Alterations of lipoprotein(a) in patients with diabetic nephropathy

Takegoshi, Tadayoshi; Haba, Toshihiro; Hirai, Junji; Kitoh, Chikashi; Saga, Takashi; Yamazaki, Yoko; Mabuchi, Hiroshi

doi:10.1016/0021-9150(90)90135-6

Cited by 64 publications

(21 citation statements)

References 9 publications

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“…collectives with diabetic nephropathies (25) and chronic renal failure (26). Our study, however, is the first to show elevated Lp(a) levels in a large group of ESRD patients.…”

Section: Discussionmentioning

confidence: 53%

Elevated plasma concentrations of lipoprotein(a) in patients with end-stage renal disease are not related to the size polymorphism of apolipoprotein(a).

Dieplinger¹,

Lackner²,

Kronenberg³

et al. 1993

J. Clin. Invest.

133

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Patients with terminal renal insufficiency suffer from an increased incidence of atherosclerotic diseases. Elevated plasma concentrations of lipoprotein(a) ILp(a)I have been established as a genetically controlled risk factor for these diseases. Variable alleles at the apo(a) gene locus determine to a large extent the Lp(a) concentration in the general population. In addition, other genetic and nongenetic factors also contribute to the plasma concentrations of Lp(a).We therefore investigated Apo(a) phenotypes and Lp(a) plasma concentrations in a large group of patients with endstage renal disease (ESRD) and in a control group. Lp(a) concentrations were significantly elevated in ESRD patients (20.1±20.3 mg/dl) as compared with the controls (12.1±15.5 mg/dl, P < 0.001). However, no difference was found in apo(a) isoform frequency between the ESRD group and the controls. Interestingly, only patients with large size apo(a) isoforms exhibited two-to fourfold elevated levels of Lp(a), whereas the small-size isoforms had similar concentrations in ESRD patients and controls. Beside elevated Lp(a) concentrations, ESRD patients had lower levels of plasma cholesterol and apolipoprotein B.These results show that elevated Lp(a) plasma levels might significantly contribute to the risk for atherosclerotic diseases in ESRD. They further indicate that nongenetic factors related to renal insufficiency or other genes beside the apo(a) structural gene locus must be responsible for the high Lp(a) levels. (J. Clin. Invest. 1993. 91:397-401.) Key words: lipoprotein(a) -apolipoprotein(a) phenotypes * terminal renal insufficiency -end-stage renal disease * atherosclerosis

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“…collectives with diabetic nephropathies (25) and chronic renal failure (26). Our study, however, is the first to show elevated Lp(a) levels in a large group of ESRD patients.…”

Section: Discussionmentioning

confidence: 53%

Elevated plasma concentrations of lipoprotein(a) in patients with end-stage renal disease are not related to the size polymorphism of apolipoprotein(a).

Dieplinger¹,

Lackner²,

Kronenberg³

et al. 1993

J. Clin. Invest.

133

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“…Lp(a) levels may also be elevated secondary to disease. In end-stage renal disease, Lp(a) levels are elevated two-to threefold over controls (24,25) (26). The development of atherosclerosis is a longlasting process that takes decades before clinical symptoms are manifest.…”

Section: Introductionmentioning

confidence: 99%

Apolipoprotein(a) phenotypes, Lp(a) concentration and plasma lipid levels in relation to coronary heart disease in a Chinese population: evidence for the role of the apo(a) gene in coronary heart disease.

Sandholzer¹,

Boerwinkle²,

Saha³

et al. 1992

J. Clin. Invest.

151

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Elevated lipoprotein(a) (Lpjal) concentrations are associated with premature coronary heart disease (CHD). In the general population, Lp(a) levels are largely determined by alleles at the hypervariable apolipoprotein(a) (apoial) gene locus, but other genetic and environmental factors also affect plasma Lp(a) levels. In addition, Lp(a) has been hypothesized tolbe an acute phase protein. It is therefore unclear whether the association of Lp(a) concentrations with CHD is primary in nature. We have analyzed apo(a) phenotypes, Lp(a) levels, total cholesterol, and HDL-cholesterol in patients with CHD, and in controls from the general population. Both samples-were Chinese individuals residing in Singapore. Lp(a) concentrations were significantly higher in the patients than in the population (mean 20.7±23.9 mg/dl vs 8.9±12.9 mg/dl). Apo(a) isoforms associated with high Lp(a) levels (B, Sl,.S2) were significantly more frequent in the CHD patients than in the population sample (16.9% vs 8.5%, P < 0.01). Higher Lp(a) concentrations in the patients were in part explained by this difference in apo(a) allele frequencies. Results from stepwise logistic regression analysis indicate that apo(a) type was a significant predictor of CHD, independent of total cholesterol and HDL cholesterol, but not independent of Lp(a) levels. The data demonstrate that alleles at the apo(a) locus determine the risk for CHD through their effects on Lp(a) levels, and firmly establish the role of Lp(a) as a primary genetic risk factor for CHD. (J. Clin. Invest.

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“…Because Lp(a) shares considerable sequence homology with plasminogen, but not its thrombolytic effect, Lp(a) may block plasminogen's action in stimu- 25 Lp(a) concentrations increased progressively with the degree of albuminuria, ranging from microalbuminuria, to marked proteinuria, to frank chronic renal failure. Half of their diabetics with proteinuria had Lp(a) levels in excess of 30 mg/dl.…”

Section: Procoagulant Statementioning

confidence: 99%