scholarly journals The role of lipoprotein (a) in chronic kidney disease

2018 ◽  
Vol 59 (4) ◽  
pp. 577-585 ◽  
Author(s):  
Jemma C. Hopewell ◽  
Richard Haynes ◽  
Colin Baigent
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Genetic Associations ◽  
Lipoprotein A ◽  
Thematic Review ◽  
And Function ◽  
Acquired Abnormalities ◽  
The Impact ◽  
The Relationship

Lipoprotein (a) [Lp(a)] and its measurement, structure and function, the impact of ethnicity and environmental factors, epidemiological and genetic associations with vascular disease, and new prospects in drug development have been extensively examined throughout this Thematic Review Series on Lp(a). Studies suggest that the kidney has a role in Lp(a) catabolism, and that Lp(a) levels are increased in association with kidney disease only for people with large apo(a) isoforms. By contrast, in those patients with large protein losses, as in the nephrotic syndrome and continuous ambulatory peritoneal dialysis, Lp(a) is increased irrespective of apo(a) isoform size. Such acquired abnormalities can be reversed by kidney transplantation or remission of nephrosis. In this Thematic Review, we focus on the relationship between Lp(a), chronic kidney disease, and risk of cardiovascular events.

scholarly journals Hyperuricemia and chronic kidney disease

2021 ◽  
pp. 77-81
Author(s):  
Olga Kompaniets
Keyword(s):  
Chronic Kidney Disease ◽  
Uric Acid ◽  
Kidney Disease ◽  
Clinical Studies ◽  
Review Of The Literature ◽  
Relationship Of ◽  
The Impact ◽  
The Relationship

The article is devoted to a review of the literature on the impact of hyperuricemia on the development and progression of chronic kidney disease (CKD). The tendency of changes of views on the role of uric acid in the pathogenesis of CKD is demonstrated. An analysis of experimental, epidemiological and clinical studies on the effects of uric acid on the physiology of the nephron and endothelial tissues, the relationship of hyperuricemia with metabolic and cardiorenal syndromes.

scholarly journals The Role of Hyperuricemia in the Pathogenesis and Progressivity of Chronic Kidney Disease

2021 ◽  
Vol 9 (F) ◽  
pp. 428-435
Author(s):  
Gede Wira Mahadita ◽  
Ketut Suwitra
Keyword(s):  
Chronic Kidney Disease ◽  
Uric Acid ◽  
Kidney Disease ◽  
Serum Uric Acid ◽  
Filtration Rate ◽  
Stage Iv ◽  
Review Of The Literature ◽  
The Relationship ◽  
Uric Acid Secretion

In humans, the end product of purine metabolism is uric acid. Over 70% of uric acid is excreted through the kidneys. When renal function is impaired, uric acid secretion is also impaired. This directly correlates the prevalence of hyperuricemia with the severity of chronic kidney disease (CKD). It has been reported that the prevalence of hyperuricemia in patients with Stage I-III CKD is 40–60% and up to 70% in patients with Stage IV-V CKD. Some studies found a link between serum uric acid levels and decreased glomerular filtration rate (GFR), an independent risk factor for CKD development. Because CKD and serum uric acid levels are related, the relationship between the two frequently generates controversy. As such, this review of the literature discusses the role of uric acid in the pathogenesis and progression of CKD.

scholarly journals Hyperuricemia and Progression of Chronic Kidney Disease: A Review from Physiology and Pathogenesis to the Role of Urate-Lowering Therapy

Diagnostics ◽  
2021 ◽  
Vol 11 (9) ◽  
pp. 1674
Author(s):  
Tao Han Lee ◽  
Jia-Jin Chen ◽  
Chao-Yi Wu ◽  
Chih-Wei Yang ◽  
Huang-Yu Yang
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Renal Disease ◽  
Disease Progression ◽  
Reciprocal Relationship ◽  
Current Evidence ◽  
Renal Disease Progression ◽  
Lowering Therapy ◽  
The Relationship

