In turn, such expansion of body fluid signs you were roofied volume can contribute to high blood pressure, a condition often seen among chronic alcoholic patients. Alcohol can produce urine flow within 20 minutes of consumption; as a result of urinary fluid losses, the concentration of electrolytes in blood serum increases. These changes can be profound in chronic alcoholic patients, who may demonstrate clinical evidence of dehydration. A cell’s function depends not only on receiving a continuous supply of nutrients and eliminating metabolic waste products but also on the existence of stable physical and chemical conditions in the extracellular fluid1 bathing it.
The treatment for alcohol-induced kidney problems depends largely on the type of kidney disease a person has sustained. According to the American Kidney Fund (AKF), there are five stages of chronic kidney disease (CKD), with stage 1 representing the earliest and mildest stage and stage 5 representing the most advanced and severe. Nonetheless, the reviewers note that alcohol metabolism produces free radicals and other harmful by-products that are known to damage the body’s organs and tissues.
Potential Mechanisms of Alcoholic Kidney Injury: Lessons From Experimental Studies
Frequent urination that goes along with this flushing of the system can lead to dehydration. This can interfere with the functioning of the kidneys and other organs. Regular and excessive alcohol use can also cause high blood pressure (hypertension) for a combination of reasons, such as disrupting hormones and affecting the muscles in blood vessels. A 2018 study found that having alcohol use disorder increased the likelihood of having a new diagnosis of CKD. However, the study authors also mentioned that more studies are needed to explore the connection between AUD and kidney function.
Know Your Kidneys – Identify and reach your kidney health goals.
One way in which alcohol directly affects the kidneys is by altering the form and structure of this pair of organs, as demonstrated by various animal studies. For example, in an early study on dogs (Chaikoff et al. 1948), investigators observed several striking alterations after chronic alcohol administration. The basement membrane of the glomerulus (see sidebar figure) became abnormally thickened and was characterized by cell proliferation. Further changes included enlarged and altered cells in the kidney tubules. In another study, Van Thiel and colleagues (1977) compared kidney structure and function in alcohol-fed and control rats. The NKF also notes that excessive drinking can cause acute kidney injury (AKI) — a sudden decrease in kidney function that usually resolves with time but may be lasting in some cases.
- Although the mechanism of alcoholic myopathy is not fully understood, it is likely that disruption of mitochondria-related energy homeostasis is important in promoting muscle cell (myocyte) injury (Eisner et al. 2014).
- As long as cirrhotic patients remain unable to excrete sodium, they will continue to retain the sodium they consume in their diet.
- In the absence of ADH, when body fluids are overly dilute, the kidneys dilute the urine, allowing more water to leave the body.
- You may need to take a complete break from alcohol for a set amount of time or reduce the amount of alcohol you consume.
It’s not as simple as one drink, one unit
Their analysis included 20 studies representing a total of 292,431 patients. In fact, IgA glomerulonephritis—acute inflammation of the kidney caused by an IgA immune response—is one of the most common types of primary glomerulonephritis worldwide (D’Amico 1987). This IgA-related kidney disease leads to clinical symptoms of renal injury and eventually progresses into renal failure (Amore et al. 1994; Bene et al. 1988; Pouria and Feehally 1999). Experimental studies suggest that heavy alcohol consumption induces IgA kidney disease (Smith et al. 1990).
Ethanol and polyphenol both have anti-oxidative effects and ethanol improves polyphenol absorption, thereby contributing to bioavailability [4,5,6]. Furthermore, alcohol has an anti-inflammatory effect, with increased serum interleukin-10 levels and decreased serum interleukin-16 levels [20]. Alcohol consumption can raise high-density lipoprotein cholesterol concentration [21,22], improve insulin sensitivity [23], and reduce platelet aggregation rate and fibrinolysis [21,22].
Studies historically have shown that alcohol consumption markedly increases magnesium excretion in the urine and may affect magnesium levels in other ways as well. For example, when rats are given alcohol, they also require significant magnesium in their diets, suggesting that alcohol disrupts absorption of this nutrient from the gut. Investigators have speculated that alcohol or an intermediate metabolite directly affects magnesium exchange in the kidney tubules (Epstein 1992). Several mechanisms may contribute to abnormally low phosphate levels (i.e., hypophosphatemia) (see box). Simply lacking an adequate amount of phosphate in the diet is one possible reason for phosphate deficiency.
Also, alcohol does not appear to make kidney disease worse or make it more likely that someone with kidney disease will need dialysis. Chronic alcoholism is the leading cause of low blood levels of magnesium (i.e., hypomagnesemia) in the United States (Epstein 1992). Often it occurs simultaneously with phosphate deficiencies, also frequently encountered among alcoholic patients. Hypomagnesemia responds readily to magnesium supplementation treatment, however. Each of the 2 million functional units (i.e., nephrons) in a pair of normal kidneys forms urine as it filters blood plasma of substances not needed by the body.
Uncoupling eventually leads to generation of damaging ROS like superoxide anion, instead of the vasorelaxant nitric oxide that maintains normal blood flow in the kidney. Another potential cause of hypophosphatemia in alcoholic patients is hyperventilation, which can occur during alcohol withdrawal. Prolonged rapid, shallow breathing results in excessive loss of carbon dioxide and decreased blood acidity (i.e., alkalosis), which in turn activates an enzyme that enhances glucose breakdown. In glucose breakdown, phosphate becomes incorporated into various metabolic compounds, ultimately lowering blood levels of phosphate.
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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.
A progressive accumulation of extracellular fluid results, and this excess fluid is sequestered foods that contain alcohol primarily in the abdominal region, where it manifests as marked swelling (i.e., ascites) (see figure). In addition, excess fluid accumulates in spaces between cells, clinically manifested as swelling (i.e., edema) of the lower back and legs. As long as cirrhotic patients remain unable to excrete sodium, they will continue to retain the sodium they consume in their diet. Consequently, they will develop increasing ascites and edema and experience weight gain. In some cases, vast amounts of abdominal fluid may collect, occasionally more than 7 gallons (Epstein 1996). Alcohol consumption also is known to induce a state of low blood sugar (i.e., hypoglycemia) and activate the portion of the nervous system that coordinates the body’s response to stress (i.e., the sympathetic nervous system).
“Normal” urine flow rate is 1 milliliter per minute (i.e., approximately 1 to what is a sponsor 1.5 L/day), but this rate can vary widely, depending on water intake or dehydration level, for instance. Alcohol causes changes in the function of the kidneys and makes them less able to filter the blood. Alcohol also affects the ability to regulate fluid and electrolytes in the body.