title: No effect of fluvastatin on the bone mineral density of children with minimal change glomerulonephritis and some focal mesangial cell proliferation, other than an ameliorating effect on their proteinuria.
abstract: OBJECTIVE
  There are conflicting data regarding the clinical benefit of the effect of HMG-CoA reductase inhibitors (statins) in osteoporosis. We have reported that fluvastatin (a statin) is effective in improving proteinuria and renal function in childhood IgA nephropathy with mild histological findings and moderate proteinuria. The aim of the present study was to clarify the effect of fluvastatin on the bone mineral density, bone metabolic markers, proteinuria, and renal function of children with minimal change glomerulonephritis with some focal mesangial cell proliferation whose glomeruli did not stain positive for IgA and on moderate proteinuria.
  
  
  METHODS
  We conducted a prospective controlled study of 36 children who had recently been diagnosed with normocholesterolemic minimal change glomerulonephritis with some focal mesangial cell proliferation and moderate proteinuria, and in whom strenuous exercise was restricted. The 36 patients were randomly assigned to receive 20 mg of fluvastatin (group 1) or 5 mg/kg of dipyridamole (group 2) for two years.
  
  
  RESULTS
  By the end of the trial, there was no difference in BMD between the groups, and there were no changes in the four bone metabolic parameters. However, the urinary protein, hematuria and BUN levels had significantly decreased in group 1 compared to baseline, and the serum total protein and albumin levels and creatinine clearance had significantly increased in group 1 compared to baseline and group 2.
  
  
  CONCLUSIONS
  The results of this study suggest that fluvastatin therapy has an antiproteinuric effect and improves renal function in moderately proteinuric patients with mild histological glomerulonephritis, but does not increase BMD.
authors.affiliation: Department of Pediatrics, Dokkyo University School of Medicine, Tochigi, Japan. k-kano@dokkyomed.ac.jp
authors.forename: K
authors.initials: K
authors.lastname: Kano
authors.forename: K
authors.initials: K
authors.lastname: Nishikura
authors.forename: Y
authors.initials: Y
authors.lastname: Yamada
authors.forename: O
authors.initials: O
authors.lastname: Arisaka
mesh_terms: D000135:Acid Phosphatase / Q000097:blood / Q000187:drug effects; D000293:Adolescent; D000328:Adult; D000469:Alkaline Phosphatase / Q000097:blood / Q000187:drug effects; D000596:Amino Acids / Q000187:drug effects / Q000652:urine; D015519:Bone Density / Q000187:drug effects*; D002648:Child; D005229:Fatty Acids, Monounsaturated / Q000494:pharmacology* / Q000627:therapeutic use; D005260:Female; D000077340:Fluvastatin; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000494:pharmacology* / Q000627:therapeutic use; D007211:Indoles / Q000494:pharmacology* / Q000627:therapeutic use; D007527:Isoenzymes / Q000097:blood / Q000187:drug effects; D008297:Male; D009393:Nephritis / Q000150:complications / Q000188:drug therapy / Q000378:metabolism*; D009402:Nephrosis, Lipoid / Q000150:complications / Q000188:drug therapy / Q000378:metabolism*; D015675:Osteocalcin / Q000097:blood / Q000187:drug effects; D011446:Prospective Studies; D000071681:Tartrate-Resistant Acid Phosphatase
chemical_list: D000596:Amino Acids; D005229:Fatty Acids, Monounsaturated; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D007211:Indoles; D007527:Isoenzymes; D015675:Osteocalcin; D000077340:Fluvastatin; C036020:deoxypyridinoline; D000469:Alkaline Phosphatase; D000135:Acid Phosphatase; D000071681:Tartrate-Resistant Acid Phosphatase