Zima T, Tesar V, Rychlík I, Nĕmecek K, Poledne R, Stejskalová A, Tĕmínová J, Stípek S, Merta M
I. ústav lékarské chemie a biochemie I. LF UK, Praha.
Cas Lek Cesk. 1995 Oct 18;134(20):658-60.
Antiproteinuric effect of pefloxacine was demonstrated in a small group of patients with minimal change nephropathy (MCN) and focal and segmental glomerulosclerosis (FSGS). This finding was not, however, confirmed by other papers. Adriamycine nephropathy is an experimental model of nephrotic syndrome with morphological changes resembling MCN and/or FSGS in patients.
Nephrotic syndrome was induced in rats by the i.v. administration of adriamycine. One part of nephrotic animals was treated from the beginning of the 4th week by daily intraperitoneal application of pefloxacine. Administration of adriamycine led in experimental animals after 3 weeks to the development of full-blown nephrotic syndrome with further progression of proteinuria in the next 3 weeks (from 1.4 +/- 1.25 to 2.23 +/- 1.89 g of protein/mmol of urinary creatinine, p < 0.05). Proteinuria did not change in nephrotic rats treated by pefloxacine (from 1.04 +/- 0.97 to 1.26 +/- 1.11 g of protein/mmol of urinary creatinine, p = n.s.). The difference in proteinuria between both groups was also significant (0.83 +/- 0.73 vs. 0.23 +/- 0.67 g of protein/mmol of urinary creatinine, p < 0.05).
Pefloxacine was antiproteinuric in experimental adriamycine nephropathy. The mechanism of this effect remains unclear and deserves further studies concentrating on glomerular cytokine network and glomerular production of reactive oxygen species.
