A study of the clinical significance of lipoprotein (a) in nephrotic syndrome.

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

doi:10.2169/internalmedicine1962.30.21

Cited by 22 publications

(12 citation statements)

References 14 publications

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“…Elevations in Lp(a) serum levels have been documented in adults with proteinuria (24)(25)(26), adults with end-stage renal failure treated by hemodialysis (27), renal allograft recipients (28), and children (33) and adults (34) with diabetes mellitus. In addition, alcohol intake (35) and possibly treatment with corticosteroids (25) may have an effect on serum Lp(a) levels.…”

Section: Discussionmentioning

confidence: 99%

“…Lp(a) can be detected in umbilical cord blood and serum of newborns (20)(21)(22), and a gradual rise in serum levels has been observed between the ages of 2 and 13 y (23). Previous studies in adults reported increased Lp(a) levels in patients with proteinChronic renal disease is often accompanied by severe dyslipi- (24)(25)(26) and in patients treated with hemdialysis (27) and demia, a known risk factor for cardiovascular disease. In adults, renal transplantation (28).…”

Section: ~H~ Distribution Of Lp(a) Levels In Normal Subjects Wasmentioning

confidence: 99%

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Lipoprotein(a) Serum Levels and Apolipoprotein(a) Phenotypes in Children with Chronic Renal Disease

et al. 1993

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ABSTRACT. Lipoprotein(a) [Lp(a)] has recently beenLp(a) is a cholesterol-rich lipoprotein resembling LDL, but characterized as a genetically determined risk factor for with a different protein composition, consisting of apo B-100 atherosclerosis and thrombosis. Normally, Lp(a) serum and apo(a). Increased blood concentrations of Lda) are strongly levels are closely related to the apo(a) phenotype. We associated with an increased risk for atherosclerosis (8-10) and studied Lp(a) serum levels and apo(a) phenotypes in 136 arterial and venous thrombosis (1 1). Notably in Young patients, young subjects, aged 0.8-24.7 y, including patients with Lda) appears to be an independent risk factor for myocardial glomerular disease and normal renal function (n = 28), infarction ( 12). The proatherogenic and prothrombotic effects of patients with chronic renal failure (n = 201, patients treated Lp Of all, 21 patients had proteinuria in the nephrotic range. and interference with the fibrinol~tic system (8, 99 13). ~h~ distribution of Lp(a) levels in normal subjects wasIn adult Caucasian populations, Lp(a) blood levels are usually skewed to the left with 97% having levels below 300 mg/ low, i.e. the distribution of normal values is shifted to the left; blood levels above 250-300 mg/L indicate a significant risk for L' A subpopulation with increased Lp(a) levels (13-42%) vascular complications, particularly in patients with elevated could be detected in all groups with renal disease, and LDL cholesterol levels (13-15). increased mean serum L P (~) levels were found in patients In individuals, L~~) serum levels are under genetic with ne~hrotic range proteinuria, in patients with chronic control and dependent on the phenotype of the apoprotein renal failure, and in patients on peritoneal dialysis. Serum apo(a). According to Utemann el (16), seven phenotypes of Lda) levels were not with age, gender, type Of different molecular weight can be differentiated by their relative renal disease, renal function or severity of proteinuria, but mobilities to apo B-100 on electrophoresis; these have been were ~ornelat* with the apo(a) phenotype. For a given designated F (faster than B-100), B (similar to B-loo), S 1, S2, phen?w9 Lda) levels knded t 0 . h higher in patients S3, S4 (all slower than B-loo), and 0 (not detectable). Serum than controls. We ~onclude that increased Lda) serum levels of Lp(a) show an inverse correlation with the size of the levels are frequently found in Young patients with chronic apoprotein phenotype, i.e. small phenotypes (F, B, Sl) are assorenal disease, possibly predisposing them to an increased ciated with high and larger phenotypes (S3, S4) with low serum risk for atherosclerosis and thrombosis. (Pediatr Res 34: levels of Lp(a) (16). Although Lp(a) levels for a given phenotype 772-776,1993) show considerable overlap, it was concluded that about 40% of the variability in the Lp(a) serum concentrations can be exAbbreviations plained by the apo(a) phenotype (17). Other researchers have identified a greater number of ...

