ACE I/D and AGT Met235Thr Polymorphisms Distinctly Affect Biomarker Levels and Risk of AKI and Exertional
Ayexa Cruz1,2, Diego Gomes1, Cintia Verdan1
1Department of Running,School of Physical Education and Sport, Universidade Federal do Rio de Janeiro, Rio de Janeiro, RJ 21949-900, Brazil.
Genetic variations in ACE and AGT may increase exertional rhabdomyolysis and acute kidney injury risk in military personnel undergoing strenuous exercise. These findings highlight potential genetic predispositions to exercise-induced muscle damage and kidney complications.
Area of Science:
- Exercise Physiology
- Genetics
- Nephrology
Background:
- Exertional rhabdomyolysis (ER) is a severe complication of strenuous exercise, particularly in military personnel.
- ER can lead to acute kidney injury (AKI) and impair physical function.
- Genetic factors, including polymorphisms in the renin-angiotensin-aldosterone system, are being investigated for their role in exercise-related injuries.
Purpose of the Study:
- To evaluate the association between ACE (rs1799752) and AGT (rs699) gene polymorphisms and exertional rhabdomyolysis risk (ERR).
- To assess the relationship between these polymorphisms and the susceptibility to AKI induced by strenuous exercise in military personnel.
Main Methods:
- Sixty-four male Brazilian Marine Corps volunteers were studied.
- Blood and urine samples were collected before and after a strenuous mission.
- Genotyping for ACE I/D and AGT M235T polymorphisms was performed.
Main Results:
- 84% of participants showed signs of ER post-exercise.
- AKI was observed in 20% of the total group and was more frequent in T allele carriers of AGT (MT+TT).
- Significant post-exercise increases in serum creatinine were noted for carriers of ACE I (II+ID) and AGT T (MT+TT) alleles.
Conclusions:
- ACE I/D and AGT M235T polymorphisms may be associated with an increased risk of AKI after intensive exercise.
- These genetic factors could play a role in the susceptibility to exercise-induced AKI in military settings.
- Further research is warranted to elucidate the precise mechanisms linking these polymorphisms to exertional rhabdomyolysis and AKI.
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