Lecithin-Cholesterol Acyltransferase (LCAT) Activity in Chronic Uremic Patients

Guarnieri, Gabriele; M, Moracchiello; Campanacci, L; Ursini, Fulvio; Ferri, Laura; Gregolin, Carlo

doi:10.1159/000401738

Cited by 37 publications

(47 citation statements)

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“…[27][28][29] Since nearly all of the circulating CE are generated within the circulation by the action of LCAT, 30 it could be that this enzyme and the acquired decrease in its activity in CRF are important in the development and progression of kidney disease. Although there have been many reports of acquired LCAT deficiency in renal disease, 19-24 there appears to have been very little interest in this phenomenon in recent years. Indeed, at least one recent study has suggested that LCAT is normal in dialysis patients, 31 but other recent studies also report low activity, 32,33 and differences may actually reflect the employment of different methodologies used to measure the activity of this enzyme.…”

Section: Discussionmentioning

confidence: 99%

“…One such enzyme is lecithin-cholesterol acyltransferase (LCAT), deficiency of which has been shown to occur in renal disease. [19][20][21][22][23][24] In the present study, we reassessed plasma lipids and lipoproteins, including both free cholesterol and CE as well as phospholipids, in patients with end-stage renal failure drawn from the multiracial population of the United Arab Emirates. The results suggest that a decreased concentration of CE relative to total cholesterol occurs commonly in renal failure and is associated with other lipid changes, while patients with high levels of cholesteryl esters show essentially normal levels of other lipids and lipoproteins.…”

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confidence: 99%

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Levels of Cholesteryl Esters and Other Lipids in the Plasma of Patients with End-Stage Renal Failure

Gillett

Obineche

Lakhani

et al. 2001

Annals of Saudi Medicine

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Background:The importance of plasma lipid abnormalities in chronic renal failure (CRF) is well recognized, but surprisingly little attention has been given to the study of some plasma lipid fractions, including cholesteryl esters (CE) and phospholipids, which might be expected to be important factors in the pathogenesis of the disease. Materials and Methods: Fasting blood samples were taken from 25 control subjects and 53 CRF patients (29 predialysis and 24 on hemodialysis). Samples were analyzed for urea nitrogen, creatinine, triacylglycerols, total and individual phospholipids, total and free cholesterol, as well as cholesterol bound to very low-, low-and high-density lipoproteins (VLDL, LDL and HDL). Plasma CE was calculated and expressed as a percentage of total cholesterol. Results: Over half of the patients had CE levels more than two standard deviations below the control value. In this subgroup of low CE patients, total, LDL-and HDL-cholesterol levels were also significantly lower than for controls, while levels of phosphatidylcholine and lysophosphatidylcholine were decreased and increased, respectively. In patients with high CE, no significant lipid abnormalities were observed. Conclusion: In this study, CE was an excellent marker for lipid disturbances-if CE was high, then the other lipid fractions were normal, but if CE was low, most other lipid fractions were abnormal. The changes noted appear to be consequences of or related to deficiency of the plasma enzyme lecithin-cholesterol acyltransferase. Ann Saudi Med 2001;21(5-6):283-286.

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Levels of Cholesteryl Esters and Other Lipids in the Plasma of Patients with End-Stage Renal Failure

Gillett

Obineche

Lakhani

et al. 2001

Annals of Saudi Medicine

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“…In addition, ApoA-1 LCAT deficiency. Serum LCAT activity and concentration levels are markedly diminished in patients with ESRD [65][66][67] . Moreover, hepatic LCAT production is downregulated in rat models of CKD and is the primary cause of LCAT deficiency 68-70. Given the critical role of LCAT in the formation of cholesterol ester-rich HDL and reverse cholesterol transport, an associated LCAT deficiency makes a notable contribution to CKD-associated impaired HDL maturation and HDL dysfunction.…”

Section: Ckd and Esrdmentioning

confidence: 98%

HDL abnormalities in nephrotic syndrome and chronic kidney disease

2015

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| Normal HDL activity confers cardiovascular and overall protection by mediating reverse cholesterol transport and through its potent anti-inflammatory, antioxidant, and antithrombotic functions. Serum lipid profile, as well as various aspects of HDL metabolism, structure, and function can be profoundly altered in patients with nephrotic range proteinuria or chronic kidney disease (CKD). These abnormalities can, in turn, contribute to the progression of cardiovascular complications and various other comorbidities, such as foam cell formation, atherosclerosis, and/or glomerulosclerosis, in affected patients. The presence and severity of proteinuria and renal insufficiency, as well as dietary and drug regimens, pre-existing genetic disorders of lipid metabolism, and renal replacement therapies (including haemodialysis, peritoneal dialysis, and renal transplantation) determine the natural history of lipid disorders in patients with kidney disease. Despite the adverse effects associated with dysregulated reverse cholesterol transport and advances in our understanding of the underlying mechanisms, safe and effective therapeutic interventions are currently lacking. This Review provides an overview of HDL metabolism under normal conditions, and discusses the features, mechanisms, and consequences of HDL abnormalities in patients with nephrotic syndrome or advanced CKD.

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“…Other reports describe a total plasma cholesterol and triglyceride increase in patients treated by CAPD ( 18). Uremic patients ( 19), but not those in other groups ( 1, 2), have also been reported to have lower rates of cholesterol esterification in plasma.…”

Section: Introductionmentioning

confidence: 94%

Plasma cholesterol metabolism in end-stage renal disease. Difference between treatment by hemodialysis or peritoneal dialysis.

Dieplinger¹,

Schoenfeld²,

Fielding³

1986

J. Clin. Invest.

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Plasma cholesterol metabolism was investigated in normotriglyceridemic patients with end-stage renal disease treated by hemo-or continuous ambulatory peritoneal dialysis (CAPD), and compared with that in a control group with normal renal function. A reversed net transport of free cholesterol from plasma to cultured fibroblasts, as well as greatly reduced levels of plasma cholesterol esterification and cholesterol ester transfer rates to low and very low density lipoproteins (LDL and VLDL), was found in the hemodialysis group compared to the controls. The LDL and VLDL contained increased amounts of free cholesterol and inhibited cholesterol ester transfer when recombined with control plasma. The LDL triglyceride content was doubled in the hemodialysis group, whereas cholesterol esters were decreased. Patients treated by CAPD, in marked contrast, had cholesterol metabolic rates that were within the normal range, as well as normal lipoprotein composition.

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Lecithin-Cholesterol Acyltransferase (LCAT) Activity in Chronic Uremic Patients

Cited by 37 publications

References 0 publications

Levels of Cholesteryl Esters and Other Lipids in the Plasma of Patients with End-Stage Renal Failure

Levels of Cholesteryl Esters and Other Lipids in the Plasma of Patients with End-Stage Renal Failure

HDL abnormalities in nephrotic syndrome and chronic kidney disease

Plasma cholesterol metabolism in end-stage renal disease. Difference between treatment by hemodialysis or peritoneal dialysis.

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