The relationship between hyperuricemia, gout, and renal disease has been investigated for several years. From the beginning, kidney disease has been considered a complication of gout; however, the viewpoints changed, claiming that hypertension and elevated uric acid (UA) levels are caused by decreased urate excretion in patients with renal impairment. To date, several examples of evidence support the role of hyperuricemia in cardiovascular or renal diseases. Several mechanisms have been identified that explain the relationship between hyperuricemia and chronic kidney disease, including the crystal effect, renin–angiotensin–aldosterone system activation, nitric oxide synthesis inhibition, and intracellular oxidative stress stimulation, and urate-lowering therapy (ULT) has been proven to reduce renal disease progression in the past few years. In this comprehensive review, the source and physiology of UA are introduced, and the mechanisms that explain the reciprocal relationship between hyperuricemia and kidney disease are reviewed. Lastly, current evidence supporting the use of ULT to postpone renal disease progression in patients with hyperuricemia and gout are summarized.

scholarly journals Pelacarsen for lowering lipoprotein(a): implications for patients with chronic kidney disease

2020 ◽  
Vol 13 (5) ◽  
pp. 753-757
Author(s):  
Raul Fernandez-Prado ◽  
Maria Vanessa Perez-Gomez ◽  
Alberto Ortiz
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Messenger Rna ◽  
Controlled Trial ◽  
Good News ◽  
Phase 2 ◽  
Phase 3 ◽  
Lipoprotein A ◽  
Increased Risk

Abstract Chronic kidney disease (CKD) patients are at an increased risk of cardiovascular disease (CVD) and statins may not be protective in advanced CKD. The reasons for the limited efficacy of statins in advanced CKD are unclear, but statins may increase plasma levels of the highly atherogenic molecule lipoprotein(a), also termed Lp(a), as well as PCSK9 (protein convertase subtilisin/kexin type 9) levels. Lp(a) has also been linked to calcific aortic stenosis, which is common in CKD. Moreover, circulating Lp(a) levels increase in nephrotic syndrome with declining renal function and are highest in patients on peritoneal dialysis. Thus, the recent publication of the Phase 2 randomized controlled trial of pelacarsen [also termed AKCEA-APO(a)-LRx and TQJ230], a hepatocyte-directed antisense oligonucleotide targeting the LPA gene messenger RNA, in persons with CVD should be good news for nephrologists. Pelacarsen safely and dose-dependently decreased Lp(a) levels by 35–80% and a Phase 3 trial [Lp(a)HORIZON, NCT04023552] is planned to run from 2020 to 2024. Unfortunately, patients with estimated glomerular filtration rate <60 mL/min or urinary albumin:creatinine ratio >100 mg/g were excluded from Phase 2 trials and those with ‘significant kidney disease’ will be excluded from the Phase 3 trial. Optimized exclusion criteria for Lp(a)HORIZON would provide insights into the role of Lp(a) in CVD in CKD patients.

scholarly journals Dietary Fiber and Gut Microbiota in Renal Diets

2019 ◽  
Author(s):  
Carla Camerotto ◽  
Adamasco Cupisti ◽  
Claudia D'Alessandro ◽  
Fulvio Muzio ◽  
Maurizio Gallieni
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
General Population ◽  
Gut Microbiota ◽  
Dietary Fiber ◽  
Intestinal Microbiota ◽  
Energy Supply ◽  
Protective Role ◽  
The Relationship

Nutrition is crucial for the management of patients affected by chronic kidney disease to slow down disease progression and to correct symptoms. The mainstay of nutritional approach to renal patients is protein restriction coupled with adequate energy supply to prevent malnutrition. However, other aspects of renal diets, including fiber content, can be beneficial. This paper summarizes the latest literature on the relationship between the type of dietary fiber and prevention and management of CKD, with special attention to intestinal microbiota and the potential protective role of renal diets. A proper amount of fiber should be recommended not only in general population but also in chronic kidney disease patients, to asses an adequate composition and metabolism of intestinal microbiota and to reduce the risks connected with obesity, diabetes and dyslipidemia.

scholarly journals THE ROLE OF MELATONIN DEFICIENCY IN THE GENESIS OF ARTERIAL HYPERTENSION IN PATIENTS WITH CHRONIC KIDNEY DISEASE

2020 ◽  
Vol 115 (1) ◽  
pp. 18-26
Author(s):  
Anna Petrova ◽  
Olena Karpenko
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Hemodialysis Patients ◽  
Laboratory Studies ◽  
Healthy Individuals ◽  
Age Dependent ◽  
Salivary Melatonin ◽  
The Relationship

