Gout and Kidney Disease

Chronic kidney disease (CKD)

Chronic kidney disease (CKD) limits the amount of waste filtration your body is capable of processing. Uric acid is not seen as a foreign matter to the body, therefore is usually last to be dealt with from a toxin filtering standpoint. This can allow for uric acid build-up, and, in turn, the increased likelihood of developing Gout. The medications used to treat kidney disease have also been associated with drug-induced cases of Gout. Diuretics and beta blockers are typically used for kidney disease induced high blood pressure and are well known to contribute to Gout development.

There is enough scientific research to confirm that kidney disease can cause Gout. How about the opposite? Can Gout lead to kidney disease? The chicken or the egg? Uric acid is filtered through the kidneys, an undeniable relation to both diseases. While this connection may be less established, the evidence is certainly present. Each condition is well-equipped to feed the other.

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Traditional Gout Medications

Most commonly prescribed Gout medication options include:

Xanthine Inhibitors: These actually block the enzyme, (xanthine oxidase) necessary for the conversion of purines to uric acid. As of result, blood serum levels are lowered and used to prevent chronic gout, stones, and hyperuricemia. It is not actually a treatment for an acute attack, and can even exacerbate an attack if used while it’s running its course. This treatment sounds good in theory, however, un-naturally stopping a very natural and necessary production such as uric acid must take its toll on the body somehow? After all, uric acid is a potent antioxidant vital to the human body. Attempting to halt its production could be detrimental to its important role as the protector of our DNA. As a result, it is necessary to monitor the liver, kidneys, and blood during its use.

Possible side effects include:

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Understanding Uric Acid

Uric Acid

Purines perform multiple important functions within our cells, including regulating energy metabolism and signaling the energy conversion from one to another.  Purines are essentially the building blocks for all living things as a necessity for the growth, proliferation and survival of all cells.  The two purine bases, adenine and guanine, create bonds that form the DNA ladder. Humans breakdown purines and convert them into uric acid.

Uric acid happens to be a potent DNA protector.  All other mammals possess an enzyme known as uricase.  Uricase converts uric acid into allantoin, which can easily travel through the bloodstream and readily eliminated through the urine.  Humans do not possess this enzyme, therefore, we cannot oxidize uric acid into the more soluble compound of allantoin.  Our liver and kidneys are left to do the all-important jobs of purine breakdown and uric acid disposal, conducted respectively.

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New evidence of increased risk of death with Febuxostat (Uloric)

According to the latest CARES trial, the Gout drug Febuxostat (Uloric) failed up against Allopurinol when it came down to a combined rate of fatal and nonfatal adverse events for those that suffer with both Gout and Cardiovascular disease.  In fact, there was a significant increased risk of death for those that took this drug for Gout while also suffering from heart disease. The trial was mandated by the FDA and consisted of 6,190 patients, 84% of which were men.  Cardiovascular risk is naturally increased in patients with Gout.  The study was attempting to look at any difference in outcome for these patients taking Febuxostat, a nonpurine xanthine oxidase inhibitor, or those taking Allopurinol, a purine base analogue xanthine oxidase inhibitor.  The patients were followed for a median of 32 months, and a maximum of 85 months.  Without diving into all of the ratio statistics, the all-cause and cardiovascular mortality rate was higher in the Febuxostat group, 34% and 22% higher respectively. Continue reading “New evidence of increased risk of death with Febuxostat (Uloric)”
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