The protective powers of L-theanine against drug-induced kidney damage.

Background: Drug-induced kidney damage (DIKD) is a significant medical concern linked to many drugs, including nonsteroidal anti-inflammatory drugs, antibiotics, and chemotherapy agents, due to its complex pathophysiology. L-theanine, a tea leaf amino acid, is explored for its protective effects against DIKD, considering its cognitive and calming benefits.

Materials and methods: In the theoretical part of the article, the role of L-theanine in combating DIKD is reviewed, highlighting its ability to mitigate oxidative stress and inflammation by neutralizing reactive oxygen species, enhancing antioxidant defenses, and modulating anti-inflammatory pathways. L-theanine's influence on cell signaling and its synergy with other nephroprotective agents are discussed. The practical part describes an experimental study using a murine model, where 60 male C57BL/6 mice were divided into four groups: a control group, a nephrotoxic group treated with cisplatin, and two treatment groups that received L-theanine either before or after cisplatin administration. Serum biomarkers (creatinine and blood urea nitrogen (BUN)), histopathological kidney damage scores, and oxidative stress markers (malondialdehyde (MDA) and superoxide dismutase (SOD)) were measured.

Results: Evidence from the murine study indicates that L-theanine protects against DIKD through antioxidative, anti-inflammatory, and anti-apoptotic mechanisms, potentially enhancing its synergy with other nephroprotective agents. In the nephrotoxic group (N), serum creatinine and BUN levels were significantly elevated, while pre-treatment with L-theanine (LTP) reduced these levels to 1.2 ± 0.3 mg/dL and 34 ± 4 mg/dL, respectively. Histopathological analysis revealed severe tubular necrosis in the N group (score: 3.8 ± 0.3), which was significantly reduced in the LTP group (1.6 ± 0.4). Oxidative stress markers, such as MDA, were markedly lowered in the LTP group compared to the N group, with corresponding increases in SOD activity, indicating enhanced antioxidant defense. These findings underscore L-theanine's potential in preserving renal health amidst pharmacotherapy-induced toxicity.

Conclusion: L-theanine emerges as a promising nephroprotective agent, particularly in the context of increasing incidence of DIKD and the associated challenges in clinical management. The practical findings from this study in a murine model provide compelling evidence that L-theanine significantly reduces serum biomarkers of renal injury, attenuates tubular necrosis, and mitigates oxidative stress, with pronounced effects observed when administered as a pre-treatment. While these results are promising, the predominance of preclinical data underscores the need for rigorous human studies to validate L-theanine's efficacy and safety in the prevention of drug-related renal injuries. Such research is crucial for advancing renal protection strategies in pharmacotherapy.