Lipoproteins and Apolipoproteins during the Progression of Chronic Renal Disease

Grützmacher, P.; März, Winfried; Peschke, Bernd; Wl, Gross; Schoeppe, W

doi:10.1159/000185138

Cited by 80 publications

(34 citation statements)

References 32 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Apolipoproteins on the other hand did not provide any additional information that was not gained from triacylglycerol, LDL-or HDL-cholesterol data. In patients without diabetes, impaired renal function has also been associated with increased triacylglycerol and VLDL-cholesterol concentrations [21,22]. Decreased levels of HDL-cholesterol have also been reported [22], but in contrast to our findings, changes in LDL-cholesterol and ApoB with impairment of renal function have been insignificant [21,22].…”

Section: Discussioncontrasting

confidence: 85%

Relationship between lipid profiles and kidney function in patients with type 1 diabetes

et al. 2007

View full text Add to dashboard Cite

Aims/hypothesis We studied the relationship between the lipid profile, estimated GFR (eGFR) and AER in patients with type 1 diabetes. We also assessed the association between the lipid profile and glycaemic control, obesity and hypertension in an environment free of manifest renal disease, as well as exploring how well the patients would have achieved the targets set in international guidelines. Methods A total of 2,927 adult patients who had type 1 diabetes and for whom lipid profiles were available were included from people participating in the nationwide, multicentre Finnish Diabetic Nephropathy Study (FinnDiane). eGFR was determined using the Cockcroft-Gault formula adjusted for body surface area. Results Patients with impaired renal function (eGFR <60 ml min −1 1.73 m −2 ) had higher total cholesterol, triacylglycerol and apolipoprotein B, and lower HDLcholesterol concentrations than patients with normal renal function (eGFR >90 ml min −1 1.73 m −2 ) or mildly impaired renal function (eGFR 60-90 ml min −1

show abstract

Section: Discussioncontrasting

confidence: 85%

Relationship between lipid profiles and kidney function in patients with type 1 diabetes

et al. 2007

View full text Add to dashboard Cite

show abstract

“…In CKD, plasma Lp(a) levels are also influenced by GFR. In some patients, plasma Lp(a) levels increase early in CKD [48] or in patients without CKD but active nephrotic syndrome [49]. Most people with CKD also exhibit increased or normal levels of ApoB [50].…”

Section: Ldl-cmentioning

confidence: 99%

Etiology and management of dyslipidemia in children with chronic kidney disease and end-stage renal disease

Khurana

Silverstein

2015

Pediatr Nephrol

View full text Add to dashboard Cite

Lipids are essential components of cell membranes, contributing to cell fuel, myelin formation, subcellular organelle function, and steroid hormone synthesis. Children with chronic kidney disease (CKD) and end-stage renal disease (ESRD) exhibit various co-morbidities, including dyslipidemia. The prevalence of dyslipidemias in children with CKD and ESRD is high, being present in 39-65 % of patients. Elevated lipid levels in children without renal disease are a risk factor for cardiovascular disease (CVD), while the risk for CVD in pediatric CKD/ESRD is unclear. The pathogenesis of dyslipidemia in CKD features various factors, including increased levels of triglycerides, triglyceride-rich lipoproteins, apolipoprotein C3 (ApoC-III), decreased levels of cholesterylester transfer protein and high-density lipoproteins, and aberrations in serum very low-density and intermediatedensity lipoproteins. If initial risk assessment indicates that a child with advanced CKD has 2 or more co-morbidities for CVD, first-line treatment should consist of nonpharmacologic management such as therapeutic lifestyle changes and dietary counseling. Pharmacologic treatment of dyslipidemia may reduce the incidence of CVD in children with CKD/ESRD, but randomized trials are lacking. Lipids are essential components of cell membranes, contributing to cell fuel, myelin formation, subcellular organelle function, and steroid hormone synthesis. Lipids are generally categorized by their density and other physical characteristics [1]. Since lipids such as cholesterol and triglycerides (TG) are insoluble in plasma, lipoproteins are required to transport all sources (e.g., diet) of lipids to areas in which the lipids can either be stored for future use or used immediately [2], although it should be noted that short-and medium-chain fatty acids also flow via the portal system as fatty acids. Specifically, low-density lipoproteins (LDL) carry the majority of cholesterol (forming LDL-C), while very low-density lipoproteins (VLDL) carry the majority of triglycerides.The broad categories of lipoproteins are chylomicrons, VLDL, LDL, and high-density lipoproteins (HDL Prevalence and sub-types of dyslipidemia in pediatric chronic kidney disease (CKD) and end-stage renal disease (ESRD)Children with CKD/ESRD exhibit various co-morbidities, including dyslipidemia. The prevalence of dyslipidemias in children with CKD and ESRD is high (39-65 %), but is significantly dependent on the cause and vintage of CKD (e.g., usually more common and severe with glomerular disease and proteinuria) and the stage of the disease [4,5]. The Chronic Kidney Disease in Children (CKiD) study included an assessment of the relationship between renal function and serum lipid levels. The most common type of dyslipidemia was hypertriglyceridemia. They found an inverse relationship between renal function (measured glomerular filtration rate, or GFR) and serum TG and total cholesterol (TC) levels; that is, as GFR declines, TG and TC levels generally increase. Conversely, there is a ...

