Date Published: , 2017
Publisher: National Institute on Alcohol Abuse and Alcoholism
Author(s): Zoltan V. Varga, Csaba Matyas, Janos Paloczi, Pal Pacher.
Chronic alcohol consumption is a well-known risk factor for tissue injury. The link between alcohol use disorder (AUD) and kidney injury is intriguing but controversial, and the molecular mechanisms by which alcohol may damage the kidneys are poorly understood. Epidemiological studies attempting to link AUD and kidney disease are, to date, inconclusive, and there is little experimental evidence directly linking alcohol consumption to kidney injury. However, studies conducted primarily in other organs and tissues suggest several possible mechanisms by which alcohol may promote kidney dysfunction. One possible mechanism is oxidative stress resulting from increased production of reactive oxygen species, which leads to an excessive amount of free radicals, which in turn trigger tissue injury and increase inflammation. 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. Notably, these mechanisms have not yet been validated experimentally in the kidney. Additional research is needed to clarify if alcohol does indeed promote kidney injury and the mechanisms by which alcohol-induced kidney injury may occur.
It is well established that cardiovascular diseases (including hypertension and ischemic heart disease) and diabetic microvascular complications are major risk factors for the development of chronic kidney diseases (Briasoulis et al. 2012; Carlsson et al. 2005; Reynolds et al. 2003; Ronksley et al. 2011). In turn, heavy alcohol consumption is implicated in the development of these cardiac diseases, with chronic, heavy drinkers at higher risk than those who consume small to moderate amounts of alcohol.
If alcohol consumption does in fact influence kidney disease, the question remains: How? There is direct and indirect evidence for several possible mechanisms. These changes are caused either by alcohol itself or by excessive amounts of the products formed when cells break down (or metabolize) alcohol, including acetaldehyde, NADH, and free radicals. These alcohol-related pathophysiologic changes in cells have been linked to damage in many organs and may play a role in kidney damage. In addition, complex interactions between organs may further complicate and accentuate the development of kidney pathology in people with AUD (see figure).
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.