The study analyzed the prevalence of hypertension and impaired melatonin-forming function of the epiphysis in patients with stage 5 chronic kidney disease treated with hemodialysis. The relationship between epiphysis dysfunction and hypertension has been identified. 130 persons (50% of men) undergoing permanent hemodialysis treatment were examined. Controls were 20 healthy individuals. The determination of daytime and nighttime levels of melatonin in saliva and clinical and laboratory studies. As a result of the study it was found that for patients with stage 5 chronic kidney disease undergoing treatment, there is a frequent violation of melatonin-forming function of the pineal gland (84.6%) and hypertension (78%). In hemodialysis patients, blood pressure increases are age-dependent and are determined with salivary melatonin levels.

scholarly journals Macrophage polarization in chronic kidney disease: a balancing act between renal recovery and decline?

2019 ◽  
Vol 317 (6) ◽  
pp. F1409-F1413 ◽  
Author(s):  
Jason E. Engel ◽  
Alejandro R. Chade
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Renal Injury ◽  
Dynamic Balance ◽  
Macrophage Polarization ◽  
M1 Phenotype ◽  
Anti Inflammatory ◽  
And Function ◽  
Injury Potential

Macrophages are heterogenous cells of the innate immune system that can fluidly modulate their phenotype to respond to their local microenvironment. They are found throughout the renal compartments, where they contribute to homeostasis and function. However, renal injury activates molecular pathways that initially stimulate differentiation of macrophages into a proinflammatory M1 phenotype. Later in the course of healing, abundant apoptotic debris and anti-inflammatory cytokines induce the production of anti-inflammatory M2 macrophages, which contribute to tissue regeneration and repair. Thus, the dynamic balance of M1 and M2 populations may outline the burden of inflammation and process of tissue repair that define renal outcomes, which has been the impetus for therapeutic efforts targeting macrophages. This review will discuss the role of these phenotypes in the progression of chronic renal injury, potential pathogenic mechanisms, and the promise of macrophage-based therapeutic applications for chronic kidney disease.

scholarly journals Renal anaemia: the role of haemoglobin control in patients with chronic kidney disease

2010 ◽  
Vol 64 (3-4) ◽  
pp. 137-143
Author(s):  
Viktorija Kuzema ◽  
Aivars Pētersons ◽  
Harijs Čerņevskis ◽  
Aivars Lejnieks
Keyword(s):  
Blood Pressure ◽  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Retrospective Chart Review ◽  
Chronic Glomerulonephritis ◽  
Advanced Degree ◽  
Renal Anaemia ◽  
Erythropoiesis Stimulating Agents ◽  
The Impact

Renal anaemia: the role of haemoglobin control in patients with chronic kidney disease Chronic kidney disease (CKD) is a significant and prevalent health problem in the world. Anaemia is one of the most common manifestations in patients with CKD. The correction of anaemia with erythropoietin normalises haemoglobin level and improves quality of life. Many aspects of the impact of anaemia treatment with erythropoiesis-stimulating agents on the progression of CKD remain unresolved and disputable. The present study is a retrospective chart review of 1654 outpatients with CKD. The data were collected from the Centre of Nephrology between 1 January 2002 and 31 December 2006. The aims of the study were to assess the causes of CKD; the prevalence of anaemia based on the current guidelines for anaemia management in CKD (Kidney Disease Dialysis Outcomes Quality Initiative; K/DOQI); to evaluate haemoglobin (Hb), systolic and diastolic blood pressure (SBP and DBP), glomerular filtration rate (GFR) at the first referral to a nephrologist and at the start of renal replacement therapy (RRT). The most common causes of CKD were arterial hypertension (17.2%), chronic glomerulonephritis (17.2%), chronic intersticial nephritis (13.3%), and diabetes (12.8%). Twenty-three percent of end-stage renal disease (ESRD) patients had diabetes mellitus. At the first visit in the renal department, 16% of the patients had an advanced degree of CKD (GFR <30 ml/min). The proportion of patients under an observation in the kidney centre for a period of six months and more was only 34% (554 of 1654). Hypertension was recorded in 72% of study subjects. The blood pressure (BP) values in patients at the first visit (n = 1633) vs. at the start of RRT (n = 154) were: mean SBP 147.4 ± 24.8 mm Hg vs. 152.2 ± 23.0 mm Hg (P < 0.05); mean DBP 88.8 ± 13.6 mm Hg vs. 88.4 ± 12.0 mm Hg (P 0.05). Anaemia was recorded in 41% of study subjects, estimated using K/DOQI recommendations. The prevalence of anaemia was increased from 30.2% to 44.8% of study patients with a rise of BP (from normal BP to hypertension; P < 0.05). The mean Hb level at the start of RRT was 9.8 ± 2.1 g/dl. Only 18% of patients with renal anaemia had used erythropoiesis-stimulating agents before RRT (28 of 155). Anaemia is the prevalent condition at moderate degrees of CKD. The severity of anaemia in the CKD population is determined by evidence of diabetes, cardiovascular disease, and renal function. Anaemia may often be unrecognised or untreated.

