Elevated Plasma Lipoprotein(a) in Patients with the Nephrotic Syndrome

Wanner, Christoph; Dj, Rader; Bartens, Werner; Kramer, Josh; Brewer, H B; Schollmeyer, P.; Wieland, Heinrich

doi:10.7326/0003-4819-119-4-199308150-00002

Cited by 145 publications

(73 citation statements)

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“…The mean Lp(a) value in nephropathy cases was 46.3 __17.6 mg/dl which were significantly raised (p<0.001) when compared to non nephropathy cases and controls. Similar findings were reported by Haffner et al (1992) Warner et al (1993), Geethanjali F.S., 1999, who showed that Lp(a) levels did not differ significantly between diabetics and controls but increased levels were seen in patients with proteinuria and diabetic nephropathy (13,14,15).…”

Section: Discussionsupporting

confidence: 85%

Serum Lp(a) in diabetics with and without evidence of clinical nephropathy—A preliminary study

Kumari

Jayaram

Vincent

et al. 2002

Indian J Clin Biochem

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Type 2 diabetes is associated with a marked increase in the risk of coronary artery disease. Dyslipidaemia is believed to be a major cause of this increased risk. Recently, elevated levels of lipoprotein (a), Lp(a), have been reported to be associated with an increased risk. However there is very little data regarding Lp(a) concentrations and type 2 diabetes from India. The objective of the study was to assess serum Lp(a) levels in type 2 diabetics with and with out evidence of clinical nephropathy. We estimated serum Lp(a) levels in 30 control subjects, 30 diabetics without evidence of clinical nephropathy and 30 diabetics with evidence of clinical nephropathy. Statistical analysis showed that Lp(a) levels were increased in diabetic patients with nephropathy (mean 46.3+_17.6 mg/dl). The Lp(a) levels however did not differ significantly between control (mean 20.2 _+15.9 mg/dl) and diabetics without nephropathy (mean 22.6 +-13.1 mg/dl). Thus diabetes per se seems to have little or no influence on serum Lp(a) levels, however elevated levels were seen in patients with nephropathy.

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Section: Discussionsupporting

confidence: 85%

Serum Lp(a) in diabetics with and without evidence of clinical nephropathy—A preliminary study

Kumari

Jayaram

Vincent

et al. 2002

Indian J Clin Biochem

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“…In subjects with IDDM and proteinuria, Lp(a) levels have been reported to be either increased or unchanged [31,[42][43][44][45][46][47]. Several studies of patients with nephrotic syndrome and/or renal failure from various causes have failed to demonstrate a difference in Lp(a) levels in subjects with IDDM compared with in subjects with other causes of renal dysfunction [20,29,65]. In the present study, most of the subjects had a normal creatinine clearance (greater than 1.17 ml [bullet] s sup-1 [bullet] 1.73 m sup-2) and level of albuminuria (less than 40 mg/24 h).…”

Section: Discussionmentioning

confidence: 99%

“…Significantly higher cholesterol levels are present in the more buoyant LDL fractions (fractions 12-18) of the intensively treated group. A trend can be seen toward lower cholesterol content in the intermediate-density lipoprotein (IDL) fractions (fractions [19][20][21][22][23][24][25][26][27][28][29][30] in the intensively treated group, although this did not reach statistical significance.…”

Section: Dgucmentioning

confidence: 99%

“…Lp(a) levels have been shown to be higher in familial hypercholesterolemia [13], chronic renal failure [14][15][16][17][18][19], and nephrotic syndrome [20][21][22][23][24][25], and lower levels have been reported in cirrhosis [26]. How Lp(a) levels might be affected by IDDM and its complications and whether Lp(a) contributes to CAD [27,28] in this population remain controversial.…”

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confidence: 99%

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Levels of lipoprotein(a), apolipoprotein B, and lipoprotein cholesterol distribution in IDDM. Results from follow-up in the Diabetes Control and Complications Trial

