scholarly journals Lipoprotein(a) in the Nephrotic Syndrome

2000 ◽  
Vol 11 (3) ◽  
pp. 507-513
Author(s):  
CHANTAL DOUCET ◽  
VINCENT MOOSER ◽  
SOPHIE GONBERT ◽  
FRANÇOISE RAYMOND ◽  
JOHN CHAPMAN ◽  
...  
Keyword(s):  
Nephrotic Syndrome ◽  
Plasma Concentrations ◽  
Lipoprotein A ◽  
Control Subjects ◽  
Large N ◽  
Catabolic Rate ◽  
Atherogenic Particle ◽  
Normal Urine ◽  
And Control

Abstract. Plasma levels of lipoprotein(a) (Lp(a)), an atherogenic particle, are elevated in kidney disease, which suggests a role of this organ in the metabolism of Lp(a). Additional evidence for a role of the kidney in the clearance of Lp(a) is provided by the fact that circulating N-terminal fragments of apolipoprotein(a) (apo(a)) are processed and eliminated by the renal route. To further understand the mechanism underlying such renal excretion, the levels of apo(a) fragments in plasma and urine relative to plasma Lp(a) levels were determined in patients with nephrotic syndrome (n = 15). In plasma, the absolute (24.7 ± 20.4 versus 2.16 ± 2.99 μg/ml, P < 0.0001) as well as the relative amounts of apo(a) fragments (4.6 ± 3.4% versus 2.1 ± 3.3% of total Lp(a), P < 0.0001) were significantly elevated in nephrotic patients compared with a control, normolipidemic population. In addition, urinary apo(a) excretion in patients with nephrotic syndrome was markedly elevated compared with that in control subjects (578 ± 622 versus 27.7 ± 44 ng/ml per mg creatinine, P < 0.001). However, the fractional catabolic rates of apo(a) fragments were similar in both groups (0.68 ± 0.67% and 0.62 ± 0.47% in nephrotic and control subjects, respectively), suggesting that increased plasma concentrations of apo(a) fragments in nephrotic subjects are more dependent on the rate of synthesis rather than on the catabolic rate. Molecular analysis of apo(a) immunoreactive material in urine revealed that the patterns of apo(a) fragments in nephrotic patients were distinct from those of control subjects. Full-length apo(a), large N-terminal apo(a) fragments similar in size to those present in plasma, as well as C-terminal fragments of apo(a) were detected in urine from nephrotic patients but not in urine from controls. All of these apo(a) forms were in addition to smaller N-terminal apo(a) fragments present in normal urine. This study also demonstrated the presence of Lp(a) in urine from nephrotic patients by ultracentrifugal fractionation. These data suggest that in nephrotic syndrome, Lp(a) and large fragments of apo(a) are passively filtered by the kidney through the glomerulus, whereas smaller apo(a) fragments are secreted into the urine.

Evidence for increased synthesis of lipoprotein(a) in the nephrotic syndrome.

1998 ◽  
Vol 9 (8) ◽  
pp. 1474-1481
Author(s):  
M G De Sain-Van Der Velden ◽  
D J Reijngoud ◽  
G A Kaysen ◽  
M M Gadellaa ◽  
H Voorbij ◽  
...  
Keyword(s):  
Nephrotic Syndrome ◽  
Synthesis Rate ◽  
Fractional Synthesis Rate ◽  
Lipoprotein A ◽  
Control Subjects ◽  
Apolipoprotein A ◽  
Catabolic Rate ◽  
Fractional Synthesis ◽  
The Mean

In patients with the nephrotic syndrome, markedly increased levels of lipoprotein(a) (Lp(a)) concentration have been frequently reported, and it has been suggested that this may contribute to the increased cardiovascular risk in these patients. The mechanism, however, is not clear. In the present study, in vivo fractional synthesis rate of Lp(a) was measured using incorporation of the stable isotope 13C valine. Under steady-state conditions, fractional synthesis rate equals fractional catabolic rate (FCR). FCR of Lp(a) was estimated in five patients with the nephrotic syndrome and compared with five control subjects. The mean plasma Lp(a) concentration in the patients (1749+/-612 mg/L) was higher than in control subjects (553+/-96 mg/L). Two patients were heterozygous for apolipoprotein(a) (range, 19 to 30 kringle IV domains), whereas all control subjects were each homozygous with regard to apolipoprotein(a) phenotype (range, 18 to 28 kringle IV domains). The FCR of Lp(a) was comparable between control subjects (0.072+/-0.032 pools/d) and patients (0.064+/-0.029 pools/d) despite the wide variance in plasma concentration. This suggests that differences in Lp(a) levels are caused by differences in synthesis rate. Indeed, the absolute synthetic rate of Lp(a) correlated directly with plasma Lp(a) concentration (P < 0.0001) in all subjects. The present results demonstrate that increased synthesis, rather than decreased catabolism, causes elevated plasma Lp(a) concentrations in the nephrotic syndrome.

