Efficacy of N-Acetylcysteine in Treatment of Overt Diabetic Nephropathy

The safety and scientific validity of this study is the responsibility of the study sponsor and investigators. Listing a study does not mean it has been evaluated by the U.S. Federal Government. Read our disclaimer for details. Identifier: NCT00556465
Recruitment Status : Completed
First Posted : November 12, 2007
Last Update Posted : November 12, 2007
Information provided by:
Shiraz University of Medical Sciences

November 9, 2007
November 12, 2007
November 12, 2007
January 2007
Not Provided
Proteinuria [ Time Frame: 3 months ]
Same as current
No Changes Posted
blood pressure,serum creatinine,GFR,c-reactive protein, [ Time Frame: 3 months ]
Same as current
Not Provided
Not Provided
Efficacy of N-Acetylcysteine in Treatment of Overt Diabetic Nephropathy
Study of N-Acetylcysteine for Treatment of Overt Diabetic Nephropathy

Diabetic nephropathy has become the single most frequent cause of end-stage renal disease.

On a molecular level, at least five major pathways have been implicated in glucose-mediated vascular and renal damage and all of these could reflect a single hyperglycaemia-induced process of overproduction of reactive oxygen species.

Recent studies have shown that inflammation, and more specifically pro-inflammatory cytokines play a determinant role in the development of micro- vascular diabetic complications, most of the attention has been focused on the implications of TNF-α in the setting of diabetic nephropathy.

Glutathione is the most abundant low-molecular-weight thiol, and Glutathione/ glutathione disulfide is the major redox couple in animal cells.

N-acetylcysteine is effective precursors of cysteine for tissue Glutathione synthesis.

Not only does N-acetylcysteine exhibit antioxidant properties, but it may also counteract the glycation cascade through the inhibition of oxidation.

N-acetylcysteine can also reduce the apoptosis elicited by reactive oxygen species .

Indeed, N-acetylcysteine has been shown to inhibit reactive oxygen species induced mesangial apoptosis and to be able to protect cells from glucose-induced inhibition of proliferation.

Not Provided
Phase 2
Phase 3
Allocation: Randomized
Intervention Model: Parallel Assignment
Masking: None (Open Label)
Primary Purpose: Treatment
  • Diabetic Nephropathy
  • Chronic Kidney Disease
  • Diabetes Type 2
Drug: N-acetylcysteine
600 mg of effervescent N-acetylcysteine tablet twice per day for three months
  • Experimental: A, 1,III
    in this arm patients took 1200 mg N-acetylcysteine
    Intervention: Drug: N-acetylcysteine
  • No Intervention: B,2, III
Not Provided

*   Includes publications given by the data provider as well as publications identified by Identifier (NCT Number) in Medline.
June 2007
Not Provided

Inclusion Criteria:

  • Diabetic patients with more than 500 mg protein in 24 hours urine protein sample
  • Males and post-menopausal non-lactating and non-pregnant females.
  • Age greater than or equal to 30 years of age.
  • Serum creatinine less than 3.0 mg/dL (265 micromoles per liter)
  • Willing and able to give informed consent

Exclusion Criteria:

  • Type 1 (insulin-dependent; juvenile onset) diabetes
  • Patients with known non-diabetic renal disease
  • Renal allograft
  • Myocardial infarction, coronary artery bypass graft surgery, or percutaneous transluminal coronary angioplasty/stent within 3 months of study entry
  • Cerebrovascular accident within 3 months of study entry
  • New York Heart Association Functional Class III or IV
  • Known allergies or intolerance to N-acetylcysteine
  • Untreated urinary tract infection or other medical condition that may impact urine protein values.
Sexes Eligible for Study: All
30 Years to 75 Years   (Adult, Senior)
Contact information is only displayed when the study is recruiting subjects
Iran, Islamic Republic of
Not Provided
Not Provided
Not Provided
Shiraz University of Medical Sciences
Not Provided
Study Director: mohammad mahdi sagheb, MD shiraz university of medical science
Shiraz University of Medical Sciences
November 2007

ICMJE     Data element required by the International Committee of Medical Journal Editors and the World Health Organization ICTRP