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Section: Discussionmentioning

confidence: 99%

Section: ~H~ Distribution Of Lp(a) Levels In Normal Subjects Wasmentioning

confidence: 99%

Lipoprotein(a) Serum Levels and Apolipoprotein(a) Phenotypes in Children with Chronic Renal Disease

et al. 1993

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“…Among the environmental factors that certainly play a role in determining plasma concentrations, renal diseases are one of the best documented. Lp(a) levels have been reported to be elevated in kidney hemodialysis patients [23][24][25][26][27][28][29][30][31][32], where they appear to be an independent risk factor for cardiovascular disease [33], in untreated patients with end-stage renal failure [34][35][36][37][38][39], and in pro teinuric syndromes [40][41][42][43][44][45]. Renal transplantation in endstage renal disease partially corrects the abnormality [25,46], A correlation of Lp(a) levels with the degree of protein uria has indeed been suspected, with the hypothesis that the decrease in scrum albumin leads to an increased hepat ic Lp(a) synthesis [43], Omega-3 fatty acids (co-3 FA) have recently been pro posed as a useful adjunct therapy in patients with renal disease [47] where they may correct some of the lipid abnormalities (notably the hypertriglyceridemia [48]) and favorably alter renal vasodilatory reserve [49], We have recently reported that a 6-week course of dietary supple mentation with co-3 FA reduces proteinuria in patients with membranous glomerulonephritis and focal glomeru lar sclerosis [50].…”

Section: Introductionmentioning

confidence: 99%

Omega-3 Fatty Acid Supplementation and Lipoprotein(a) Concentrations in Patients with Chronic Glomerular Diseases

Lenzi

Caprioli

Rindi

et al. 1996

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Renal disease patients often exhibit alterations in the lipid profile which may become an important risk of accelerated atherosclerosis and contribute to disease progression. Among such alterations, increased levels of lipoprotein(a) [Lp(a)] are common and may be related, in part, to the degree of proteinuria. Omega-3 polyunsaturated fatty acids (ω-3 FA) have been reported to decrease Lp(a) concentrations in nonrenal subjects. In addition, they have recently been shown to reduce proteinuria in patients with chronic glomerular disease. We therefore tested the hypothesis that ω-3 FA treatment in patients with chronic glomerular disease may reduce Lp(a) concentrations. Eight patients (2 with membranous glomerulonephritis, 6 with focal glomerular sclerosis) were submitted to a total of 13 six-week courses of treatment with ω-3 FA, at a dose of 3 g/day with a triglyceride preparation (n = 4) and of 7.7 g/day with an ethyl-ester preparation (n = 9). Both treatments significantly increased the proportions of ω-3 to ω-6 FA in total serum lipids, documenting compliance to treatment. Both treatments were also effective in decreasing serum thromboxane (from mean 490 ± (SEM) 70 to 325 ± 49 ng/ml, p < 0.05, in the high-dose group) and prolonging the bleeding time (from 5.8 ± 0.4 to 7.7 ± 0.5 min, p < 0.05, in the high-dose group), thus documenting the biological efficacy of treatment. However, despite a significant reduction in serum triglyceride levels (from 137 ± 20 to 104 ± 19 mg/dl in the high-dose group), Lp(a) concentrations did not change (292 ± 120 U/l before, 315 ± 130 U/l after the high-dose therapy). Treatment-related changes in proteinuria (from 2.9 ± 0.5 to 2.1 ± 0.7 g/24 h) were not related at all to changes in Lp(a) levels. We conclude that ω-3 FA do not decrease Lp(a) concentrations in renal patients with chronic glomerular diseases and that Lp(a) levels are unlikely to be related to the degree of proteinuria within the short-term modifications induced by ω-3 FA.

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“…Numerous studies have reported that Lp(a) levels are significantly elevated in patients with nephrotic syndrome [8][9][10][11][12][13][14][15][16][17][18]. However, it was never systematically investigated whether and how the apo(a) kringle-IV repeat polymorphism contributes to this increase.…”

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confidence: 99%