scholarly journals A case of nephrotic syndrome due to IgA nephropathy complicated by acute renal failure and ameriolated by low density lipoprotein(LDL) apheresis.

1994 ◽  
Vol 27 (3) ◽  
pp. 233-236 ◽  
Author(s):  
Tetsuo Shibata ◽  
Eiji Okabe ◽  
Akihiro Sumie ◽  
Takanori Ishii ◽  
Tadashi Tomo ◽  
...  
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Nephrotic Syndrome ◽  
Iga Nephropathy ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Low Density ◽  
Ldl Apheresis

scholarly journals Preoperative Low-Density Lipoprotein Apheresis for Preventing Recurrence of Focal Segmental Glomerulosclerosis after Kidney Transplantation

2018 ◽  
Vol 2018 ◽  
pp. 1-5 ◽  
Author(s):  
Akihito Sannomiya ◽  
Toru Murakami ◽  
Ichiro Koyama ◽  
Kosaku Nitta ◽  
Ichiro Nakajima ◽  
...  
Keyword(s):  
Renal Failure ◽  
Kidney Transplantation ◽  
Focal Segmental Glomerulosclerosis ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Low Density ◽  
Ldl Apheresis ◽  
Segmental Glomerulosclerosis ◽  
Living Related ◽  
Observation Period

Background. Focal segmental glomerulosclerosis (FSGS) often develops rapidly and frequently progresses to renal failure, while the recurrence rate after kidney transplantation is 20–50%. We performed low-density lipoprotein (LDL) apheresis before kidney transplantation in FSGS patients to prevent recurrence. Methods. Five adult patients with chronic renal failure due to FSGS undergoing living related donor kidney transplantation were investigated retrospectively. LDL apheresis was done 1-2 times before transplantation. Postoperative renal function and recurrence of FSGS were assessed. Results. The patients were two men and three women aged 24 to 41 years. The observation period ranged from 60 days to 22 months. Preoperative LDL apheresis was performed once in one patient and twice in four patients. Blood LDL cholesterol levels were normal before LDL apheresis and remained normal both after LDL apheresis and after kidney transplantation. Additional LDL apheresis was performed once in one patient with mild proteinuria after transplantation. The renal graft survived in all patients and there was no evidence of recurrent FSGS. Conclusions. Although the observation period was short, FSGS did not recur in all 5 patients receiving preoperative LDL apheresis. These results suggest that LDL apheresis can be effective in preventing recurrence of FSGS after kidney transplantation.

Low density lipoprotein metabolism in rats with puromycin aminonucleoside-induced nephrotic syndrome

Metabolism ◽  
1989 ◽  
Vol 38 (5) ◽  
pp. 491-495 ◽  
Author(s):  
J. Joven ◽  
L. Masana ◽  
C. Villabona ◽  
E. Vilella ◽  
T. Bargalló ◽  
...  
Keyword(s):  
Nephrotic Syndrome ◽  
Low Density Lipoprotein ◽  
Lipoprotein Metabolism ◽  
Density Lipoprotein ◽  
Low Density ◽  
Puromycin Aminonucleoside

scholarly journals Markedly Increased Small Dense Low-Density Lipoprotein During Acute Phase in Childhood and Adolescent Nephrotic Syndrome

2020 ◽  
Author(s):  
Keisuke Sugimoto ◽  
Kohei Miyazaki ◽  
Takuji Enya ◽  
Tomoki Miyazawa ◽  
Yuichi Morimoto ◽  
...  
Keyword(s):  
Nephrotic Syndrome ◽  
Acute Phase ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Lipid Profiles ◽  
Atherogenic Index ◽  
Childhood And Adolescence ◽  
Low Density ◽  
Ldl Particles ◽  
Initial Onset

