This case presents an interesting question: if alcohol metabolism occurs mainly in the liver, how did renal failure occur, and how did this result in a shriveled kidney? The answer to the first part of the question is well understood. Literature has reported several possible mechanisms by which chronic alcohol ingestion induces renal failure. One such mechanism is cell proliferation, resulting in kidney hypertrophy (Epstein). This nephromegaly eventually leads to renal failure, which can develop alongside common conditions like hypokalemia, hypomagnesemia, hypophosphatemia, hypoglycemia, ketoacidosis, and lactic acidosis (Ibrahim). These conditions are mediated by poor intake and alcohol's inhibition of antidiuretic hormone, which results in the enhanced urinary excretion. For example, the National Health and Nutrition Examination Survey reported that most Americans consume less than the recommended amount of magnesium (Moshfegh). Magnesium deficiency and chronic alcohol ingestion would therefore lead to a case of hypomagnesemia and an increased risk of renal failure. Another mechanism that could have led to the renal failure is the promoting of atherogenic risk factors by alcohol, which can happen in an acute or chronic manner (Singh). Collectively, these mechanisms might explain the nephrotoxicity problems that led to the renal failure, addressing the first part of our question.
The second part of the question regarding how the kidney ended up shriveled remains to be answered. If I was in contact with my friend (the patient), I might ask her myself, but this is not an option. I propose, therefore, that kidney failure and hypertrophy preceded necrosis, where eventually the nonfunctional kidney began to degrade, leading to the condition found at diagnosis. That's my guess, what do you guys think?
Thankfully, persons with a solitary kidney, including my friend, can live an unperturbed life assuming appropriate dietary restrictions and precautions. This is all to say that at the end of a stressful finals period, make sure to drink in moderation (assuming you can legally ingest alcohol).
References:
Epstein M. 1997. Alcohol's impact on kidney function. Alcohol Health and Research World. 21(1): 84-93.
Ibrahim AS, Dikin M, Soubani AO. 2005. Critical care aspects of alcohol abuse. South Med J. 98(3): 372-381.
Moshfegh A, Goldman J, Ahuja J, Rhodes D, LaComb R. 2009. What We Eat in America, NHANES 2005-2006: Usual Nutrient Intakes from Food and Water Compared to 1997 Dietary Reference Intakes for Vitamin D, Calcium, Phosphorus, and Magnesium. U.S. Department of Agriculture, Agricultural Research Service.
Singh VP, Singh N, Jaggi AS. 2013. A review on renal toxicity profile of common abusive drugs. Korean J Physiol Pharmacol. 17(4):347-357.
Mr. Le,
ReplyDeleteThis is terrifying.
Also, I wonder what other factors may have contributed to your friend's kidney failure. I would hope that one week of solid drinking wasn't the only reason she experienced this misfortune, otherwise, you may just spark up a lot of paranoia in undergrads all over the United States. In all seriousness, I've found a few resources online claiming that a ureter blockage could induce acute kidney failure (Khalaf et al). The blockage may have increased the pressure inside the kidneys, decreasing the pressure gradient into the kidneys and that may explain the low GFR? But the body is so resilient that I find this absolutely puzzling. Luckily we don't need both kidneys to survive.
As for the necrosis of the kidney, maybe accumulation of waste products induced oxidative damage to the kidney cells and apoptosis. Some of these waste products entering the blood could wind up right back in the same kidney for filtration and exacerbate the problem. Subsequent inflammation and maybe a little edema could put additional pressure on the kidney, further reducing GFR and stressing the structural integrity of the cells. What do you think?
Khalaf IM, Shokeir AA, El-Gyoushi FI, Amr HS, Amin MM. 2004. Recoverability of renal function after treatment of adult patients with unilateral obstructive uropathy and normal contralateral kidney: a prospective study. Urology. 64(4): 664-8.
Mr Le and Mr Olson,
ReplyDeleteI find this terrifying as well. I think I may be able to add to this paranoia that Ben has mentioned. It seems like binge drinking could be a lot more dangerous to the kidneys than many might suspect. I found a few articles as well that state that binge drinking can lead to acute tubular necrosis due to volume depletion, adverse reaction to alcohol, or rhabdomyolysis (Jung et al.). Rhabdomyolysis, for those that may not know is, when damaged skeletal muscle is broken down and gets released into the bloodstream as myoglobin and can be quite damaging to the kidneys. The paper mentions that acute tubular necrosis is reversible but excessive binge drinking may worsen it. The paper, specifically, focuses on one patient who acquired renal cortical necrosis, which is pretty rare but dangerous due to binge drinking. They believe that vitamin deficiency may have been aggravated by the excessive drinking and contributed to the renal cortical necrosis in this patient since alcohol can lead to vitamin deficiency, such as choline deficiency. This in turn can increase risk for other factors like arterial thrombosis (Remacha et al.).
I'm not sure if your friend had either of these types of necrosis, but its pretty scary how damaging alcohol can be not to just your liver, but to other organs too. I remember we talked about alcohol and esophageal cancer in one of our classes as well. So I guess the moral of this story is listen to your mama: drink moderately and take your vitamins (this is what my mama tells me, at least).
Jung YS, Shin HS, Rim H, Jang K, Park M, Park JS, Lee CH, Kim GH, Kang CM. 2012. Bilateral Renal Cortical Necrosis Following Binge Drinking. Alcohol Alcohol. 47: 140-142. Available at: http://alcalc.oxfordjournals.org/content/47/2/140.full#ref-11
Remacha AF, Souto JC, Rámila E, Perea G, Sarda MP, Fontcuberta J. 2002. Enhanced risk of thrombotic disease in patients with acquired vitamin B12 and/or folate deficiency: role of hyperhomocysteinemia. Ann Hematol. 81:616-21. Available at: http://www.ncbi.nlm.nih.gov/pubmed/12454698