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Ozone Therapy Renal Failure

Ozone therapy renal failure

Ozone Therapy Renal Failure

Ozone Therapy: A Possible Agent that Delays the Chronic Renal Failure 

Sarahí del Río1, Ernesto Barber1, Silvia Menéndez *2, Angel Concepción1 and Jorge Bacallao1
1Institute of Basic and Preclinical Sciences “Victoria de Girón”, Havana, Cuba
2Ozone Research Center. POBox 6880, Havana, Cuba

Abstract

Chronic renal failure (CRF) represents a world health problem. The aim of this paper  is  to  evaluate  the  effect  of  ozone  therapy,  in  the  renal  function  and morphology, in an experimental model of CRF. Rats were divided into 4 groups:

1-negative control, rats without any treatment;
2-positive control, rats submitted to 5/6 reduction of the total renal mass (right kidney nephrectomy, with 2 branches of  the  renal  arteria,  of  the  left  kidney,  clamped);
3-ozone,  as  group 2,  but receiving, rectally, 7 sessions of ozone (0.5 mg/kg), previously to the surgery procedure and twice per week (during 10 weeks) after the partial nephrectomy;
4-oxygen, as group  3, but receiving oxygen instead of ozone. Ozone oxidative preconditioning effect protected the tissues against the oxidative stress present in the CRF, being in correspondence with the positive histological results obtained.

Introduction

Chronic renal failure (CRF) represents a world health problem. CRF, once established, goes irreversibly to a final stage, provoking the patient death. In contrast with the capacity of the kidneys to regain function following acute renal injury, renal injury of a more prolonged nature often leads to progressive and irreversible destruction of nephron mass  (1). Such reduction of renal mass, in turn, causes structural and functional hypertrophy of surviving nephrons. This compensatory hypertrophy is due to an adaptive hyperfiltration mediated by increases in glomerular capillary pressures and flows. Eventually, these adaptations prove maladaptive, in that they predispose to sclerosis of the residual glomerular population (1-4). The intrarenal vasculature is the most affected structure, preventing an appropriate blood flow,  favoring  the  glomerular  sclerosis (1-5).  For  that  reason,  the  improvement  of  the rheological properties of the blood could delay the progression of the CRF.

Glomerulonephritis was the most common initiating cause of CRF in the past. Possibly because  of  more  aggressive  treatment  of  glomerulonephritis,  diabetes  mellitus  and hypertensive renal diseases are now leading causes of CRF. The inexorable course to renal failure often is accompanied by anemia, malnutrition, impaired metabolism of carbohydrates, fats and proteins, impaired platelet function and defective utilization of energy (1).

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