Abstract Background: Hyperlipidemia is an important characteristic feature of idiopathic nephrotic syndrome (NS) in children. This study was conducted to examine the lipid profiles, including small dense low-density lipoprotein (sdLDL-C), in childhood-onset NS.Methods: This retrospective study enrolled patients diagnosed with initial-onset NS in childhood and adolescence. Study parameters included lipid profiles. The “alternative LDL window” comprises the number and sizes of LDL particles estimated according to non-HDL-C and TG levels.Results: A total of 39 patients were enrolled who exhibited markedly increased lipid abnormalities, including TC, TG, LDL-C, and non-HDL-C levels (TC, 409.7 TC, TG, and sizes of LDL particles estimated as non-HDL-C, 332.3). Of the 39 patients, 32 (82%) were categorized in the area of hyper-TG/-non-HDL levels, which is considered as sdLDL. A positive correlation was found between non-HDL-C and TC (r = 0.96, P < 0.001), TG (r = 0.38, P = 0.018), LDL-C (r = 0.84, P < 0.001), TC/HDL (r = 0.53, P < 0.001), and atherogenic index of plasma (r = 0.42, P = 0.008).Conclusions: Our study demonstrated markedly increased lipid profiles during the acute phase of NS. Evaluation of lipid profiles using the “alternative LDL window” may help understand the state of hyperlipidemia in NS.

Changes in Bradykinin and Prostaglandins Plasma Levels during Dextran-sulfate Low-density-lipoprotein Apheresis

1997 ◽  
Vol 20 (3) ◽  
pp. 178-183 ◽  
Author(s):  
S. Kojima ◽  
M. Ogi ◽  
Y. Yoshitomi ◽  
M. Kuramochi ◽  
J. Ikeda ◽  
...  
Keyword(s):  
Plasma Levels ◽  
Dextran Sulfate ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Guanosine Monophosphate ◽  
Prostaglandin E ◽  
Plasma Kallikrein ◽  
Low Density ◽  
Ldl Apheresis

The negative charges of dextran-sulfate (DS) used for low-density-lipoprotein (LDL) apheresis initiate the intrinsic coagulation pathway in which plasma kallikrein acts on the high-molecular-weight kininogen to produce large amounts of bradykinin. This study was undertaken to assess whether bradykinin generated during DS LDL apheresis has any physiologic effects in vivo. The plasma levels of bradykinin, prostaglandins and cyclic guanosine monophosphate (cGMP) were compared, when either of two anticoagulants, heparin or nafamostat mesilate (NM), was used during DS LDL apheresis. Although anticoagulative action by NM depends on the inhibition of thrombin activity, this substance also inhibits the activity of plasma kallikrein. During apheresis using heparin, the plasma levels of prostaglandin E2 (PGE2) increased significantly (5.6 ± 1.2 (mean ± SE, n=4) pg/ml before apheresis and 33.4 ± 13.2 after apheresis, p < 0.05) in association with an increase in bradykinin levels (17.9 ± 2.6 pg/ml before apheresis and 470 ± 135 after apheresis, p < 0.01). Interestingly, these changes were suppressed during apheresis using NM. There were no appreciable changes in cGMP during DS LDL apheresis with either of the anticoagulants. This finding suggests that bradykinin generated during apheresis has some pathophysiological effects via activation of the prostaglandin system. Our results support the view that in patients taking angiotensin-convertingenzyme inhibitors, the anaphylactoid reaction occurring during apheresis may be caused by an excessive rise in the bradykinin levels.

Upregulation of lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) in endothelial cells by nitric oxide deficiency

2004 ◽  
Vol 287 (1) ◽  
pp. F25-F32 ◽  
Author(s):  
I. V. Smirnova ◽  
T. Sawamura ◽  
M. S. Goligorsky
Keyword(s):  
Nitric Oxide ◽  
Renal Failure ◽  
Endothelial Cells ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Common Denominator ◽  
Low Density ◽  
Lipoprotein Receptor ◽  
Low Density Lipoprotein Receptor ◽  
Density Lipoprotein Receptor

Endothelial cell dysfunction (ECD) is emerging as a common denominator for diverse cardiovascular abnormalities associated with inhibition of endothelial nitric oxide (NO) synthase (eNOS). Elevated levels of asymmetric dimethylarginine (ADMA), a potent eNOS inhibitor, are common in renal failure and may contribute to ECD. Through DNA microarray screening of genes modulated in human umbilical vein endothelial cells (HUVEC) by NG-nitro-l-arginine methyl ester (l-NAME), we found a 1.8-fold increase in low-density lipoprotein receptor-1 (LOX-1) expression. LOX-1 is a major endothelial receptor for oxidized low-density lipoproteins (OxLDL) and is assumed to play a role in the initiation and progression of atherosclerosis. Here, we confirmed the upregulation of LOX-1 mRNA and protein level by quantitative RT-PCR and Western blot analysis. Increased expression of LOX-1 was associated with the accumulation of DiI-labeled OxLDL (DiI-OxLDL) in ADMA- and l-NAME-pretreated HUVEC. To evaluate the contribution of LOX-1 in ADMA-induced accumulation of OxLDL by HUVEC, we used the competitive receptor inhibitor, soluble LOX-1. Treatment of HUVEC with soluble LOX-1 was associated with an approximately two- to threefold inhibition of DiI-OxLDL uptake in l-NAME- or ADMA-treated HUVEC. In conclusion, ADMA- or l-NAME-induced NO deficiency leads to the increased expression of LOX-1 mRNA and protein in HUVEC, which in turn results in the accumulation of OxLDL. Competition with LOX-1-soluble extracellular domain reduces OxLDL accumulation. In summary, elevated ADMA levels, i.e., in patients with renal failure, may be responsible for endothelial accumulation of OxLDL via upregulated LOX-1 receptor, thus contributing to endothelial lipidosis and dysfunction.

