Treatment of Hyperlipidemia in Nephrotic Syndrome: Time for a Change?

Olbricht, Christoph J.; Koch, Karl-Martin

doi:10.1159/000187019

Cited by 17 publications

(15 citation statements)

References 35 publications

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“…This finding matches those reported by Olbricht and Koch [11]who were surprising for the high drop in TG levels in their simvastatin-treated patients when compared to placebo. The observed reduction in TG values might have been due to diminished LDL-cholesterol synthesis and as increased ratio of TG/cholesterol in VLDL [14].…”

Section: Discussionsupporting

confidence: 92%

“…The relatively small number of cases (10 cases) as well as the large dosage of fluvastatin they used might explain the earlier reduction in LDL and cholesterol they observed. Also, our observation goes hand in hand with the degree of reduction in total and LDL cholesterol reported by Olbricht and Koch [11]on using simvastatin in nephrotic patients. Todd and Goa [12]achieved a 25–30% reduction in plasma LDL within 4 weeks which was maintained with continued treatment with 20–40 mg fluvastatin daily.…”

Section: Discussionsupporting

confidence: 75%

“…Jacobson et al [18]reported an increase in liver enzymes, while Olbricht and Koch [11]and Matzkies et al [10]reported satisfactory tolerance of statin in their nephrotic patients.…”

Section: Discussionmentioning

confidence: 99%

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Impact of Treatment of Dyslipidemia on Renal Function, Fat Deposits and Scarring in Patients with Persistent Nephrotic Syndrome

Gheith

Sobh

Mohamed

et al. 2002

Nephron

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In this study 43 patients with idiopathic nephrotic syndrome were randomly distributed into 2 age- and sex-matched groups. The first group was given fluvastatin while the second was used as control. The cases in the 2 groups were evaluated clinically, biochemically (creatinine clearance, albumin, 24-hour proteinuria, and lipogram), neurologically, and histopathologically (examination of renal biopsies obtained basally and after 1 year of treatment with fluvastatin). In the fluvastatin-treated group but not in the control group, we observed a significant reduction in cholesterol, low-density lipoprotein, and triglyceride. Clinical and laboratory assessment showed satisfactory tolerance of the drug by the patients. Proteinuria, serum albumin and creatinine clearance values were significantly better in the statin-treated patients. There was no difference in glomerular sclerosis between the 2 groups while interstitial fibrosis and renal fat deposits were less in the statin-treated group. The reduction in renal fat deposits in the statin-treated group was highly significant, while that of interstitial fibrosis was not. We conclude that: (1) statin can be safely and effectively used in the treatment of dyslipidemia in patients with persistent idiopathic nephrotic syndrome; (2) control of dyslipidemia in nephrotic patients is associated with better control of proteinuria and creatinine clearance; (3) statin treatment may cause regression of renal fat deposits in patients with nephrotic syndrome, and (4) longer term studies are still required to study further possible beneficial effects on renal histology and disease progression.

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Section: Discussionsupporting

confidence: 92%

Section: Discussionsupporting

confidence: 75%

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Impact of Treatment of Dyslipidemia on Renal Function, Fat Deposits and Scarring in Patients with Persistent Nephrotic Syndrome

Gheith

Sobh

Mohamed

et al. 2002

Nephron

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“…Dear Sir, Several recent reports have focused atten tion on the efficacy of the HMG-CoA reduc tase inhibitor drugs (lovastatin, simvastatin), reducing the hyperlipidemia associated with persistent nephrotic syndrome (NS) [1][2][3][4][5][6]. The experience is, however, still limited to a small number of patients and to short-term treat ment.…”

Section: Rem Ission Of Nephrotic Syndrom E On Lovastatin Treatm Entmentioning

confidence: 99%

Remission of Nephrotic Syndrome on Lovastatin Treatment

Gonzalo

Pascual

Mampaso

et al. 1994

Nephron

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“…However, in later studies, both gonadal and adrenal functions have been shown to be preserved in these patients [2][3][4][5], In recent years, there has been great interest in treating the disorders of lipid metabolism from which some patients with chronic renal failure suffer, with P-hydroxyl-(3-methylglutaryl-CoA re ductase inhibitors as such treatment may either facilitate the prevention of the associated atheromatous vascular disease or slow down the progressive course of chronic renal failure [6][7][8], However, hyperlipidemic patients with chronic renal failure have impaired LDL uptake both in hepatic and extrahepatic tissues [9][10][11], Likewise, they may suffer from a primary defect in testosterone syn thesis by the Leydig cells and a primary defect of adrenal function [12][13][14]. Since lovastatin inhibits de novo cellu lar synthesis of cholesterol, it may further reduce the amount of cholesterol available for steroid synthesis and, in this way, aggravate the deficit in steroid hormone in these patients.…”

Section: Introductionmentioning

confidence: 99%

Prospective Case Control Study to Determine the Effect of Lovastatin on Serum Testosterone and Cortisol Concentrations in Hyperlipidemic Nephrotic Patients with Chronic Renal Failure

Segarra

Chacón²,

Vilardell³

et al. 1996

Nephron

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In order to investigate the effects of lovastatin on adrenal and gonadal function, we prospectively determined the basal and gonadorelin-stimulated concentrations of testosterone, follicle-stimulating hormone (FSH) and luteiniz-ing hormone (LH) and the cortisol response to adrenocorticotropic hormone (ACTH) in a sample of 25 male patients with advanced chronic renal failure, hypercholesterolemia and proteinuria. Hormone studies were done prior to and after lovastatin treatment. The values of these patients were compared with those of a matched healthy control group. Before starting treatment with lovastatin, the patients showed significantly lower testosterone concentration and higher LH concentration than the control group. After stimulation with gonadorelin, they also showed a lower increase in testosterone and LH. After 12 months of lovastatin treatment, a significant decrease in the concentration of cholesterol, LDL C, VLDL C and apo B was observed, but neither the basal testosterone concentration nor the response to gonadorelin stimulation was modified. Before treatment, basal and ACTH-stimulated serum cortisol levels did not differ from those of the control group. After lovastatin treatment, neither the basal serum cortisol levels nor the response to ACTH was modified. We conclude that in the patients studied, although the decrease in testosterone concentration may be partially attributable to a decrease in its synthesis, lovastatin treatment does not increase testosterone deficit. This is either because this drug does not inhibit gonadal hydroxymethylglutaryl CoA reductase at the dose given or because the cholesterol which LDL C provides the cell with is enough to maintain testosterone synthesis.

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Treatment of Hyperlipidemia in Nephrotic Syndrome: Time for a Change?

Cited by 17 publications

References 35 publications

Impact of Treatment of Dyslipidemia on Renal Function, Fat Deposits and Scarring in Patients with Persistent Nephrotic Syndrome

Impact of Treatment of Dyslipidemia on Renal Function, Fat Deposits and Scarring in Patients with Persistent Nephrotic Syndrome

Remission of Nephrotic Syndrome on Lovastatin Treatment

Prospective Case Control Study to Determine the Effect of Lovastatin on Serum Testosterone and Cortisol Concentrations in Hyperlipidemic Nephrotic Patients with Chronic Renal Failure

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