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Background <p>Oxidative stress is considered a significant contributing factor of chronic kidney disease (CKD). To date, there is a paucity of clinical data in the literature regarding the effect of N-Acetylcysteine (NAC) in cats with naturally developing CKD. The aim of the study is to evaluate whether the addition of NAC in the treatment of cats with acute exacerbations of CKD could improve kidney function biomarkers over the use of intravenous fluid therapy alone.</p> Methods <p>A total of 50 client-owned cats were included in the study. The inclusion criteria comprised cats previously diagnosed with azotemic CKD (IRIS stage 2–4) in addition to ultrasonographic evidence of bilaterally decreased renal mass, rough surface contours, and alteration of renal cortical echogenicity. All cats were examined using standard clinical procedures, including clinical examination, blood analyses, abdominal ultrasonography, dipstick urinalysis and urine culture. Computer-generated randomisation was utilised to assign the cats into the following groups: NAC (<i>n</i>:40): N-acetylcysteine (70&#xa0;mg/kg, diluted in 50&#xa0;ml 0.9% saline solution, administered intravenously over a period of seven days, and a placebo group (<i>n</i>:10) 50&#xa0;ml 0.9% saline solution, IV for 7 days. Blood analyses and dipstick urinalysis were repeated on the eighth day of treatment. Between-group differences in baseline age and weight were assessed using the Student’s t-test, while sex distribution was evaluated with the Fisher’s exact test. Treatment effects across time were analysed using a two-way mixed-design ANOVA, with “Group” and “Time” entered as fixed factors and their interaction term included in the model.</p> Results <p>SDMA and creatinine concentrations decreased significantly in both groups, but the concentrations of both were significantly lower in the NAC group after treatment (Day 8 values: SDMA NAC 16.5 ± 1.21&#xa0;µg/dl versus placebo 27 ± 3.89&#xa0;µg/dl; <i>P</i> = 0.04 and Creatinine NAC 4.01 ± 0.25&#xa0;mg/dl versus placebo 6.44 ± 0.9&#xa0;mg/dl; <i>P</i> &lt; 0.001). UPC and BUN decreased significantly in the NAC group, but no change was observed in the placebo group.</p> Conclusion <p>The incorporation of NAC into treatment regimens demonstrates potential as a treatment strategy for cats with acute-on-chronic kidney disease.</p>

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N-acetylcysteine reduces serum creatinine, blood urea nitrogen, symmetric dimethylarginine and urine protein to creatinine ratio in cats with chronic kidney disease: a double-blind, placebo-controlled clinical trial

  • 期刊论文

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  • 发表日期：

    2026年2月3日

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  • Hadi Ali̇hossei̇ni̇,
  • Ekrem Çagatay Çolakoğlu,
  • Ali Evren Haydardedeoğlu,
  • Doğukan Özen

摘要

Background

Oxidative stress is considered a significant contributing factor of chronic kidney disease (CKD). To date, there is a paucity of clinical data in the literature regarding the effect of N-Acetylcysteine (NAC) in cats with naturally developing CKD. The aim of the study is to evaluate whether the addition of NAC in the treatment of cats with acute exacerbations of CKD could improve kidney function biomarkers over the use of intravenous fluid therapy alone.

Methods

A total of 50 client-owned cats were included in the study. The inclusion criteria comprised cats previously diagnosed with azotemic CKD (IRIS stage 2–4) in addition to ultrasonographic evidence of bilaterally decreased renal mass, rough surface contours, and alteration of renal cortical echogenicity. All cats were examined using standard clinical procedures, including clinical examination, blood analyses, abdominal ultrasonography, dipstick urinalysis and urine culture. Computer-generated randomisation was utilised to assign the cats into the following groups: NAC (n:40): N-acetylcysteine (70 mg/kg, diluted in 50 ml 0.9% saline solution, administered intravenously over a period of seven days, and a placebo group (n:10) 50 ml 0.9% saline solution, IV for 7 days. Blood analyses and dipstick urinalysis were repeated on the eighth day of treatment. Between-group differences in baseline age and weight were assessed using the Student’s t-test, while sex distribution was evaluated with the Fisher’s exact test. Treatment effects across time were analysed using a two-way mixed-design ANOVA, with “Group” and “Time” entered as fixed factors and their interaction term included in the model.

Results

SDMA and creatinine concentrations decreased significantly in both groups, but the concentrations of both were significantly lower in the NAC group after treatment (Day 8 values: SDMA NAC 16.5 ± 1.21 µg/dl versus placebo 27 ± 3.89 µg/dl; P = 0.04 and Creatinine NAC 4.01 ± 0.25 mg/dl versus placebo 6.44 ± 0.9 mg/dl; P < 0.001). UPC and BUN decreased significantly in the NAC group, but no change was observed in the placebo group.

Conclusion

The incorporation of NAC into treatment regimens demonstrates potential as a treatment strategy for cats with acute-on-chronic kidney disease.