Clinical Trial Details
— Status: Completed
Administrative data
NCT number |
NCT04420897 |
Other study ID # |
The effect of Pa02 in KT |
Secondary ID |
|
Status |
Completed |
Phase |
|
First received |
|
Last updated |
|
Start date |
May 1, 2020 |
Est. completion date |
December 1, 2020 |
Study information
Verified date |
December 2020 |
Source |
Akdeniz University |
Contact |
n/a |
Is FDA regulated |
No |
Health authority |
|
Study type |
Observational
|
Clinical Trial Summary
We evaluated the prognostic role of the intraoperative arterial oxygen partial pressures
(PaO2) on postoperative patient and graft survival in living donor kidney transplantations.
Description:
Undoubtedly, one of the most important elements of life on earth is oxygen. Aerobic organisms
adapted to the 20.8% oxygen ratio in the atmosphere have survived even lower than this
concentration by developing various defense mechanisms. The real question is whether high
levels of oxygen in the blood, which are administered iatrogenically, leads to tissue
destruction.
Reactive Oxygen Species (ROS), which is a result of hyperoxia and may be useful even at low
levels, may cause tissue loss due to oxidative stress, also called oxygen-free radicals. ROS,
whose toxicity is very destructive with its accumulation, may cause damage to macromolecular
structures such as lipids, protein, mitochondrial and nuclear DNA. On the organs of the
exposed oxidative stress; For lung, asthma, chronic obstructive pulmonary disease (COPD),
acute respiratory distress syndrome (ARDS), cardiovascular system, ischemic heart disease
(IHD), hypertension, shock, heart failure, while kidney failure and glomerulonephritis can
cause unwanted complications.
The kidneys get for circulation, only 20% of the cardiac output. Since the arterial and
venous (AV) structures in the kidneys are anatomically parallel to each other, the oxygen
concentration in the renal vein may be relatively higher than the efferent arteriole and
cortex because of the oxygen shunt. Thanks to this mechanism, in clinical situations where
partial oxygen pressure (Pa02) is high, the oxygen concentration presented to the kidney
tissues remains within a certain limit. In fact, AV shunt protects kidney tissue with a
structural antioxidant mechanism. Thus, the increase in renal blood flow (RBF) will cause an
increase in AV oxygen shunt in parallel, the blood coming to the kidneys participates in the
systemic circulation without entering the renal microcirculation. It has been suggested that
shunt occurs to protect from hyperoxia at the tissue level by decreasing blood volume in the
kidneys. Oxidative stress, which is inevitable as a result, will increase tissue hypoxia
paradoxically by increasing the oxygen consumption of the kidneys. It is stated that uremic
toxin, especially indoxyl sulfate (IS) accumulation is the cause of the mentioned table.
Apart from IS, phenyl sulfate and ρ-cresy sulfate make tubular cells susceptible by reducing
glutathione levels. Thus, increased renal hypoxia, renal oxidative stress will result in
renal inflammation and fibrosis.
According to recent studies, the antioxidant defense mechanism has been shown not only to be
limited to AV shunt. But also the dynamic regulation of intrarenal oxygenation in RBF
changes. However, mechanisms developed to prevent hyperoxia have made kidney tissue sensitive
to hypoxia. The increase in AV oxygen shunt causes an increase in tissue hypoxia.
Although endogenous antioxidant mechanisms play a major role against free radicals, the
postoperative effects of iatrogenic hyperoxia on transplanted kidney grafts and patient
survival remain a subject to be investigated. That's why we aim to understand the impact of
iatrogenic hyperoxia during the living donor kidney transplantation operations by
retrospective data analyzing.