKD patient. The assessment of fracture risk and diagnosis of the underlying skeletal pathology in CKD patients is a significant clinical challenge. Non-invasive imaging techniques are not totally reliable in the general population, and the presence of advanced CKD (stages 4, 5, and 5D) renders them largely useless. Bone strength is not determined only by quantity of bone, and renal osteodystrophy can significantly affect bone quality, rendering it liable to fracture even in the presence of a normal bone density measurement. Currently, the only reliable method of assessing both quantity and quality of bone is the examination of trans-iliac bone biopsy, which is generally, but probably incorrectly, perceived to be overly invasive. However, identifying the cause of reduced bone strength and fractures may influence the choice of therapy. For example, in the presence of low-turnover states such as adynamic bone, antiresorptive agents may be ineffective. Pharmaceuticals licensed for the treatment of osteoporosis in the general population can be used similarly in patients with CKD 1–3 without dosage alteration. In CKD 4, post-hoc analyses suggest denosumab is effective and safe, based on a 3-year study that included 73 such patients. In CKD 5 and 5D no dependable data exists to guide therapy, and it should probably be reserved for patients who have already suffered and survived a fracture, and are therefore at high risk of death from a second event.
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Malyszko, Jolanta, and Iain C. Macdougall. Iron metabolism in chronic kidney disease. Edited by David J. Goldsmith. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0125.
Full textAbstract:
While whole-body (‘absolute’) iron deficiency is common and probably increased in frequency in chronic kidney disease (CKD), functional iron deficiency is a particular problem in CKD. Absolute iron deficiency is likely to be present in advanced CKD when the ferritin falls below 100 ng/mL and the TSAT falls below 20%. Functional iron deficiency is characterized by the presence of adequate iron stores (as defined by conventional criteria), but with an inability to mobilize this iron rapidly enough to adequately support erythropoiesis with the administration of erythropoietin. Among such patients, the serum ferritin level is either normal or elevated (usually between 100 and 800 ng/mL), with a TSAT typically ≤20%. Hepcidin, a novel peptide discovered at the turn of the twenty-first century, is an iron gatekeeper that plays a key role in functional iron deficiency, and the ‘anaemia of chronic disease’. The main function of hepcidin is homeostatic regulation of iron metabolism and mediation of host defence and inflammation. Hepcidin is the predominant negative regulator of iron absorption in the small intestine, iron transport across the placenta, and iron release from the macrophages. Novel strategies that modulate hepcidin and its target ferroportin for the treatment of anaemia of chronic diseases are currently undergoing extensive research.
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Biggar, Patrick, Hansjörg Rothe, and Markus Ketteler. Epidemiology of calcium, phosphate, and parathyroid hormone disturbances in chronic kidney disease. Edited by David J. Goldsmith. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0109_update_001.
Full textAbstract:
Chronic kidney disease-mineral and bone disorders (CKD-MBD), calcium, phosphate, and parathyroid hormone are biomarkers of mortality and cardiovascular risk. Hyperphosphataemia is a prominent and pathophysiologically most plausible risk indicator. Calcium balance and load appear to be more important than serum concentrations. Parathyroid hormone is a less reliable marker with a relatively wide range extending above that applicable for a normal population especially when used as a singular laboratory parameter without additional assessment of bone metabolism, for example, bone-specific alkaline phosphatase and bone biopsy. There is not a single prospective controlled hard-outcome study that provides us with unequivocal evidence that such an isolated laboratory parameter-based treatment approach will lead to significant clinical improvements. As CKD-MBD is complex, clinical decisions would be made easier by informative prospective trials.
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Voinescu, Alexandra, Nadia Wasi Iqbal, and Kevin J. Martin. Management of chronic kidney disease-mineral and bone disorder. Edited by David J. Goldsmith. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0118_update_001.
