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Effect of losartan on proteinuria and urinary angiotensinogen excretion in non-diabetic patients with chronic kidney disease
  1. Yu-Ji Lee1,
  2. Seong Cho1,
  3. Sung Rok Kim1,
  4. Hye Ryoun Jang2,
  5. Jung Eun Lee2,
  6. Wooseong Huh2,
  7. Dae Joong Kim2,
  8. Ha Young Oh2,
  9. Yoon-Goo Kim2
  1. 1Department of Medicine, Samsung Changwon Hospital, Sungkyunkwan University School of Medicine, Changwon, Republic of Korea
  2. 2Department of Medicine, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Republic of Korea
  1. Correspondence to Yoon-Goo Kim, Department of Medicine, Samsung Medical Center, Sungkyunkwan University School of Medicine, 50 Irwon-dong, Gangnam-Gu, 135-710 Seoul, Korea;{at}


Purpose Activation of the rennin–angiotensin system (RAS) is thought to contribute to hypertension and proteinuria, and eventually to the progression of chronic kidney disease (CKD). Recent evidence suggests that urinary angiotensinogen (UAGT) excretion reflects activation of the intrarenal RAS. This study was performed to determine the effect of losartan on proteinuria and UAGT excretion in non-diabetic patients with CKD with non-nephrotic-range proteinuria.

Study design Thirty-two patients with non-nephrotic-range proteinuria (0.045–0.23 g/mmol creatinine) and normal renal function between April 2005 and April 2006 were randomised to a losartan (n=17) or a control (n=15) group. Patients in the losartan group received losartan 50 mg/day, and the doses were titrated up to 100 mg/day after 6 weeks. Serum and urinary angiotensinogen concentrations were measured by sandwich ELISA. The primary end point was the percentage change in proteinuria. The secondary end points were changes in estimated glomerular filtration rate and UAGT excretion. The follow-up period was 24 months.

Results Baseline characteristics in the two groups were similar. After 24 months, losartan had reduced urinary protein excretion by 43% (from mean±SD 0.13±0.04 to 0.073±0.03 g/mmol, p<0.0001), but proteinuria had not changed in the control group. The percentage change in mean arterial pressure did not differ between the groups. Losartan decreased logarithmically converted UAGT excretion (from 1.58±0.47 to 1.00±0.52, p=0.001). Estimated glomerular filtration rate decreased significantly only in the control group.

Conclusion Losartan significantly decreased proteinuria and UAGT excretion, and preserved renal function in non-diabetic patients with CKD.

  • Angiotensin II receptor blocker
  • angiotensinogen
  • non-diabetic chronic kidney disease
  • proteinuria
  • renal function
  • nephrology
  • biochemistry

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  • Funding This study was funded by Merck & Co.

  • Competing interests None.

  • Patient consent Obtained.

  • Ethics approval The study protocol was approved by the institutional review board of Samsung Medical Center.

  • Provenance and peer review Not commissioned; externally peer reviewed.

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