Complete Remission of the Nephrotic Syndrome due to Focal Glomerular Sclerosis Achieved with Low Density Lipoprotein Adsorption Alone

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.

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Rituximab-Resistant Nephrotic Syndrome With Successful Induction of Remission by Low-Density Lipoprotein Apheresis

Therapeutic Apheresis and Dialysis ◽

10.1111/1744-9987.12561 ◽

2017 ◽

Vol 21 (3) ◽

pp. 295-296 ◽

Cited By ~ 4

Author(s):

Hiroyuki Suzuki ◽

Tatsuo Tsukamoto ◽

Eri Muso

Keyword(s):

Nephrotic Syndrome ◽

Low Density Lipoprotein ◽

Density Lipoprotein ◽

Low Density ◽

Lipoprotein Apheresis ◽

Successful Induction

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Effect of simvastatin on plasma lipid and lipoprotein concentrations and low-density lipoprotein metabolism in the nephrotic syndrome

Clinical Science ◽

10.1042/cs0820701 ◽

1992 ◽

Vol 82 (6) ◽

pp. 701-708 ◽

Cited By ~ 15

Author(s):

G. L. Warwick ◽

C. J. Packard ◽

L. Murray ◽

D. Grierson ◽

J. P. Stewart ◽

...

Keyword(s):

Nephrotic Syndrome ◽

Apolipoprotein B ◽

Cholesterol Synthesis ◽

Low Density Lipoprotein ◽

Plasma Lipid ◽

Lipoprotein Metabolism ◽

Density Lipoprotein ◽

Cholesterol Concentration ◽

Low Density ◽

Coa Reductase

1. The effect of inhibiting the rate-limiting enzyme (3-hydroxy-3-methylglutaryl-CoA reductase, EC 1.1.1.88) in cholesterol synthesis on plasma lipid and lipoprotein concentrations was investigated in 16 patients with primary glomerular disease, heavy proteinuria, well-preserved renal function and hypercholesterolaemia. 2. Detailed studies of low-density lipoprotein metabolism were performed on eight patients before and after 12 weeks of simvastatin therapy. Radioiodinated tracers were used to quantify the fractional catabolic rate of low-density lipoprotein by apolipoprotein B/E receptors and alternative pathways. 3. Simvastatin produced consistent reductions in total plasma cholesterol concentration (median 36.9%), plasma low-density lipoprotein-cholesterol concentration (43.6%) and apolipoprotein B pool size (29.9%). 4. In contrast, the changes in kinetic parameters of low-density lipoprotein metabolism showed no clear pattern. Although an increase in the receptor-mediated catabolism of low-density lipoprotein was demonstrated in five patients, no change or a slight decrease was seen in three patients. Production rates were not significantly altered, although there was a slight decrease in the median value (from 12.4 to 9.7 mg day−1 kg−1). Plasma lathosterol concentration was reduced in all eight patients (range 34–71%), indirectly confirming significant inhibition of cholesterol synthesis. 5. These results suggest that, as in patients with primary moderate hyperlipidaemia, the significant cholesterol-lowering effect of 3-hydroxy-3-methylglutaryl-CoA reductase inhibitors in the nephrotic syndrome is accompanied by variable changes in lipoprotein metabolism. The reasons for this heterogeneous response are unclear. This reflects our limited understanding of the metabolic basis of nephrotic hyperlipidaemia and the relationship between hepatic sterol synthesis and plasma lipoprotein kinetics.

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