Effect of α-1-adrenolytic agent and 5-α-reductase inhibitor on renal function in an experimental model of hyperprolactinemia-induced benign prostatic hyperplasia

Pol Merkur Lekarski. 2020 Jun 17;48(285):188-194.

Abstract

The standard pharmacotherapy of benign prostatic hyperplasia (BPH) may also alleviate potential kidney dysfunction resulting from the development of obstructive uropathy in the course of BPH.

Aim: The aim of study was to evaluate the effect of treatment with α-1- adrenolytic agent (tamsulosin) and 5-α-reductase inhibitor (finasteride) on renal function in rats.

Materials and methods: Four groups of rats were studied: 1 - controls, 2 - rats with metoclopramide-induced hyperprolactinemia BPH model, 3 - rats with BPH treated with tamsulosin, 4 - rats with BPH treated with finasteride. BPH presence was verified by histopathological examination. The renal function was assessed by histopathological examination, and the laboratory assessment of the classic nitrogen parameters and new kidney function markers (cystatin C; CysC, kidney injury molecule-1; KIM-1).

Results: In group 2, BPH development was confirmed by histopathological examination, without simultaneous significant kidney disturbances. Compared to the controls, BPH animals exhibited significant proteinuria, and increased concentration and daily urinary excretion of CysC and KIM- 1. Treatment with tamsulosin significantly improved the histopathological image of the prostate without affecting renal structure and led to reduced blood urea and proteinuria. Treatment with finasteride also significantly reduced the histopathological signs of BPH without changing the image of the kidneys, and reduced CysC concentration and daily CysC excretion with urine compared to group 2 individuals.

Conclusions: In the course of experimental hyperprolactinemiainduced BPH, kidney tubulopathy developed, which was indicated by KIM-1 and CysC disturbances in urine. The administration of finasteride reduced renal dysfunction to a higher degree, bringing the concentration and daily excretion of CysC back to normal.

Keywords: benign prostatic hyperplasia; cystatin C; hyperprolactinemia; kidney; kidney injury molecule-1; rats.

MeSH terms

  • 5-alpha Reductase Inhibitors* / therapeutic use
  • Animals
  • Hyperprolactinemia* / drug therapy
  • Male
  • Models, Theoretical
  • Oxidoreductases
  • Prostatic Hyperplasia* / drug therapy
  • Rats

Substances

  • 5-alpha Reductase Inhibitors
  • Oxidoreductases