Full textAbstract:
In all patients with chronic kidney disease (CKD) stages 3–5, regular monitoring of serum markers of CKD-mineral and bone disorder, including calcium (Ca), phosphorus (P), parathyroid hormone (PTH), 25-hydroxyvitamin D, and alkaline phosphatase, is recommended. Target ranges for these markers are endorsed by guidelines. The principles of therapy for secondary hyperparathyroidism include control of hyperphosphataemia, correction of hypocalcaemia, use of vitamin D sterols, use of calcimimetics, and parathyroidectomy. of hyperphosphataemia is crucial and may be achieved by means of dietary P restriction, use of P binders, and P removal by dialysis. Dietary P restriction requires caution, as it may be associated with protein malnutrition. Aluminium salts are effective P binders, but they are not recommended for long-term use, as Aluminium toxicity (though from contaminated dialysis water rather than oral intake) may cause cognitive impairment, osteomalacia, refractory microcytic anaemia, and myopathy. Ca-based P binders are also quite effective, but should be avoided in patients with hypercalcaemia, vascular calcifications, or persistently low PTH levels. Non-aluminium, non-Ca binders, like sevelamer and lanthanum carbonate, may be more adequate for such patients; however, they are expensive and may have several side effects. Furthermore, comparative trials have failed so far to provide conclusive evidence on the superiority of these newer P binders over Ca-based binders in terms of preventing vascular calcifications, bone abnormalities, and mortality. P removal is about 1800–2700 mg per week with conventional thrice-weekly haemodialysis, but may be increased by using haemodiafiltration or intensified regimens, such as short daily, extended daily or three times weekly nocturnal haemodialysis. Several vitamin D derivatives are currently used for the treatment of secondary hyperparathyroidism. In comparison with the natural form calcitriol, the vitamin D analogue paricalcitol seems to be more fast-acting and less prone to induce hypercalcaemia and hyperphosphataemia, but whether these advantages translate into better clinical outcomes is unknown. Calcimimetics such as cinacalcet can significantly reduce PTH, Ca, and P levels, but they have failed to definitively prove any benefits in terms of mortality and cardiovascular events in dialysis patients. Parathyroidectomy is often indicated in CKD patients with severe persistent hyperparathyroidism, refractory to aggressive medical treatment with vitamin D analogues and/or calcimimetics. This procedure usually leads to rapid improvements in biochemical markers (i.e. significant lowering of serum Ca, P, and PTH) and clinical manifestations (such as pruritus and bone pain); however, the long-term benefits are still unclear.
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Kinsella, Sinead, and John Holian. The effect of chronic renal failure on critical illness. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0218.
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The incidence of chronic kidney disease (CKD) and end-stage kidney disease (ESKD) is increasing, reflecting an increase in the incidence and prevalence of hypertension and type 2 diabetes. Patients with CKD and ESKD frequently experience episodes of critical illness and require treatment in an intensive care unit (ICU)setting. Management requires specific consideration of their renal disease status together with their acute illness. Mortality in critically-ill patients with ESKD is frequently related to their co-morbid conditions, rather than their ESKD status. Illness severity scoring systems allocate high points for renal variables and tend to overestimate actual mortality. Patients with ESKD and CKD requiring ICU admission have better ICU and in-hospital survival than patients with denovo acute kidney injury requiring renal replacement therapy. Appropriately selected patients benefit from ICU admission and full consideration for ICU care should be given to these patients if required, despite their renal disease status. Cardiovascular disease and sepsis account for the majority of ICU admissions in this population and the aetiology of these conditions differs from that in patients without kidney disease. Optimal critical care management of patients with ESKD and CKD requires that these differences are recognized.
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Wong, Muh Geot, Bruce A. Cooper, and Carol A. Pollock. Preparation for renal replacement therapy. Edited by David J. Goldsmith. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0143_update_001.
Full textAbstract:
Although the primary aim of management in chronic kidney disease (CKD) is to prevent progression to stage 5 CKD, for many patients renal replacement therapy (RRT) is inevitable. Planning for the initiation of dialysis is aimed at ensuring that it takes place in a supported environment in which adverse events will be minimized, that the modality chosen is appropriate for the individual circumstances, and the patient has full knowledge of what RRT entails. Beginning dialysis inevitably involves medical, psychological, family, and social issues, and preparation for RRT is optimally managed by a team with appropriate expertise in these areas. Multidisciplinary education programmes that inform patients and their families about their disease and the treatment options are likely to result in patients starting dialysis in a planned and elective manner.
