Author: Gary Jackson

Alcohol Consumption Can be a Double-Edged Sword for Chronic Kidney Disease Patients PMC

Free radicals (also called reactive oxygen species [ROS]) are one of the by-products of alcohol metabolism and are known to cause cellular damage, unless the body can use antioxidants to clean them up. Oxidative stress occurs when the body cannot detoxify free radicals as fast as they are being produced, and it is pivotal in triggering alcohol-related tissue injury. Studies suggest that several mechanisms produce ROS in alcohol-damaged organs, including the liver (Cederbaum et al. 2009), heart (Tan et al. 2012; Varga et al. 2015), and kidney (Latchoumycandane et al. 2015). CYP2E1 is of particular interest when thinking about potential mechanisms for alcohol-related kidney damage.

As an example, Puddey and colleagues (1985) evaluated the effects of hormones that regulate kidney function. Their results show not only how alcohol disrupts homeostasis but also how the body reacts to restore it. Following moderate alcohol consumption—about 24 oz—of nonalcoholic beer with 1 milliliter of alcohol per kilogram of body weight added, the investigators noted several effects. Alcohol-induced urination reduced the subjects’ plasma volume, resulting in an increased concentration of plasma sodium. In addition, the subjects’ blood pressure and plasma potassium concentration decreased. These changes in fluid volume, electrolyte balance, and blood pressure may have stimulated the activity of hormones to return body fluid volume and composition back to normal, which occurred soon after consumption.

Limitations of Existing Studies

Another study by Plotnikov and colleagues (2009) showed that mitochondria isolated from rat kidneys were damaged by oxidative stress when incubated with myoglobin. This finding suggests that rhabdomyolysis and myoglobin toxicity may trigger oxidative stress in the kidney via mitochondrial injury. In summary, there is no exact evidence that alcohol consumption aggravates the state of CKD or increases all-cause mortality in CKD, and the protective effect of abstinence on such patients is unclear. Although many studies stated that people should not start drinking for any reason, and alcohol consumption can increase disease risk [125], we also cite many studies demonstrating the protective effects of light-to-moderate alcohol consumption in our review. Abstinence is one of the characteristics of human drinking habits; many doctors will encourage patients to stop drinking, which may be good for their health [121]. As for the kidney damage caused by alcohol, some studies discovered that the patients’ renal function recovered after abstinence [1].

As the plasma filtrate passes along this channel, the substances the body needs to conserve are reabsorbed into an extensive network of capillaries that wrap the nephron tubule. Small amounts of unwanted substances also are secreted directly into the nephron tubules. Together, the filtered and secreted substances form urine (see figure) and eventually trickle into a series of progressively larger collecting ducts.

How does alcohol harm the kidneys?

Follow a low-fat, healthy diet that has plenty of fresh fruits and vegetables. See your doctor to treat kidney stones or a kidney infection if they are the cause. Seeing a doctor as soon as possible helps ensure appropriate treatment and can reduce the risk of complications.

In addition, AUD’s effect on other major organs (liver, heart, intestines, and skeletal muscle) appears to promote unfavorable pathological processes that are harmful to the kidneys.
In addition, long-term alcohol consumption can lead to injuries of renal tubules [1,2,30,39,51].
You may need to take a complete break from alcohol for a set amount of time or reduce the amount of alcohol you consume.
In the kidneys, ROS is generated via both enzymatic and non-enzymatic processes [22,23,27,32,36,37].
Several mechanisms may contribute to abnormally low phosphate levels (i.e., hypophosphatemia) (see box).