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Cholesterol-lowering therapy may retard the progression of diabetic nephropathy.

Abstract

There is experimental evidence to suggest that hypercholesterolaemia may play a pathogenetic role in progressive glomerular injury. We investigated the effect of cholesterol-lowering therapy on the progression of diabetic nephropathy in 34 patients with non-insulin-dependent diabetes mellitus. Patients were randomly assigned in a single-blind fashion to treatment with either lovastatin, an HMG CoA reductase inhibitor (n = 16; mean dose 30.0 +/- 12.6 mg/day) or placebo (n = 18) for 2 years. Renal function was assessed by serially measuring the serum creatinine, glomerular filtration rate (using Cr51-EDTA), and 24-h urinary protein excretion. Lovastatin treatment was associated with significant reductions in total cholesterol (p < 0.001), LDL-cholesterol (p < 0.001) and apo B (p < 0.01), the reductions at 24 months being 26, 30 and 18%, respectively. Beneficial effects on serum triglyceride, HDL-cholesterol and apo A1 levels were also observed. Lp(a) showed no significant change in both groups. Glomerular filtration rate deteriorated significantly in the placebo group after 24 months (p < 0.025) but showed no significant change in the lovastatin-treated patients. The increase in serum creatinine was statistically significant (p < 0.02) in placebo-treated patients at 12 and 24 months, and in the lovastatin group after 24 months. Twenty-four hour urinary protein excretion increased in both groups (p < 0.05). Lovastatin treatment was not associated with significant elevations in liver or muscle enzymes. We conclude that effective normalisation of hypercholesterolaemia may retard the progression of diabetic nephropathy.

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  • Authors+Show Affiliations

    ,

    Department of Medicine, University of Hong Kong, Queen Mary Hospital.

    , ,

    Source

    Diabetologia 38:5 1995 May pg 604-9

    MeSH

    Anticholesteremic Agents
    Apolipoprotein A-I
    Apolipoproteins
    Apolipoproteins B
    Apoprotein(a)
    Blood Pressure
    Body Mass Index
    Cholesterol
    Cholesterol, HDL
    Cholesterol, LDL
    Creatinine
    Diabetes Mellitus, Type 2
    Diabetic Nephropathies
    Diet, Diabetic
    Female
    Follow-Up Studies
    Glomerular Filtration Rate
    Glycated Hemoglobin A
    Humans
    Hydroxymethylglutaryl-CoA Reductase Inhibitors
    Lipoprotein(a)
    Lovastatin
    Male
    Middle Aged
    Placebos
    Single-Blind Method
    Time Factors
    Triglycerides

    Pub Type(s)

    Clinical Trial
    Comparative Study
    Journal Article
    Randomized Controlled Trial

    Language

    eng

    PubMed ID

    7489845

    Citation

    Lam, K S., et al. "Cholesterol-lowering Therapy May Retard the Progression of Diabetic Nephropathy." Diabetologia, vol. 38, no. 5, 1995, pp. 604-9.
    Lam KS, Cheng IK, Janus ED, et al. Cholesterol-lowering therapy may retard the progression of diabetic nephropathy. Diabetologia. 1995;38(5):604-9.
    Lam, K. S., Cheng, I. K., Janus, E. D., & Pang, R. W. (1995). Cholesterol-lowering therapy may retard the progression of diabetic nephropathy. Diabetologia, 38(5), pp. 604-9.
    Lam KS, et al. Cholesterol-lowering Therapy May Retard the Progression of Diabetic Nephropathy. Diabetologia. 1995;38(5):604-9. PubMed PMID: 7489845.
    * Article titles in AMA citation format should be in sentence-case
    TY - JOUR T1 - Cholesterol-lowering therapy may retard the progression of diabetic nephropathy. AU - Lam,K S, AU - Cheng,I K, AU - Janus,E D, AU - Pang,R W, PY - 1995/5/1/pubmed PY - 1995/5/1/medline PY - 1995/5/1/entrez SP - 604 EP - 9 JF - Diabetologia JO - Diabetologia VL - 38 IS - 5 N2 - There is experimental evidence to suggest that hypercholesterolaemia may play a pathogenetic role in progressive glomerular injury. We investigated the effect of cholesterol-lowering therapy on the progression of diabetic nephropathy in 34 patients with non-insulin-dependent diabetes mellitus. Patients were randomly assigned in a single-blind fashion to treatment with either lovastatin, an HMG CoA reductase inhibitor (n = 16; mean dose 30.0 +/- 12.6 mg/day) or placebo (n = 18) for 2 years. Renal function was assessed by serially measuring the serum creatinine, glomerular filtration rate (using Cr51-EDTA), and 24-h urinary protein excretion. Lovastatin treatment was associated with significant reductions in total cholesterol (p < 0.001), LDL-cholesterol (p < 0.001) and apo B (p < 0.01), the reductions at 24 months being 26, 30 and 18%, respectively. Beneficial effects on serum triglyceride, HDL-cholesterol and apo A1 levels were also observed. Lp(a) showed no significant change in both groups. Glomerular filtration rate deteriorated significantly in the placebo group after 24 months (p < 0.025) but showed no significant change in the lovastatin-treated patients. The increase in serum creatinine was statistically significant (p < 0.02) in placebo-treated patients at 12 and 24 months, and in the lovastatin group after 24 months. Twenty-four hour urinary protein excretion increased in both groups (p < 0.05). Lovastatin treatment was not associated with significant elevations in liver or muscle enzymes. We conclude that effective normalisation of hypercholesterolaemia may retard the progression of diabetic nephropathy. SN - 0012-186X UR - https://www.unboundmedicine.com/medline/citation/7489845/full_citation L2 - https://medlineplus.gov/diabetickidneyproblems.html DB - PRIME DP - Unbound Medicine ER -