Alcohol Consumption and Risk of Chronic Kidney Disease: A Nationwide Observational Cohort Study PMC

Along with oxidative stress, increasing evidence suggests that some nonoxidative mechanisms also factor into alcohol-related organ damage. Specifically, ethanol metabolism produces fatty acid ethyl esters in various organs (Laposata and Lange 1986), which can cause ethanol-induced organ damage. Calabrese and Rizza (1999) found that ethanol induced a significant increase in the levels of fatty acid ethyl esters. They measured the highest levels in the heart, followed by kidney, brain, and liver. Studies suggest that ethanol consumption may increase renal expression of other potential sources of free radicals involving a family of enzymes called nitric oxide synthases (Tirapelli et al. 2012).

1. Data Collection

As a result, excess carbon dioxide accumulates, and the body’s acid level subsequently increases. Respiratory acidosis is rare but carries an ominous prognosis when it occurs. Low blood levels of phosphate commonly occur acutely in hospitalized alcoholic patients, appearing in more than one-half of severe alcoholism cases. The kidney tubules play an important role in keeping the body’s water and electrolyte levels in equilibrium.

Nutrition and Kidney Disease, Stages 1-5 (Not on Dialysis)

Subjects fun addiction group activities that were aged more than 18 years old were selected from the 2001, 2005, and 2009 NHIS. Those with a diagnosis of CKD in the medical insurance record before the interview date were excluded. The follow-up duration began since the interview date and censored on the date of incident CKD, death, or Dec 31, 2013, which ever come first. With your support, we are proud to serve the 1 in 7 Americans who have kidney disease.

In hyponatremic patients, the amount of fluid retained by the kidneys is disproportionately greater than the amount of sodium retained. In other words, the kidneys’ ability to excrete excess fluid by way of dilute urine is impaired, and too much fluid is reabsorbed. Hyponatremia probably is the single most common electrolyte disturbance encountered in the management of patients with cirrhosis of the liver (Vaamonde 1996). This abnormality may xanax for sleep vs ambien reflect the severity of liver disease, but the available data do not allow correlation of kidney impairment with the degree of clinical signs of liver disease, such as ascites or jaundice. One example of an alcohol-related acid-base disturbance already has been mentioned in relation to low levels of phosphate (i.e., respiratory alkalosis resulting from hyperventilation during alcohol withdrawal). Other acid-base disturbances are possible as a result of excessive alcohol consumption.

An often-overlooked problem: kidney disease in people with cerebral palsy and other neurodevelopmental disabilities

Although hepatorenal syndrome often ensues after an event that reduces blood volume (e.g., gastrointestinal bleeding), it also can occur without any apparent precipitating factor. Some observers have noted that patients with cirrhosis frequently develop hepatorenal syndrome following hospital admission, possibly indicating that a hospital-related event can trigger the syndrome. Regardless of the precipitating factor, patients who develop kidney failure in the course of alcoholic cirrhosis have a grave prognosis. Despite the multiple possible causes of acidosis, disturbances in acid-base balance are more frequently manifested as low acidity (i.e., alkalosis).

1. Both of those conditions are the most common causes of chronic kidney disease in the United States.
2. Additional research is needed to clarify if alcohol does indeed promote kidney injury and the mechanisms by which alcohol-induced kidney injury may occur.
3. 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.
4. People older than age 50 overcome suppression of ADH more quickly than their younger counterparts do, despite reaching similar serum electrolyte concentrations after alcohol consumption.
5. Their analysis included 20 studies representing a total of 292,431 patients.

Although resilient, the kidneys can deteriorate as a result of malnutrition, alcohol abuse or dependence, or liver and other staying motivated in recovery diseases. Healthy kidneys are vital to the function of all the body’s organs and systems. In addition to their role in regulating the body’s fluid composition, the kidneys produce hormones that influence a host of physiological processes, including blood pressure regulation, red blood cell production, and calcium metabolism. Besides producing hormones, the kidneys respond to the actions of regulatory hormones produced in the brain, the parathyroid glands in the neck, and the adrenal glands located atop the kidneys. In terms of alcohol’s effects on the kidneys, the National Kidney Foundation (NKF) states that drinking too much alcohol can harm kidney function and worsen existing kidney disease.

Check with your doctor, especially if you take medications that might be affected by using alcohol. Women, older people, and those with smaller bodies should be especially careful. Ask your healthcare provider if it is safe for you to drink, especially if you have a medical condition or take medicines that might be affected by using alcohol. They filter waste from your blood, regulate the balance of water and minerals in your body and produce hormones. Some wines and beers pose potential problems around the amount of potassium they contain.

You can make mocktails in a fancy glass if you want to drink something special, especially in social situations. This is the area at the back of your abdomen, under your ribcage on both sides of your spine. This pain may be felt as a sudden, sharp, stabbing pain or more of a dull ache. It may be mild or severe and can be felt on one or both sides of the body. However, it is important to note that alcohol-induced kidney damage may not always cause kidney pain.

This massive induction of CYP2E1 in the kidneys results in oxidative stress that modifies phospholipids in cell membranes. Such modified phospholipids may in turn activate immune cells called neutrophil granulocytes, which further aggravates oxidative stress, promoting a vicious cycle (Latchoumycandane et al. 2015). Another study with dogs (Beard et al. 1965) disclosed that the effects of chronic alcohol consumption endured even longer. The investigators noted increased plasma and extracellular fluid volume 1 week after chronic alcohol ingestion, and these volume expansions persisted for the remaining 7 weeks of the study. Similar alterations have been found in body fluid volumes among chronic alcoholic patients. As noted above, there is much to learn about alcoholic kidney disease and the complex interplay among multiple organs affected by alcohol consumption.

Although research suggests several potential mechanisms by which alcohol may directly or indirectly affect the kidneys, they have not yet been validated experimentally. Future research will hopefully explore these hypotheses to provide a better understanding of alcoholic kidney injury. This article highlights the effects of other organs on kidney and renal function; however, it should be noted that alcoholic kidney injury itself may have negative metabolic consequences. One such complication is impaired vitamin D metabolism (Shankar et al. 2008), which may influence the function of several other organs, creating a vicious cycle. Chronic or acute heart failure can lead to chronic or acute dysfunction in the kidneys, known as cardiorenal syndrome (Cleland et al. 2012). The overactivation of RAAS further aggravates oxidative stress in chronic alcoholism (Ungvari et al. 2004).

As the rate of glucose breakdown increases, profound hypophosphatemia potentially can result. “Beer drinkers’ hyponatremia” is a syndrome that appears to result from an intake of excessive fluid in the form of beer. Hilden and Svendsen (1975) observed hyponatremia in five patients who drank at least 5 liters of beer per day (L/d) without any other nourishment. The few studies focusing on alcohol’s direct effects on perfusion in human kidneys suggest that regulatory mechanisms retain control over this component of kidney function despite alcohol consumption. Even at high blood alcohol levels, only minor fluctuations were found in the rates of plasma flow and filtration through the kidneys (Rubini et al. 1955).

Though it’s reversible with treatment, it can increase the risk of developing chronic kidney disease. Chronic alcohol consumption induces profound injury in several organs that may affect and aggravate the deleterious effect of ethanol on the kidney. Ethanol itself markedly induces the expression of the microsomal ethanol oxidation system (CYP2E1), producing reactive oxygen species as a byproduct. Increased gastrointestinal permeability and endotoxin load may lead to alcoholic steatohepatitis resulting in excessive immunoglobulin A (IgA) load (due to increased intestinal production and decreased hepatic IgA clearance).