Endocrinological Consequences of the Nephrotic Syndrome

Nd, Vaziri

doi:10.1159/000168650

Cited by 32 publications

(15 citation statements)

References 17 publications

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“…However, most of the anemic cases had renal dysfunction and the causation seems inconclusive. The subsequent work by the same group has shown impaired biosynthesis of erythropoietin as well as the urinary loss in experimen tal NS [9,10]. The data obtained from our case are in agreement with these reports in the sense that plasma erythropoietin is inappropriately low in NS patients with anemia.…”

Section: Discussionsupporting

confidence: 92%

Successful Erythropoietin Treatment for Severe Anemia in Nephrotic Syndrome without Renal Dysfunction

Ishimitsu

Ono²,

Sugiyama³

et al. 1996

Nephron

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A 62-year-old woman presented with nephrotic syndrome and severe anemia although the renal function was not impaired. Renal biopsy revealed the histology of membranoproliferative glomerulonephritis, and the proteinuria was resistant to steroid therapy. Iron deficiency, bleeding and other causes of anemia were ruled out, however, her serum erythropoietin level was inappropriately low. The anemia was rapidly corrected by administration of recombinant human erythropoietin. It is suggested that inappropriately low erythropoietin level, in part at least, accounts for the anemia in nephrotic syndrome. It is proposed that erythropoietin therapy should be taken into consideration for severe anemia in nephrotic syndrome even when the renal function is not impaired.

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Section: Discussionsupporting

confidence: 92%

Successful Erythropoietin Treatment for Severe Anemia in Nephrotic Syndrome without Renal Dysfunction

Ishimitsu

Ono²,

Sugiyama³

et al. 1996

Nephron

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“…The presence of nephrotic syndrome may contribute to reduce the Epo production [16][17][18][19][20]. This possibility was excluded in the present group of FAP patients by the finding of similar values in patients with or without proteinuria.…”

Section: Discussionmentioning

confidence: 78%

Kidney and anemia in familial amyloidosis type I

Beirão¹,

Lobato²,

Costa³

et al. 2004

Kidney International

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“…Although the cause of this disorder has not been completely defined, low testos terone levels associated to high gonadotropin secretion suggest a primary defect in the response of the Leydig cell to pituitary stimulation. Moreover, in nephrotic patients, this deficit might be aggravated by increased urinary losses of testosterone along with the sex-hormone-binding protein [17,18], In our patients, although the cumulative cyclophosphamide amount was low and a 6-month period had elapsed between cyclophosphamide withdrawal and hormone studies, increased baseline FSH levels could still be due to the effect of this drug. However, since the toxic effect of cyclophosphamide on the testes is specific for the germinal epithelium [19], low testosterone levels could not be attributed to the cyclophosphamide effect.…”

Section: Discussionmentioning

confidence: 73%

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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Endocrinological Consequences of the Nephrotic Syndrome

Cited by 32 publications

References 17 publications

Successful Erythropoietin Treatment for Severe Anemia in Nephrotic Syndrome without Renal Dysfunction

Successful Erythropoietin Treatment for Severe Anemia in Nephrotic Syndrome without Renal Dysfunction

Kidney and anemia in familial amyloidosis type I

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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