Unraveling the Mechanisms of Magnesium Supplementation in Alleviating Chronic Kidney Disease Complications and Progression: Balancing Risks and Benefits.

Chronic kidney disease (CKD) is a major cause of death and disability worldwide. It is usually diagnosed at early levels because of its slow progression. Treatment should consider CKD complications (such as electrolyte level imbalance, vascular calcification, and bone mineral disorders), as well as the development of CKD itself. Large-scale studies have shown that current treatment guidelines are nearly ineffective and fail to achieve treatment goals. Guidelines have not paid as much attention to magnesium (Mg) as the other electrolytes, while Mg has a significant role in the treatment goals of CKD. Hypomagnesemia is the only electrolyte imbalance that is equally prevalent in all stages of CKD. A lower plasma Mg level in each stage of CKD is associated with a higher risk of CKD progression and cardiac events. Magnesium exerts its effects both directly and via other ions. Mg supplementation increases insulin sensitivity while reducing proteinuria and inflammation. It lowers blood pressure and inhibits vascular calcification primarily because of its effects on calcium and phosphate, respectively. Vitamin D supplementation for low-active vitamin D in CKD patients increases vascular calcification and cardiac events, but magnesium supplementation enhances vitamin D levels and activity without increasing the risk of cardiac events. However, careful attention is required due to the potential threats of hypermagnesemia, particularly in advanced CKD stages. Starting magnesium supplementation early in patients' treatment plans will result in fewer side effects and more advantages. More original research is needed to determine its optimal dose and serum levels.

Kinin-kallikrein system: New perspectives in heart failure.

Heart failure (HF) is a pervasive clinical challenge characterized by compromised cardiac function and reduced quality of life. The kinin-kallikrein system (KSS), a multifaceted peptide cascade, has garnered substantial attention due to its potential role in HF. Through activation of B1 and/or B2 receptors and downstream signaling, kinins modulate various physiological processes, including inflammation, coagulation, pain, blood pressure control, and vascular permeability. Notably, aberrations in KKS components have been linked to HF risk. The elevation of vasodilatory bradykinin (BK) due to kallikrein activity reduces preload and afterload, while concurrently fostering sodium reabsorption inhibition. However, kallikrein's conversion of prorenin to renin leads to angiotensinsII upregulation, resulting in vasoconstriction and fluid retention, alongside increased immune cell activity that fuels inflammation and cardiac remodeling. Importantly, prolonged KKS activation resulting from volume overload and tissue stretch contributes to cardiac collagen loss. The conventional renin-angiotensin-aldosterone system (RAAS) inhibitors used in HF management may inadvertently intensify KKS activity, exacerbating collagen depletion and cardiac remodeling. It is crucial to balance the KKS's role in acute cardiac damage, which may temporarily enhance function and metabolic parameters against its detrimental long-term effects. Thus, KKS blockade emerges as a promising strategy to impede HF progression. By attenuating the link between immune system function and tissue damage, KKS inhibition can potentially reduce cardiac remodeling and alleviate HF symptoms. However, the nuanced roles of BK in various acute conditions necessitate further investigation into the sustained benefits of kallikrein inhibitors in patients with chronic HF.

Prevalence of amiodarone-induced hypothyroidism; A systematic review and meta-analysis.

Amiodarone is a common anti-arrhythmic agent mostly used to treat and prevent different kinds of arrhythmia with several considerable side effects, most commonly on the thyroid gland. We aimed to assess the frequency of hypothyroidism among chronic amiodarone users. PubMed/Medline, Web of Science, and Scopus databases were screened in the title and abstract sections with no time limitation. Relevant published records reported amiodarone-induced hypothyroidism (AIH) among patients with normal thyroid function at baseline were recruited with further analysis according to gender and study locations. We found 29 records on 14143 individuals. Total population age ranged from 18 to 92 years (males: 58.2% (8158 out of 13,999)). The AIH prevalence was found to be 14% (95% confidence interval (CI): 12-17%). Further gender stratified showed an insignificant higher AIH frequency in females versus males (17%, 95% CI: 13-22% vs. 14%, 95% CI: 11-19% P= 0.304, respectively). Despite no significant difference in AIH prevalence according to different continents, African subjects had marginally lower AIH frequency compared to Asian (7%, 95% CI: 4-13% vs. 15%, 95% CI: 12-19%, P= 0.012) and South American persons (7%, 95% CI: 4-13% vs. 54%, 95% CI: 9-93%, P= 0.038). This review suggests the occurrence of AIH is quite considerable regardless of gender and area of residence, and several periodic thyroid assessment strategies should be developed for earlier recognition and therapeutic interventions in clinical settings.

Ameliorative effect of lycopene effect on cisplatin-induced nephropathy in patient.

BACKGROUND: Nephrotoxicity is one of the most important limitations of cisplatin-based chemotherapies which associated with many complications and high mortality rate. OBJECTIVES: To investigate the effect of lycopene on cisplatin-induced nephrotoxicity in patients with cancer. PATIENTS AND METHODS: In this double-blind, randomized clinical trial, 120 patients were randomly assigned to two groups, case (treated with lycopene + standard regimen of kidney injury prevention) and control (treated with only the standard regimen of kidney injury prevention). Lycopene was orally taken from 24 hours before to 72 hours after cisplatin administration. Blood urea nitrogen (BUN), serum creatinine (Cr), and glomerular filtration rate (GFR) were measured and recorded. The data were analyzed using SPSS. RESULTS: Changes in Cr were not significantly different between the two groups (P = 0.131). However, a significant decreasing trend was seen in GFR during the study, which was more marked in the control group (P = 0.004). BUN significantly decreased during the study (P = 0.002), and a significant decrease of BUN on the day three in both groups was seen (P = 0.001). However, BUN increased in the case group on the day 21 of treatment. The corresponding increase was less marked in the control group. CONCLUSIONS: Lycopene can be considered a useful adjuvant therapy to decrease the complications due to cisplatin-induced nephrotoxicity in patients with cancer.