Purnell¹,

Marcovina²,

Hokanson³

et al. 1995

Diabetes

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Levels of lipoprotein (a) [Lp(a)], apolipoprotein (apo) B, and lipoprotein cholesterol distribution using density-gradient ultracentrifugation were measured as part of a cross-sectional study at the final follow-up examination (mean 6.2 years) in the Diabetes Control and Complications Trial. Compared with the subjects in the conventionally treated group (n = 680), those subjects receiving intensive diabetes therapy (n = 667) had a lower level of Lp(a) (Caucasian subjects only, median 10.7 vs. 12.5 mg/dl, respectively; P = 0.03), lower apo B (mean 83 vs. 86 mg/dl, respectively; P = 0.01), and a more favorable distribution of cholesterol in the lipoprotein fractions as measured by density-gradient ultracentrifugation with less cholesterol in the very-low-density lipoprotein and the dense low-density lipoprotein fractions and greater cholesterol content of the more buoyant lowdensity lipoprotein. Compared with a nondiabetic Caucasian control group (n = 2,158), Lp(a) levels were not different in the intensive treatment group (median 9.6 vs. 10.7 mg/dl, respectively; NS) and higher in the conventional treatment group (9.6 vs. 12.5 mg/dl, respectively; P less than 0.01). No effect of renal dysfunction as measured by increasing albuminuria or reduced creatinine clearance on Lp(a) levels could be demonstrated in the diabetic subjects. Prospective follow-up of these subjects will determine whether these favorable lipoprotein differences in the intensive treatment group persist and whether they influence the onset of atherosclerosis in insulin-dependent diabetes. Lp(a) is formed by a molecule of a carbohydrate-rich protein named apo(a) linked by a single disulfide bond to the apo B of an LDL-like lipoprotein. Like LDL, Lp(a) is thought to be atherogeic. Because of the structural homology of apo(a) to plasminogen, it is also thought to have thrombogenic properties. This potential combination of proatherogenic and prothrombotic properties has led to a surge of research into the role of Lp(a) in atherosclerosis. KeywordsIn several case-controlled and prospective studies consisting primarily of white men with at least one preexisting cardiac risk factor, such as a family history of heart disease or an elevated LDL cholesterol level, an increased Lp(a) level has been shown to be an independent risk factor for CAD [5,10,11].Because up to 91 percent of the variability in plasma Lp(a) levels between individuals has been attributed to the apo(a) isoform [5,12], the contribution of age, sex, diet, and exercise to Lp(a) levels is thought to be small. Lp(a) levels have been shown to be higher in familial hypercholesterolemia [13], chronic renal failure [14][15][16][17][18][19], and nephrotic syndrome [20][21][22][23][24][25], and lower levels have been reported in cirrhosis [26]. How Lp(a) levels might be affected by IDDM and its complications and whether Lp(a) contributes to CAD [27,28] in this population remain controversial. Some investigators found elevated Lp(a) levels in subjects with IDDM compared with normoglycemic co...

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“…5,6 For instance, modifications in the levels of plasminogen may be related to age, in view of the fact that low levels have been found in nephrotic children 7,8 and normal or increased levels have been found in nephrotic adults. 9,10 In contrast, increased concentrations of Lp(a), the lipoprotein particle containing apo(a), a glycoprotein genetically related and structurally homologous to plasminogen, have been reported in nephrotic adults 9,[11][12][13] and in children. 14,15 Because high plasma levels of Lp(a) are now recognized as a risk factor in cerebrovascular and cardiovascular diseases, 16 -18 increased concentrations of Lp(a) may represent an added thrombotic risk in nephrotic subjects.…”

mentioning

confidence: 99%

Effect of Individual Plasma Lipoprotein(a) Variations In Vivo on Its Competition With Plasminogen for Fibrin and Cell Binding

Soulat

Loyau

Baudouin

et al. 2000

ATVB

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Abstract-Simultaneous natural changes in lipoprotein(a) [Lp(a)] and plasminogen occur in the nephrotic syndrome and offer a unique opportunity to investigate their effects on plasminogen activation under conditions fashioned in vivo. Plasminogen, Lp(a), and apolipoprotein(a) in plasma were characterized, and their competitive binding to carboxyterminal lysine residues of fibrin and cell membrane proteins was determined in nephrotic children during a flare-up of the disease (61 cases) and after 6 weeks (33 cases) and 6 months (42 cases) of remission. Low plasminogen concentrations (median 1.34 mol/L, range 0.39 to 1.96 mol/L) and high Lp(a) levels (median 0.27 g/L, range 0.07 to 2.57 g/L) were detected at flare-up. These changes were associated with an increased Lp(a) binding ratio onto fibrin (3.13Ϯ0.48) and cells (1.53Ϯ0.24) compared with binding ratios of control children (1.31Ϯ0.19 and 1.05Ϯ0.07, respectively) with normal plasminogen and low Lp(a) (median 0.071 g/L). After 6 weeks and 6 months of remission, the values for net decrease in Lp(a) binding to fibrin were 1.7Ϯ0.22 (after 6 weeks) and 1.88Ϯ0.38 (after 6 months) and were correlated with low Lp(a) concentrations (median 0.2 g/L, range 0.07 to 0.8 g/L; and median 0.12 g/L, range 0.07 to 1.34 g/L) and inversely associated with increased plasminogen levels (median 1.82 mol/L, range 1.4 to 2.1 mol/L; and median 1.58 mol/L, range 1.1 to 2.1 mol/L). These studies provide the first quantitative evidence that binding of Lp(a) to lysine residues of fibrin and cell surfaces is directly related to circulating levels of both plasminogen and Lp(a) and that these glycoproteins may interact as competitive ligands for these biological surfaces in vivo. This mechanism may be of relevance to the atherothrombotic role of Lp(a), particularly in nephrotic patients.

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Elevated Plasma Lipoprotein(a) in Patients with the Nephrotic Syndrome

Cited by 145 publications

References 0 publications

Serum Lp(a) in diabetics with and without evidence of clinical nephropathy—A preliminary study

Serum Lp(a) in diabetics with and without evidence of clinical nephropathy—A preliminary study

Levels of lipoprotein(a), apolipoprotein B, and lipoprotein cholesterol distribution in IDDM. Results from follow-up in the Diabetes Control and Complications Trial

Effect of Individual Plasma Lipoprotein(a) Variations In Vivo on Its Competition With Plasminogen for Fibrin and Cell Binding

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