Lipoprotein(a) Levels in the Nephrotic Syndrome.

Kanno, Hiroaki; Saito, Eiji; Fujioka, Takayuki; Yasugi, Tadao

doi:10.2169/internalmedicine.31.1004

Cited by 9 publications

(6 citation statements)

References 23 publications

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“…Since Lp(a) is a potential independent risk factor for vascular disease in renal patients, addition al studies on the effects of co-3 FA in this patient category appear warranted. This is even more so since it has been suspected that proteinuria, possibly via a decrease in serum albumin, may lead to an increased hepatic Lp(a) synthesis [43], Therefore we elected to study the effects of co-3 FA in patients with chronic glomerular diseases, with the idea that a possible weak 'direct' effect on Lp(a) plas ma levels might be magnified by the reduction in protein uria occurring in these patients under co-3 FA treatment.…”

Section: Lipoprotein (A)mentioning

confidence: 99%

“…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]. In addition, some reports have indicated that plasma levels of Lp(a) were reduced by co-3 FA [51][52][53].…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

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

Lenzi

Caprioli

Rindi

et al. 1996

Nephron

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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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Section: Lipoprotein (A)mentioning

confidence: 99%

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

Nephron

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“…Lee et al 22) reported the effects of hyperlipidemia on the pharmacokinetics of tadalafil in rats with experimental hyperlipidemia. They administered tadalafil to control rats and rats with poloxamer-407-induced hyperlipidemia.…”

Section: Discussionmentioning

confidence: 99%

“…They suggested that the alterations in the pharmacokinetics of tadalafil observed in hyperlipidemia rats may be attributable to a decrease in the unbound fraction of tadalafil in the plasma. 22) Kanno et al 23) suggested that a decrease in serum albumin led to increased hepatic lipoprotein synthesis. The observed range of the total cholesterol concentrations were 115-232 mg/dL in patient #1, and 92-144 mg/dL in patient #2, which were generally in the normal range.…”

Section: Discussionmentioning

confidence: 99%

Determination of the Serum Unbound Fraction of Tadalafil in Children with Protein-Losing Enteropathy and Its Specific Binding to Human Serum Proteins <i>in Vitro</i>

Shigetomi

Kamiya

Takamori

et al. 2019

Biological & Pharmaceutical Bulletin

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The purpose of this study was to determine the serum protein binding of tadalafil in children with protein-losing enteropathy (PLE) and to evaluate the specific binding of the drug to human serum-derived proteins in vitro. Seventeen serum samples from two PLE patients used after biochemical tests were collected, and the unbound fraction of tadalafil was determined by an ultrafiltration method. The serum albumin concentrations observed in patients #1 and #2 were 2.4-4.2 and 2.9-3.5 g/dL, respectively. The ranges of unbound fraction of tadalafil in patients #1 and #2 were 3.9-13 and 5.0-7.0%, respectively. This suggested that serum albumin was at least a binding carrier for tadalafil because the unbound fraction of tadalafil and serum albumin were slightly correlated. The unbound fraction of tadalafil at the total concentration of 300 ng/mL was negatively dependent on the serum albumin concentration (range: 1.0-5.0 g/dL) in vitro. In the presence of albumin, the additive effect of γ-globulin on the unbound fraction of tadalafil was marginal, but the addition of α 1-acid glycoprotein to test samples decreased the unbound fraction of the drug. The decrease in the unbound fraction of tadalafil was greater at low albumin levels (2 g/dL). The addition of lipoprotein to test samples also decreased the unbound fraction of tadalafil, suggesting that lipoprotein was also a binding carrier of the drug. These results suggested that the disposition and/or response to tadalafil in PLE patients was altered by the change in protein bindings of the drug.

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“…Among these changes are an increase in serum total cholesterol, very-low and lowdensity-lipoprotein (VLDL and LDL) cholesterol, and triglycerides [1][2][3][4]. Recent studies have shown that serum lipoprotein (a) (Lp(a)) is also elevated in proteinuric patients [5][6][7][8]. Lp(a) is an LDL-like particle that contains apolipoprotein(a), which is covalently linked to apolipoprotein B-100 [9].…”

Section: Introductionmentioning

confidence: 99%

Symptomatic antiproteinuric treatment decreases serum lipoprotein (a) concentration in patients with glomerular proteinuria

Gansevoort

Heeg²,

Dikkeschei³

et al. 1994

Nephrology Dialysis Transplantation

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Elevated serum levels of the atherogenic and thrombogenic lipoprotein (a) (Lp(a)) have been recognized as a feature of the nephrotic syndrome associated hyperlipidaemia. To examine a possible relationship between serum Lp(a) concentration and proteinuria, serum albumin, or blood pressure, we studied nine patients with nephrotic-range proteinuria both at baseline and after various forms of antihypertensive and antiproteinuric treatment. In fixed order, patients received conventional antihypertensive treatment (either a-methyldopa or clonidine), subsequently ACEinhibition therapy (lisinopril), ACE inhibition combined with an NSAID (indomethacin), and finally NSAID plus conventional antihypertensive therapy. Measurements were performed at the end of each 2-month study period. When compared to controls (n = 29), proteinuric patients before treatment showed increased levels of total cholesterol, very-low and low-density lipoprotein (VLDL + LDL) cholesterol, triglycerides and apolipoprotein B (apoB), while high-density lipoprotein (HDL) HDL cholesterol was lower. Lp(a) was significantly higher in patients (107 (95% CI: 55-208) mg/1) as compared to controls (25 (13-49) mg/1, P<0.01). Conventional antihypertensive treatment did not reduce proteinuria, while Lp(a) remained unaffected. ACE-inhibitor treatment lowered proteinuria, raised serum albumin, while La(a) tended to fall (-11 ±8%). Addition of an NSAID induced a further fall in proteinuria and a rise in serum albumin. Lp(a) now fell by 40±5% from baseline values (/) <0.01). Both serum total, HDL and VLDL + LDL cholesterol fell significantly. Finally, during subsequent single therapy with NSAID most parameters, including proteinuria and Lp(a), returned towards values obtained during single therapy with ACE inhibition. Multiple regression analysis showed a strong relation of Lp(a) with the amount of proteinuria (P = 0.001), while serum albu

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Lipoprotein(a) Levels in the Nephrotic Syndrome.

Cited by 9 publications

References 23 publications

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

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

Determination of the Serum Unbound Fraction of Tadalafil in Children with Protein-Losing Enteropathy and Its Specific Binding to Human Serum Proteins <i>in Vitro</i>

Symptomatic antiproteinuric treatment decreases serum lipoprotein (a) concentration in patients with glomerular proteinuria

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