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Comorbidities in Chronic Kidney Disease (CKD). MDPI, 2021. http://dx.doi.org/10.3390/books978-3-03936-669-9.
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Herrington, William G., Aron Chakera, and Christopher A. O’Callaghan. Chronic kidney disease. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0163.
Full textAbstract:
Chronic kidney disease (CKD) is defined as abnormalities of kidney structure or function, where the abnormalities have been present for >3 months and have implications for health. It is characterized by a reduced estimated glomerular filtration rate (eGFR) or other renal abnormalities. CKD is staged according to the eGFR or the degree of albuminuria. The KDIGO (Kidney Disease: Improving Global Outcomes) criteria for CKD is either an eGFR that is <60 ml/min 1.73 m−2 and has been present for >3 months, or one or more markers of kidney damage, when these have been present for >3 months.
Book chapters on the topic "Chronic kidney disease, CKD, CKD treatment"
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Alshayeb, Hala M., and L. Darryl Quarles. "Treatment Of Chronic Kidney Disease Mineral Bone Disorder (CKD-MBD)." In Primer on the Metabolic Bone Diseases and Disorders of Mineral Metabolism, 640–50. Ames, USA: John Wiley & Sons, Inc., 2013. http://dx.doi.org/10.1002/9781118453926.ch78.
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Zhang, Yilin, Dongwei Liu, and Zhangsuo Liu. "Fine Particulate Matter (PM2.5) and Chronic Kidney Disease." In Reviews of Environmental Contamination and Toxicology Volume 254, 183–215. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/398_2020_62.
Full textAbstract:
AbstractThe impact of ambient particulate matter (PM) on public health has become a great global concern, which is especially prominent in developing countries. For health purposes, PM is typically defined by size, with the smaller particles having more health impacts. Particles with a diameter <2.5 μm are called PM2.5. Initial research studies have focused on the impact of PM2.5 on respiratory and cardiovascular diseases; nevertheless, an increasing number of data suggested that PM2.5 may affect every organ system in the human body, and the kidney is of no exception. The kidney is vulnerable to particulate matter because most environmental toxins are concentrated by the kidney during filtration. According to the high morbidity and mortality related to chronic kidney disease, it is necessary to determine the effect of PM2.5 on kidney disease and its mechanism that needs to be identified. To understand the current status of PM2.5 in the atmosphere and their potential harmful kidney effects in different regions of the world this review article was prepared based on peer-reviewed scientific papers, scientific reports, and database from government organizations published after the year 1998. In this review, we focus on the worldwide epidemiological evidence linking PM2.5 with chronic kidney disease and the effect of PM2.5 on the chronic kidney disease (CKD) progression. At the same time, we also discuss the possible mechanisms of PM2.5 exposure leading to kidney damage, in order to emphasize the contribution of PM2.5 to kidney damage. A global database on PM2.5 and kidney disease should be developed to provide new ideas for the prevention and treatment of kidney disease.
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Müller, Andreas, and Martin Meier. "Assessment of Renal Volume with MRI: Experimental Protocol." In Methods in Molecular Biology, 369–82. New York, NY: Springer US, 2021. http://dx.doi.org/10.1007/978-1-0716-0978-1_21.