Temperature, Mitochondria, and Reye's Syndrome

PEDIATRICS ◽  
1983 ◽  
Vol 71 (6) ◽  
pp. 985-986
Author(s):  
R. DON BROWN ◽  
JOHN T. WILSON
Keyword(s):  
Mitochondrial Damage ◽  
Reye's Syndrome ◽  
Enhancing Effect ◽  
Control Subjects ◽  
Epidemiologic Data ◽  
Higher Temperature ◽  
And Control

In Reply.— El-Mallakh raises hypothetical questions about an enhancing effect of fever on mitochondrial damage associated with Reye's syndrome. Our article on aspirin and Reye's syndrome1 emphasized the role of prodromal illness in use of aspirin. Fever was only one of several [See table in the PDF] prodormal illness events that were different in patients as compared with control subjects. Results of our analysis of the epidemiologic data from the Ohio study reveal a statistically significant higher temperature in those children which Reye's syndrome as compared with unmatched control subjects (Table) as well as in patients and control subjects matched for record temperatures.1

Taurine transport in epilepsy.

1980 ◽  
Vol 26 (3) ◽  
pp. 414-419 ◽  
Author(s):  
H O Goodman ◽  
B M Connolly ◽  
W McLean ◽  
M Resnick
Keyword(s):  
Genetic Control ◽  
Plasma Concentrations ◽  
Taurine Transport ◽  
Taurine Concentration ◽  
Control Subjects ◽  
Principal Finding ◽  
Idiopathic Epilepsies ◽  
And Control

Abstract Previous studies of plasma taurine concentrations in epileptics have yielded equivocal results. We measured plasma and urinary taurine in 41 epileptic and 68 control subjects and found plasma concentrations among epileptics to be comparable in general to those of controls, but that two or three classes of plasma taurine concentrations, possibly genetically regulated, occur in both epileptic and control subjects. Our previous studies and data from the present study on taurine excretion revealed three excretion classes under genetic control. The principal finding is that epileptics include disproportionate numbers of low excretors (high reabsorbers), who are presumptive homozygotes for the allele effecting higher reabsorption. If confirmed, these findings suggest that the transport of taurine, rather than absolute taurine concentration, may explain the efficacy of taurine administration in some epileptics but not in others. The locus involved may be one component in the polygenic diathesis to the idiopathic epilepsies.

scholarly journals Lipoprotein (a) level as a risk factor for stroke and its subtype: A systematic review and meta-analysis

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Pradeep Kumar ◽  
Priyanka Swarnkar ◽  
Shubham Misra ◽  
Manabesh Nath
Keyword(s):  
Systematic Review ◽  
Risk Factor ◽  
Meta Analysis ◽  
Predictive Marker ◽  
Large Artery ◽  
Lipoprotein A ◽  
Control Subjects ◽  
Toast Classification ◽  
Subtype A

AbstractThe role of lipoprotein-A [Lp (a)] as a risk factor for stroke is less well documented than for coronary heart disease. Hence, we conducted a systematic review and meta-analysis for the published observational studies in order to investigate the association of Lp (a) levels with the risk of stroke and its subtypes. In our meta-analysis, 41 studies involving 7874 ischemic stroke (IS) patients and 32,138 controls; 13 studies for the IS subtypes based on TOAST classification and 7 studies with 871 Intracerebral hemorrhage (ICH) cases and 2865 control subjects were included. A significant association between increased levels of Lp (a) and risk of IS as compared to control subjects was observed (standardized mean difference (SMD) 0.76; 95% confidence interval (CIs) 0.53–0.99). Lp (a) levels were also found to be significantly associated with the risk of large artery atherosclerosis (LAA) subtype of IS (SMD 0.68; 95% CI 0.01–1.34) as well as significantly associated with the risk of ICH (SMD 0.65; 95% CI 0.13–1.17) as compared to controls. Increased Lp (a) levels could be considered as a predictive marker for identifying individuals who are at risk of developing IS, LAA and ICH.