scholarly journals Vitamin D supplementation on anemia markers and the impact on PTH in patients with chronic kidney disease

2021 ◽  
Vol 10 (9) ◽  
pp. e53310917752
Author(s):  
Letícya Thaís Mendes Viana ◽  
Larissa Lages Rodrigues ◽  
Jurandy do Nascimento Silva ◽  
Maria Márcia Dantas de Sousa ◽  
Fhanuel Silva Andrade ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Vitamin D ◽  
Kidney Disease ◽  
Vitamin D Supplementation ◽  
Beneficial Effects ◽  
Search And Selection ◽  
The Impact ◽  
Anemia Of Inflammation ◽  
Selection Of

Chronic Kidney Disease (CKD) is an injury that causes progressive impairment of exocrine and endocrine renal functions. A very common complication is anemia, caused by reduced erythropoietin production, iron deficiency and inflammation. Evidence demonstrates that vitamin D has effects on anemia of inflammation, through the increase in erythrocytes and decrease in pro-inflammatory cytokines. This study aims to review the effects of vitamin D supplementation on 25(OH)D2 concentrations, on anemia markers and on PTH levels. This is an integrative review carried out through the search and selection of original publications, in english and portuguese, indexed in PubMed, Web of Science and Science Direct databases belonging to the 2010-2020 range. The results pointed to 25(OH)D2 concentrations compatible with normality after vitamin D supplementation. In five studies, there was no change in hemoglobin and PTH levels, and in four studies there was a reduction in the dose of EPO or erythroid stimulating agent, attributing such effect on the role of calcitriol as a substrate for bone marrow erythropoietic cells. The study concluded that vitamin D supplementation had beneficial effects for correction of 25(OH)D2 deficiency, however, it reinforces the controversy about the behavior of vitamin D on the improvement of anemia markers and PTH levels in patients with DRC. Therefore, it is suggested that the beneficial effect of vitamin D on anemia in renal patients may be independent of PTH suppression.

Exploring the role of excess fluoride in chronic kidney disease: A review

2018 ◽  
Vol 38 (3) ◽  
pp. 269-279 ◽  
Author(s):  
RW Dharmaratne
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Adverse Effects ◽  
Soft Tissues ◽  
Human Kidney ◽  
Kidney Damage ◽  
The Body ◽  
Excessive Consumption ◽  
The Impact

This review covers nearly 100 years of studies on the toxicity of fluoride on human and animal kidneys. These studies reveal that there are direct adverse effects on the kidneys by excess fluoride, leading to kidney damage and dysfunction. With the exception of the pineal gland, the kidney is exposed to higher concentrations of fluoride than all other soft tissues. Therefore, exposure to higher concentrations of fluoride could contribute to kidney damage, ultimately leading to chronic kidney disease (CKD). Among major adverse effects on the kidneys from excessive consumption of fluoride are immediate effects on the tubular area of the kidneys, inhibiting the tubular reabsorption; changes in urinary ion excretion by the kidneys disruption of collagen biosynthesis in the body, causing damages to the kidneys and other organs; and inhibition of kidney enzymes, affecting the functioning of enzyme pathways. This review proposes that there is a direct correlation between CKD and the consumption of excess amounts of fluoride. Studies particularly show immediate adverse effects on the tubular area of human and animal kidneys leading to CKD due to the consumption of excess fluoride. Therefore, it is very important to conduct more investigations on toxicity studies of excess fluoride on the human kidney, including experiments using human kidney enzymes, to study more in depth the impact of excess fluoride on the human kidney. Further, the interference of excess fluoride on collagen synthesis in human body and its effect on human kidney should also be further investigated.

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