Full textAbstract:
AbstractRenal length and volume are important parameters in the clinical assessment of patients with diabetes mellitus, kidney transplants, or renal artery stenosis. Kidney size is used in primary diagnostics to differentiate between acute (rather swollen kidneys) and chronic (rather small kidney) pathophysiology. Total kidney volume is also an established biomarker in studies for the treatment of autosomal dominant polycystic kidney disease (ADPKD). There are several factors influencing kidney size, and there is still a debate on the value of the measured kidney size in terms of renal function or cardiovascular risk. The renal volume is most often calculated by measuring the three axes of the kidney, on the assumption that the organ resembles an ellipsoid. By default, the longitudinal and transverse diameters of the kidney are measured. In animal models renal length and volume1 are also important parameters in the assessment of organ rejection after transplantation and in determination of kidney failure due to renal artery stenosis, recurrent urinary tract infections, or diabetes mellitus. In general total kidney volume (TKV) is a valuable parameter for predicting prognosis and monitoring disease progression in animal models of human diseases like polycystic kidney disease (PKD) or acute kidney injury (AKI) and chronic kidney disease (CKD).This chapter is based upon work from the COST Action PARENCHIMA, a community-driven network funded by the European Cooperation in Science and Technology (COST) program of the European Union, which aims to improve the reproducibility and standardization of renal MRI biomarkers. This analysis protocol is complemented by two separate chapters describing the basic concept and experimental procedure.
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Iyengar, Arpana A., and Bethany J. Foster. "Chronic Kidney Disease (CKD)." In Manual of Pediatric Nephrology, 373–400. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-12483-9_9.
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Hiß, Marcus, and Jan T. Kielstein. "Chronic Kidney Disease (CKD)." In Urology at a Glance, 145–50. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-54859-8_30.
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Abbasi, Adeel, Francis DeRoos, José Artur Paiva, J. M. Pereira, Brian G. Harbrecht, Donald P. Levine, Patricia D. Brown, et al. "Chronic Kidney Disease (CKD)." In Encyclopedia of Intensive Care Medicine, 556. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-642-00418-6_1348.
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Rees, Lesley. "Chronic Kidney Disease (CKD)." In Textbook of Clinical Pediatrics, 2921–28. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-642-02202-9_313.
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Cavalier, Etienne. "PTH Measurement in CKD." In Parathyroid Glands in Chronic Kidney Disease, 93–102. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-43769-5_6.
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Gupta, Maitreyee M., and William Dennis Coffey. "Screening Tests for CKD Detection." In Approaches to Chronic Kidney Disease, 25–50. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-83082-3_3.
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Cozzolino, Mario, Paola Monciino, Michela Frittoli, Francesco Perna, Eliana Fasulo, Roberta Casazza, and Masafumi Fugakawa. "Parathyroid Glands in CKD: Anatomy, Histology, Physiology and Molecular Biology in CKD." In Parathyroid Glands in Chronic Kidney Disease, 1–19. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-43769-5_1.
Full textConference papers on the topic "Chronic kidney disease, CKD, CKD treatment"
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Al-Baniali, Asmaa, Banan Shoair, Maha Al‐ Asmakh, Ola Aljamal, and Mohammad Sohail. "Quantifying Gut Microbiome in Rats with Adenine-Induced Chronic Kidney Disease and the effect of Treatment with Gum Arabic." In Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2020. http://dx.doi.org/10.29117/quarfe.2020.0200.
Full textAbstract:
Chronic kidney disease (CKD) affects ~10% of Qatar’s population. Recently, dysbiosis in the gut microbiome has been associated with CKD. It is not understood whether CKD affects the gut microbiome or the dysbiotic gut microbiome leads to CKD. Gum Arabic (GA) is a fiber-rich dietary substance that has a potential to enhance the gut microbiome, therefore it could treat CKD. The aim of this study is to quantify the gut microbiome in CKD rats and to evaluate the GA as a potential treatment for CKD.
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Rafeeque, Ameena, and Mohammed Fasihul Alam. "The effect of Renin Angiotensin System Blockers versus Calcium Channel Blockers on Progression towards Hypertensive Chronic Kidney Disease: A comprehensive systematic review based on Randomized Controlled Trials." In Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2020. http://dx.doi.org/10.29117/quarfe.2020.0162.
