ACE inhibition induces regression of proteinuria and halts progression of renal damage in a genetic model of progressive nephropathy

A. Remuzzi, A. Fassi, T. Bertani, N. Perico, G. Remuzzi

Research output: Contribution to journalArticle

Abstract

Experimental data consistently indicate that renal disease progression is fully prevented in proteinuric glomerulopathies by long-enough angiotensin-converting enzyme (ACE) inhibition therapy. Whether regression of established proteinuria to normal can be achieved is, however, ill defined. The current study was designed with the aim to clarify whether ACE inhibition may induce regression of established proteinuria and renal structural damage in MWF rats, a genetic model of progressive proteinuria and renal injury. Animals treated with the ACE inhibitor lisinopril from 20 weeks of age (time when proteinuria is already important) and age-matched untreated rats were followed for 10 weeks. ACE inhibition normalized systolic blood pressure and progressively reduced proteinuria (from 172 ± 79 to 81 ± 23 mg/24 hours). In these animals, a highly significant correlation was obtained between baseline proteinuria and antiproteinuric response. At variance in untreated rats, proteinuria showed a marked increase in the 10-week follow-up period (from 165 ± 57 to 325 ± 86 mg/24 hours). Lisinopril prevented the progression of renal damage, as documented by a significantly lower incidence of glomeruli affected by sclerotic lesions (P <0.01) than in untreated animals after the 10-week study period. Kidney tissue damage was comparable in lisinopril-treated rats and in untreated animals at 20 weeks of age, indicating that structural changes were arrested by the treatment. Thus, in proteinuric MWF rats, late-onset ACE inhibition normalized blood pressure, effectively and progressively restored high protein excretion rate toward normal values, and arrested progression of tissue damage.

Original languageEnglish
Pages (from-to)626-632
Number of pages7
JournalAmerican Journal of Kidney Diseases
Volume34
Issue number4
Publication statusPublished - 1999

Fingerprint

Genetic Models
Peptidyl-Dipeptidase A
Proteinuria
Kidney
Lisinopril
Blood Pressure
Enzyme Therapy
Angiotensin-Converting Enzyme Inhibitors
Disease Progression
Reference Values
Incidence
Wounds and Injuries
Proteins

Keywords

  • Angiotensin-converting enzyme (ACE) inhibitor
  • Proteinuria
  • Rat
  • Regression
  • Renal disease progression
  • Renal structural damage

ASJC Scopus subject areas

  • Nephrology

Cite this

ACE inhibition induces regression of proteinuria and halts progression of renal damage in a genetic model of progressive nephropathy. / Remuzzi, A.; Fassi, A.; Bertani, T.; Perico, N.; Remuzzi, G.

In: American Journal of Kidney Diseases, Vol. 34, No. 4, 1999, p. 626-632.

Research output: Contribution to journalArticle

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