Low-density lipoprotein (LDL) oxidizability before and after LDL apheresis

Metabolism ◽  
1999 ◽  
Vol 48 (7) ◽  
pp. 881-886 ◽  
Author(s):  
Markus G. Donner ◽  
Klaus G. Parhofer ◽  
Werner O. Richter ◽  
Peter Schwandt
Keyword(s):  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Low Density ◽  
Ldl Apheresis ◽  
Before And After

Oxidized Low-Density Lipoprotein Biomarkers in Patients with End-Stage Renal Failure: Acute Effects of Hemodialysis

2007 ◽  
Vol 25 (5-6) ◽  
pp. 457-465 ◽  
Author(s):  
Maurizio Bossola ◽  
Luigi Tazza ◽  
Esther Merki ◽  
Stefania Giungi ◽  
Giovanna Luciani ◽  
...  
Keyword(s):  
Renal Failure ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Low Density ◽  
Acute Effects ◽  
Oxidized Low Density Lipoprotein ◽  
End Stage Renal Failure ◽  
End Stage

Urinary Neopterin and Microalbuminuria in Patients Treated by Low-density Lipoprotein Apheresis

Pteridines ◽  
2005 ◽  
Vol 16 (4) ◽  
pp. 174-183 ◽  
Author(s):  
Melanie Cermanová ◽  
Bohuslav Melichar ◽  
Dagmar Solichová ◽  
Milan Bláha ◽  
Vladimir Bláha ◽  
...  
Keyword(s):  
Ldl Cholesterol ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Atheromatous Plaque ◽  
Specific Marker ◽  
Low Density ◽  
Creatinine Ratio ◽  
Ldl Apheresis ◽  
Urinary Neopterin ◽  
Lipoprotein Disorders

Abstract Low-density lipoprotein (LDL)-apheresis is a method of extracorporeal elimination of LDL-cholesterol in patients with severe primary lipoprotein disorders. LDL-cholesterol activates macrophages, which play an important role in atheromatous plaque formation. In the present study, we have investigated urinary neopterin, a specific marker of macrophage activation and microalbuminuria, an indicator of generalized vascular dysfunction, after a single LDL-apheresis procedure in 10 patients with severe primary lipoprotein disorder. The urinary neopterin/creatinine ratio was increased in patients compared to controls. No significant changes of the neopterin/creatinine and albumin/creatinine ratios were observed after LDL-apheresis, except a significant (p < 0.006) decrease of urinary neopterin/creatinine ratio in the evening after the apheresis. This decrease showed significant negative correlation with the pre-apheretic levels of atherogenic cholesterol fractions (p < 0.05) and with cholesterol decrease during the apheresis (p < 0.05). Urinary albumin/creatinine ratio correlated positively with total and LDL-cholesterol levels before the apheresis and with the evening urinary neopterin/creatinine ratio after the apheresis, but did not correlate with glycemia and triacylglycerides. Elevated urinary neopterin in the patients with severe primary lipoprotein disorders reflects the presence of atherosclerosis. A single LDL-apheresis procedure did not significantly affect microalbuminuria. The decrease of urinary neopterin in the evening after the apheresis corresponds with the diurnal rhythm of neopterin excretion and was less pronounced in patients with more severe hypercholesterolemia. The correlations between microalbuminuria, neopterin and pre-apheretic cholesterol concentrations indicate a possible connection between microvascular dysfunction, macrophage activity and severity of hyperlipidemia, but these results should be interpreted with caution because of small number of subjects evaluated.

Sign in / Sign up

Export Citation Format

Share Document