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Background: Decline in estimated Glomerular filtration rate (eGFR) is associated with further progression of chronic kidney disease. Evidence suggests that Renin Angiotensin System blockers (RAS), which can be angiotensin-receptor blockers (ARBs) or Angiotensin converting enzymes Inhibitors (ACEIs), have reno- protective effect, but results are variable. Similarly, effects of Calcium channel blockers (CCBs) are shown to have a role in protecting renal function but differ across studies. Hence, the relative effect of ARBs or ACEIs as well as CCBs, and their administration as monotherapy, remain uncertain. Purpose: To summarize and determine the pooled effect of RAS versus CCBs on progression towards hypertensive CKD amongst diabetic as well as non-diabetic patients with CKD of any stage from I-IV. Data sources: All language studies in PubMed, the Cochrane Library Central, Clinical Registry of unpublishedTrials, WHO, Embase, Scopus, ProQuest, reference lists, and expert contacts up to September 2019. Study selection: This study included all the full text articles that studied diabetic and non-diabetic patients with eGFR ≥ 15 ml/min per 1.73m3 or Urinary albumin excretion levels (UAE) ≤ 300mg/d during RAS based treatment an intervention in direct comparison with CCBs treatment based approach as comparator at baseline and at the end of follow-up. However, pooling of all the included studies using meta-analysis was not feasible due to substantial study heterogeneity and the small number of included studies that are meta-analyzable. So, studies were selected for systematic review, and out of which, all the meta-analyzable studies were quantitatively analyzed on the basis of main outcomes such as (i) Relative risk for CKD progression and (ii) Mean differences in SBP and DBP for both the arms. Doi plot and funnel plot were used for detection of publication bias. Results: Review with seven included trials, and metaanalysis using IVhet model was done on three studies for primary CKD outcome and four studies for secondary BP outcomes. RAS blockers and CCBs did not show any statistically significant differences in terms of its effects on further progression CKD with RR of 0.90 [95% CI 0.69, 1.16]. Moreover, there was no statistically significant difference in BP from baseline to final end points between CCBs and RAS inhibitors with WMD of -2.09 mmHg [95% CI -5.96, 1.79] for mean SBP change and -0.71 mmHg [95% CI -2.16, 0.73] for mean DBP change. Conclusion: Evidence asserts no difference between RAS and CCB concerning the risk of progression for CKD and in terms of mean BP differences. However, the study have its own set of limitations due to which more well designed and well conducted RCTs with robust findings are required to confirm the inferences based on this review.
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Ganapathi Raju, N. V., K. Prasanna Lakshmi, K. Gayathri Praharshitha, and Chittampalli Likhitha. "Prediction of chronic kidney disease (CKD) using Data Science." In 2019 International Conference on Intelligent Computing and Control Systems (ICCS). IEEE, 2019. http://dx.doi.org/10.1109/iccs45141.2019.9065309.
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Vashisth, Shubham, Ishika Dhall, and Shipra Saraswat. "Chronic Kidney Disease (CKD) Diagnosis using Multi-Layer Perceptron Classifier." In 2020 10th International Conference on Cloud Computing, Data Science & Engineering (Confluence). IEEE, 2020. http://dx.doi.org/10.1109/confluence47617.2020.9058178.
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Alsharif, Abdullah H. "Review of mobile Applications for Managing Chronic Kidney Disease (CKD)." In 2020 International Conference on Computing and Information Technology (ICCIT-1441). IEEE, 2020. http://dx.doi.org/10.1109/iccit-144147971.2020.9213762.
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Inayatullah and Huma Qayyurn. "An improved comparative model for chronic kidney disease (CKD) prediction." In 2020 14th International Conference on Open Source Systems and Technologies (ICOSST). IEEE, 2020. http://dx.doi.org/10.1109/icosst51357.2020.9333097.
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Zhmurov, V. A., D. V. Zhmurov, and V. G. Yarkova. "CHRONIC KIDNEY DISEASE AND THE STATE OF THE CARDIOVASCULAR SYSTEM IN LOCOMOTIVE CREW WORKERS." In The 16th «OCCUPATION and HEALTH» Russian National Congress with International Participation (OHRNC-2021). FSBSI “IRIOH”, 2021. http://dx.doi.org/10.31089/978-5-6042929-2-1-2021-1-208-211.
