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2010 | 57 | 4 | 547-552

Article title

Atorvastatin improves tubular status in non-diabetic patients with chronic kidney disease - placebo controlled, randomized, cross-over study

Content

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EN

Abstracts

EN
Background. There is evidence that dyslipidemia is associated with chronic kidney disease (CKD) and it has been implicated in the progression of renal damage. Optimal management of dyslipidemia should therefore lead to renal benefits. A number of experimental models demonstrate a beneficial effect of statins in ameliorating renal damage. However, the exact mechanism by which statins protect against renal damage remains unclear. Methods. In a placebo-controlled, randomized, cross-over study we evaluated the influence of atorvastatin (ATO) 40 mg/day added to the renin-angiotensin-aldosterone systeme (RAAS) blockade on proteinuria and surrogate biomarkers of tubular damage or injury in 14 non-diabetic patients with proteinuria (0.4-1.8 g per 24 h) with normal or declined kidney function (eGFR 55-153 ml/min). In the eight-week run-in period, therapy using angiotensin converting enzyme inhibitors (ACEI) and/or angiotensin II subtype 1 receptor antagonists (ARB) was adjusted to achieve a blood pressure below 130/80 mm Hg. Next, patients were randomly assigned to one of two treatment sequences: ATO/washout/placebo or placebo/washout/ATO. Clinical evaluation and laboratory tests were performed at the randomization point and after each period of the study. The primary end point of this study was a change in proteinuria measured as 24-h urine protein excretion (DPE). Secondary end points included urine N-acetyl-β-d-glucosaminidase (NAG) and α1-microglobulin (α1m) excretion. Results. The ATO therapy significantly reduced urine excretion of α1m (p=0.033) and NAG (p=0.038) as compared to placebo. There were no differences in proteinuria, blood pressure, eGFR and serum creatinine between the ATO and placebo groups. Conclusion. Atorvastatin treatment is safe and improves biomarkers of tubular damage or injury in non-diabetic patients with CKD.

Year

Volume

57

Issue

4

Pages

547-552

Physical description

Dates

published
2010
received
2010-05-21
revised
2010-10-16
accepted
2010-11-06
(unknown)
2010-11-16

Contributors

author
  • Department of Nephrology, Transplantology and Internal Medicine, Medical University of Gdansk, Gdansk, Poland
  • Department of Nephrology, Transplantology and Internal Medicine, Medical University of Gdansk, Gdansk, Poland
  • Department of Nephrology, Transplantology and Internal Medicine, Medical University of Gdansk, Gdansk, Poland
  • Blood Brain Barrier and Neuro-Oncology Program, Oregon Health & Science University, Portland, Oregon, USA
  • Department of Nephrology, Transplantology and Internal Medicine, Medical University of Gdansk, Gdansk, Poland
  • Department of Internal Medicine, Connective Tissue Diseases and Geriatrics, Medical University of Gdansk, Gdansk, Poland
  • Department of Clinical Nutrition and Laboratory Diagnostics, Medical University of Gdansk, Gdansk, Poland
  • Department of Clinical Nutrition and Laboratory Diagnostics, Medical University of Gdansk, Gdansk, Poland
  • Department of Nephrology, Transplantology and Internal Medicine, Medical University of Gdansk, Gdansk, Poland

References

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Document Type

Publication order reference

Identifiers

YADDA identifier

bwmeta1.element.bwnjournal-article-abpv57p547kz
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