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Last updated January 1, 2014

Protein, Gout and Renal Failure in Reptiles

©200 Melissa Kaplan


Protein is one of the building blocks of life: our bodies are made from it and we need to eat it to grow and develop properly and maintain health.

Animals have evolved to process different types of protein: animal protein (from eating prey or raised-to-be-eaten animals) and plant (vegetable) protein. While they are all made up of the same amino acids, the amount of the amino acids vary between protein types, and plant proteins are often incomplete, missing some or all of one or more amino acids. To further complicate matters, animal and plant proteins are not metabolized the same, with each type of animal being physiologically adapted to either animal or plant protein. That is why carnivores need animal protein and do not do well when forced into being vegans or vegetarians, and why herbivores do not do well in the long run on animal protein. As for omnivores, they need to eat a combination of plant and animal protein, in ratios appropriate for their species.

Dietary nucleic acids are broken down by nucleases into nucleotides. Free pryimidine and free purine bases are formed once the nucleotides undergo enzymatic hydrolysis. Other free pyrimidine and purine are synthesized by the liver from amino acids. If these free bases are not used by the body, they are broken down further and excreted. Pyrimidines catabolize into CO2 (carbon dioxide) and NH3 (ammonia).

In some vertebrates, such as some reptiles (including iguanas), humans and non-human primates, birds, and Dalmatians, the end product of purine breakdown is uric acid; in some other reptiles, it is allantoin.

In reptiles, uric acid is filtered from the blood by the tubules in the kidneys. While it has been documented that dehydration does not impair uric acid excretion in alligators, dehydration does affect other reptiles. Renal function is impaired in all reptiles they are kept at temperatures too cool for proper systemic functioning.

In the blood, uric acid usually presents as monosodium urate. Both the urate salts and free uric acid are largely insoluble in water. When the serum concentration of either free uric acid or urate salts is elevated, hyperuricemia develops. Crystals, called tophi, are formed which may circulate through the blood or the synovial (joint) fluid, resulting in the deposition of crystals in tissues, organs and joints throughout the body. When they are deposited by the synovial fluid in joints, gouty arthritis or periarticular arthritis forms, both painful inflammatory conditions. When crystals are deposited in the subcutaneous and internal tissues, it is called visceral gout. Tophi, which appear as small, white crystalline nodules, are easily seen by the naked eye when looking at affected tissues. Gout may also be caused by the presence of monosodium urate crystals. Pseudogout, another acute inflammatory condition, is caused by crystals other than sodium urates.

The most common sites for tophi deposition are the kidneys, liver, spleen, lungs, pericardial sac, subcutaneous tissues, and other soft tissue. Since the liver is the body's first line of defense, filtering the blood of wastes and toxins, if the liver function is impaired, it will ultimately affect the kidneys, which then get a higher level of unfiltered wastes and toxins that they can handle. This may result in kidney failure before liver failure, especially if there are other factors that have impaired renal function, such as dehydration, the use of nephrotoxic drugs (including aminoglycosides and sulfonamides), purine-rich (animal protein) diets fed to herbivores, or acute or chronic inflammatory conditions which have been inadequately addressed.

With reptiles, environmental factors are most often implicated in gout leading to renal failure, especially chronic dehydration, diet, and suboptimum temperatures for the species

Kidney stones in reptiles may be 100% monosodium urate, or they may be calcium oxalate (as from feeding a diet high in plant foods containing oxalate), or calcium phosphate. The monosodium urate stones are transparent on radiographs; those made from calcium oxalate or other calcium combinations, will be visible on x-rays.


As discussed above, serum monosodium urate levels may be increased, but stones formed of this matter will not be seen on x-rays. Serum blood-urea-nitrogen (BUN), creatinine and uric acid levels may be within normal range in lizards. Serum phosphorous is generally very high, and calcium very low, with a ratio of less than 1:1 Ca:P; however, in some cases, phosphorous will be normal while the calcium is up on the hypercalcemic range. X-rays, ultrasound and kidney biopsy may be used to detect the presence of tophi and other problems.

Treatment at this point is mostly supportive, including ensuring adequate hydration, and dietary and environmental correction. Phosphate binders can be used to reduce high phosphate levels, and reduced a protein diet can be fed during recovery from acute stages. If the reptile is not self-feeding during the acute state, a slurry can be made to get the necessary nutrients in to the reptile while reducing the stress associated with feeding prey or the usual herbivorous diet.

See reptile veterinarian Stephen Divers' article, Clinician's approach to renal disease in lizards, for more information on diagnosis and treatment.



Barten, SL. 1996. Lizards. In, Reptile Medicine & Surgery. DR Mader, editor. WB Saunders, NY.

Divers, SJ. 1997. Clinician's approach to renal disease in lizards. Proceedings of the Association of Reptilian and Amphibian Veterinarians, October 24-27, Sacramento, CA.

Kaplan, M. 1997. Reptile rehabilitation. In, The Biology Husbandry, and Health Care of Reptiles. Lowell Ackerman, DVM, ed. Vol. III, pp. 898-941. TFH Publishing, Neptune City, NJ.

Mader, DR. 1996. Gout. In, Reptile Medicine & Surgery. DR Mader, editor. WB Saunders, NY.

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