Abstract 236: Lipoprotein Metabolism in APOB L343V Familial Hypobetalipoproteinemia

2014 ◽  
Vol 34 (suppl_1) ◽  
Author(s):  
Amanda J Hooper ◽  
Ken Robertson ◽  
Liesl V Heeks ◽  
Danie Champain ◽  
P Hugh R Barrett ◽  
...  
Keyword(s):  
Plasma Concentrations ◽  
Area Under The Curve ◽  
Lipoprotein Metabolism ◽  
Compartmental Modeling ◽  
Apo B ◽  
Control Subjects ◽  
Modeling Analysis ◽  
Catabolic Rate ◽  
Postprandial Lipoprotein ◽  
Familial Hypobetalipoproteinemia

Familial hypobetalipoproteinemia (FHBL) is a codominant disorder of lipoprotein metabolism characterized by decreased plasma concentrations of LDL-cholesterol and apolipoprotein (apo) B. We examined the effect of heterozygous APOB L343V FHBL on fasting and postprandial lipoprotein metabolism. VLDL, IDL-, and LDL-apoB kinetics were determined in the fasting state using stable isotope methods and compartmental modeling. VLDL-apoB concentrations in FHBL subjects (n=2) were reduced by more than 75% compared to healthy, normolipidemic control subjects ( P <0.01). VLDL-apoB fractional catabolic rate (FCR) was more than 5-fold higher in the FHBL subjects ( P =0.07). ApoB production rates and IDL- and LDL-apoB FCRs were not different between FHBL subjects and controls. To assess postprandial lipoprotein metabolism, a standardized oral fat load was given after a 12 h fast to heterozygous APOB L343V FHBL subjects (n=3) and normolipidemic controls. The postprandial incremental area under the curve (0-10 h) in FHBL subjects was decreased for large TRL-triglyceride (-77%; P <0.0001), small TRL-cholesterol (-83%; P <0.001), small TRL-triglyceride (-88%; P <0.0.001) and plasma apoB (-63%; P <0.0001) compared with controls. Compartmental modeling analysis showed that apoB-48 production was decreased (-91%; P <0.05) compared with controls. We conclude that when compared to controls, APOB L343V FHBL heterozygotes show decreased TRL production with normal postprandial TRL particle clearance. In contrast, VLDL-apoB production was normal, while the FCR was higher in heterozygotes compared with lean control subjects. These mechanisms account for the marked hypolipidemic state observed in these FHBL subjects.

scholarly journals Production of Interferons and β-Chemokines by Placental Trophoblasts of HIV-1-Infected Women

2001 ◽  
Vol 9 (2) ◽  
pp. 95-104 ◽  
Author(s):  
Bang-Ning Lee ◽  
Hunter Hammill ◽  
Edwina J. Popek ◽  
Stanley Cron ◽  
Claudia Kozinetz ◽  
...  
Keyword(s):  
Enzyme Linked Immunosorbent Assay ◽  
Control Subjects ◽  
Trophoblastic Cells ◽  
Inflammatory Protein ◽  
Β Protein ◽  
Immunodeficiency Virus ◽  
Vertical Transmission Of Hiv ◽  
And Control ◽  
Hiv 1