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Abstract: 967 employees of locomotive crews (drivers and their assistants of the Sverdlovsk railway of JSC «Russian Railways») were examined. It was revealed that CKD occurs in 12, 09% of employees of locomotive crews. As the CKD stage increases, the progression of changes in the cardiovascular system was found in locomotive crew workers. A high percentage of the prognostically unfavorable variant of left ventricular remodeling - eccentric myocardial hypertrophy (25% - 39.1%, depending on the stage of CKD) was found. These changes may be a factor of adverse cardiovascular events in employees of locomotive crews, which must be taken into account when admitting to professional activities.
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Sridharan, Anush, Sandeep K. Kasoji, Emily H. Chang, and Paul A. Dayton. "Contrast-enhanced ultrasound (CEUS) in patients with chronic kidney disease (CKD)." In 2017 IEEE International Ultrasonics Symposium (IUS). IEEE, 2017. http://dx.doi.org/10.1109/ultsym.2017.8092753.
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Sridharan, Anush, S. Kasoji, E. Chang, and P. A. Dayton. "Contrast-enhanced ultrasound (CEUS) in patients with chronic kidney disease (CKD)." In 2017 IEEE International Ultrasonics Symposium (IUS). IEEE, 2017. http://dx.doi.org/10.1109/ultsym.2017.8092855.
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Abuomar, O., and P. Sogbe. "Classification and Detection of Chronic Kidney Disease (CKD) Using Machine Learning Algorithms." In 2021 International Conference on Electrical, Computer and Energy Technologies (ICECET). IEEE, 2021. http://dx.doi.org/10.1109/icecet52533.2021.9698666.
Full textReports on the topic "Chronic kidney disease, CKD, CKD treatment"
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Zhang, Mingzhu, Wujisiguleng Bao, Luying Sun, Zhi Yao, and Xiyao Li. Efficacy and safety of finerenone in chronic kidney disease associated with type 2 diabetes: meta-analysis of randomized clinical trials. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, March 2022. http://dx.doi.org/10.37766/inplasy2022.3.0020.
Full textAbstract:
Review question / Objective: To assess the beneficial effect and safety of finerenone for patients with chronic kidney disease associated with type 2 diabetes. Condition being studied: Chronic kidney disease (CKD) is a major contributor to morbidity and mortality from non-communicable diseases, affecting almost 700 million people worldwide. Approximately 40% of patients with diabetes have CKD, which exposes them to a 3-fold higher risk of cardiovascular death versus those with T2D alone. Strategies to protect the kidneys of patients with CKD and T2D may reduce their risk of cardiovascular events. Finerenone, a nonsteroidal, selective mineralocorticoid receptor antagonist, reduced composite kidney and cardiovascular outcome in trials involving patients with chronic kidney disease. Recently, quite a few clinical studies have been conducted to compare finerenone and placebo. Our meta-analysis aimed to investigate the efficacy and safety of finerenone in chronic kidney disease associated with T2D. 1st author* - Mingzhu Zhang and Wujisiguleng Bao contributed equally to this study.
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Horvit, Andrew, and Donald Molony. A Systematic Review and Meta-Analysis of Mortality and Kidney Function in Uranium – Exposed Individuals. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, April 2022. http://dx.doi.org/10.37766/inplasy2022.4.0122.
Full textAbstract:
Review question / Objective: 1) In humans, how does environmental and/or occupational exposure to uranium affect the risk of mortality due to primary kidney disease compared to unexposed individuals? (2) In humans, how does environmental and/or occupational exposure to uranium affect the risk of developing kidney failure compared to unexposed individuals? Eligibility criteria: We included cohort studies that evaluate the risk of CKD/ESKD due to uranium exposure. We also included cohort studies that evaluate standardized mortality due to all-cause mortality, kidney cancer, chronic kidney disease, diabetes, and cardiovascular disease in humans with exposure to uranium. We also included cross sectional studies that evaluate renal function in humans exposed to uranium via biomarkers and hard clinical measures (such as creatinine clearance) compared to humans with low/no uranium exposure. In order to not include the same cohort multiple times in the statistical analyses, we selected studies that evaluated an outcome of interest for a given cohort for the longest follow-up period. When this was not possible (due to multiple studies using different combinations of cohorts with varying lengths of follow up), the study with the largest study population size was selected.