show abstract

“…Lipid abnormalities are frequent in renal patients, and chronic renal failure is associated with accelerated atherosclerosis and high cardiovascular risk [2, 3]. Because hypertriglyceridemia is positively correlated with coronaropathy incidence, lipid-lowering medications are fully justified in renal patients refractory to dietary treatment.…”

Section: Introductionmentioning

confidence: 99%

Fenofibrate Increases Creatininemia by Increasing Metabolic Production of Creatinine

Hottelart

Esper

Rosé

et al. 2002

Nephron

166

128

View full text Add to dashboard Cite

Fenofibrate is a potent hypolipemic agent, widely used in patients with renal insufficiency in whom dyslipidemia is frequent. A moderate reversible increase in creatinine plasma levels is an established side effect of fenofibrate therapy, which mechanism remains unknown. We have previously reported that in 13 patients with normal renal function or moderate renal insufficiency, two weeks of fenofibrate therapy increased creatininemia without any changes in renal plasma flow and glomerular filtration rate [1]. In 13 additional patients, muscular enzymes (AST, GPT, CPK, LDH) and myoglobin were measured before and after 2 weeks on fenofibrate, and the values of creatininemia obtained by the Jaffé technique and HPLC were compared. CPK and AST activity and plasma myoglobin increased in 2 patients with fenofibrate, but muscular enzymes remained unchanged in the population as a whole, and were not correlated to the changes in creatininemia. The changes in creatininemia induced by fenofibrate measured by the Jaffé technique were strongly correlated to those measured by HPLC (r² = 0.675, p = 0.0006). Analysis of the pooled data of the two arms of the study showed in 26 patients that two weeks of fenofibrate therapy efficiently reduced total cholesterol and triglycerides plasma levels, and raised creatininemia from 139 ± 8 to 160 ± 10 µmol/l (p < 0.0001), but confirmed that creatininuria also increased to the extent that creatinine clearance remained unchanged (68 ± 6 vs. 67 ± 6 ml/min, n.s.). It is concluded that the increase in creatininemia induced by fenofibrate in renal patients does not reflect an impairment of renal function, nor an alteration of tubular creatinine secretion, and is not falsely increased by a dosage interference. Fenofibrate-induced increase of daily creatinine production is neither readily explained by accelerated muscular cell lysis. It is proposed that fenofibrate increases the metabolic production rate of creatinine.

show abstract

Lipoproteins and Apolipoproteins during the Progression of Chronic Renal Disease

Cited by 80 publications

References 32 publications

Relationship between lipid profiles and kidney function in patients with type 1 diabetes

Relationship between lipid profiles and kidney function in patients with type 1 diabetes

Etiology and management of dyslipidemia in children with chronic kidney disease and end-stage renal disease

Fenofibrate Increases Creatininemia by Increasing Metabolic Production of Creatinine

Contact Info

Product

Resources

About