Objective:The mechanism whereby the placental cells of a human immunodeficiency virus (HIV)-1-infected mother protect the fetus from HIV-1 infection is unclear. Interferons (IFNs) inhibit the replication of viruses by acting at various stages of the life cycle and may play a role in protecting against vertical transmission of HIV-1. In addition the β-chemokines RANTES (regulated on activation T cell expressed and secreted), macrophage inflammatory protein-1-α (MIP-1α), and MIP-1β can block HIV-1 entry into cells by preventing the binding of the macrophage-trophic HIV-1 strains to the coreceptorCCR5. In this study the production of IFNs and β-chemokines by placental trophoblasts of HIV-1-infected women who were HIV-1 non-transmitters was examined.Methods:Placental trophoblastic cells were isolated from 29 HIV-1-infected and 10 control subjects. Supernatants of trophoblast cultures were tested for the production of IFNs and β-chemokines by enzyme linked immunosorbent assay (ELISA). Additionally, HIV-1-gag and IFN-β transcripts were determined by a semi-quantitative reverse transcription polymerase chain reaction (RT-PCR) assay.Results:All placental trophoblasts of HIV-1-infected women contained HIV-1-gag transcripts. There were no statistical differences in the median constitutive levels of IFN-α and IFN-γ produced by trophoblasts of HIV-1- infected and control subjects. In contrast, trophoblasts of HIV-1-infected women constitutively produced significantly higher levels of IFN-β protein than trophoblasts of control subjects. Furthermore, the median levels of β-chemokines produced by trophoblasts of HIV-infected and control women were similar.Conclusions:Since there was no correlation between the placental HIV load and the production of interferons or β-chemokines, the role of trophoblast-derived IFNs and β-chemokines in protecting the fetus from infection with HIV-1 is not clear.

The Role of the False Neurotransmitter Octopamine in the Hypotension of Fulminant Hepatic Failure

1977 ◽  
Vol 52 (3) ◽  
pp. 305-310 ◽  
Author(s):  
P. N. Trewby ◽  
R. A. Chase ◽  
M. Davis ◽  
R. Williams
Keyword(s):  
Cardiac Output ◽  
Fulminant Hepatic Failure ◽  
Hepatic Failure ◽  
Pressor Response ◽  
Peripheral Resistance ◽  
Control Subjects ◽  
Arteriovenous Shunts ◽  
Resting Blood Pressure ◽  
And Control

1. An investigation was carried out into the mechanism of unexplained hypotension in patients with fulminant hepatic failure. The cardiac output and peripheral resistance were compared in normotensive and hypotensive patients. In addition, the serum concentration of the false neurotransmitter octopamine and the pressor response to noradrenaline, and to the indirectly acting sympathomimetic agent tyramine, were measured in hypotensive and normotensive patients with fulminant hepatic failure and in healthy subjects. 2. The cardiac output and the peripheral resistance were decreased in the hypotensive patients, and their mean heart rate was slower than in the normotensive patients. Although the serum octopamine concentration was significantly elevated in the patients compared with the control subjects, the highest octopamine concentrations were unexpectedly found in the normotensive patients and a significant positive correlation could be demonstrated between the resting blood pressure and the serum octopamine concentration. The pressor response to tyramine and noradrenaline were similar in the hypotensive patients, the normotensive patients and control subjects. 3. These results suggest that neither increased serum concentrations of the false neurotransmitter octopamine, nor end-organ insensitivity to released noradrenaline are responsible for the hypotension. A more likely explanation is toxic depression of the vasomotor centre. The opening of peripheral arteriovenous shunts, possibly as a result of endotoxaemia, might be an additional factor.

Characteristic Plasma Hormone Changes in Alzheimer's Disease

1987 ◽  
Vol 150 (5) ◽  
pp. 674-681 ◽  
Author(s):  
J. E. Christie ◽  
L. J. Whalley ◽  
J. Bennie ◽  
H. Dick ◽  
I. M. Blackburn ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Plasma Concentrations ◽  
High Plasma ◽  
Hormonal Changes ◽  
Alzheimer Type ◽  
Control Subjects ◽  
Alzheimer Type Dementia ◽  
Plasma Gh ◽  
And Control

A systematic endocrine investigation in dementia, depression and control subjects showed that plasma growth hormone (GH) was higher in the morning and plasma TSH concentrations were higher throughout the day in Alzheimer-type dementia (ATD) than in age-matched depressed patients (MDD), and plasma TSH concentrations were also higher throughout the day in female ATD compared with age-matched female control subjects. The increased plasma TSH concentrations could not be due to reduced negative feedback because plasma T3, T4 and rT3 were in the normal range. Plasma concentrations of oestrogen-stimulated neurophysin (ESN) were lower throughout the day in ATD compared with MDD and controls and lower in the morning compared with other dementias. The high plasma GH and TSH concentrations in ATD may reflect the reduced hypothalamic content of somatostatin in ATD, and the reduced concentrations of ESN may reflect reduced cholinergic activity in ATD prain. These selective hormonal changes provide a useful diagnostic test for Alzheimer's disease.

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