Chronic Renal Failure and Nephrolithiasis in a Two-Toed Sloth (Choloepus didactylus)
American Association of Zoo Veterinarians Conference 2005

Julia E. Napier1, DVM; Tiffany A. Moore2, DVM

1Potawatomi Zoo, South Bend, IN, USA; 2Riverbanks Zoo and Garden, Columbia, SC, USA


A 9-year-old, female, two-toed sloth (Choloepus didactylus) presented with acute illness and expired within 24 hours. On necropsy, two nephroliths were located in the renal pelvis of the right kidney. The bladder walls were dark and thickened. The right ureter was enlarged and filled with a mucopurulent substance. Histologically, the diagnosis was chronic renal disease with marked chronic interstitial nephritis and severe gastric mucosal mineralization. The composition of the kidney stones was determined to be struvites. Previous exams of this animal that included radiographs and bloodwork were unremarkable. Urinalyses had not been performed. Performance of routine physical exams, bloodwork, radiographs, and urinalyses may be important tools for antemortem diagnosis of renal disease and/or stones in this species. Evaluation of husbandry and diet provided for captive two-toed sloths may illuminate causes for increased incidence of this disease in these animals.


Chronic renal failure (CRF) is a common diagnosis in many species.5 As shown in a recent retrospective study, this clinical problem is a leading cause of death in two-toed sloths (Choloepus sp.).6 Replacement fibrosis of the renal parenchyma that occurs with CRF often obscures the specific etiology of end-stage kidney disease regardless of species.5 Sloths have an alkaline urine pH that contributes to formation of crystals and urinary tract stones, conditions that can set the stage for renal failure. Clinical signs in sloths with renal failure may be nonspecific such as weakness, dehydration, anorexia, and weight loss. Many sloths with CRF die acutely, showing little indication of disease. Routine physical exams are often not performed on captive sloths and little data exists for sloth urinalysis in normal or diseased states.6

Case Report

Abnormally thickened, viscous saliva was noted in a 9-year-old, female, two-toed sloth. This animal displayed acute anorexia and exhibited difficulty in clinging to tree branches. Physical exam revealed a body temperature of 33.3°C, heart rate of 85 bpm, and respiratory rate of 12 brpm. Emergency treatment under manual restraint consisted of enrofloxacin (Baytril, Bayer Corporation, Agriculture Division, Animal Health, Shawnee Mission, KS, USA) 2.5 mg/kg IM, Dexamethasone (Dexamethasone Solution, Phoenix Pharmaceuticals Inc., St. Joseph, MO, USA) 1 mg/kg IM and LRS (Lactated Ringer’s, USP, Abbott Laboratories, North Chicago, IL, USA) 200 ml SC. The sloth was placed in a crate with a heat source underneath it and was closely monitored. It did not respond to supportive care and died 24 hours after initial clinical signs were observed.

A cystocentesis completed immediately postmortem showed urine pH of 8, specific gravity of 1.013, trace blood, the presence of 1–2 triple phosphate crystals per HPF, 4+ bacteria, and 3+ protein (DiaScreen Reagent strips, Hypoguard, Minneapolis, MN, USA). Urine culture was not performed. At necropsy, the entire bladder wall appeared thickened and black. The right ureter was approximately twice the size of the left ureter and filled with a mucopurulent substance. Two nephroliths were found in the right kidney. On analysis, the stones were composed of magnesium ammonium phosphate hexahydrate (struvites). Chronic renal disease with lymphoplasmacytic interstitial nephritis and severe gastric mucosal mineralization was diagnosed histologically. Gastric mineralization has been documented as a secondary finding in other sloths with end-stage renal disease.6

Radiographs, taken 11 months prior to the animal’s death, did not indicate a difference in kidney size and nephroliths were not visualized. Serum chemistry at that time was unremarkable relative to ISIS values for this species. However, serum calcium was 10.4 mg/dl, showing an increase to the high-normal range as compared to a serum calcium measured approximately 2 years prior to the animal’s death (8.2 mg/dl). A urinalysis had not previously been performed.


An understanding of normal excretory processes in the sloth is important when considering potential causes of urinary tract disease in this species. Sloths urinate and defecate simultaneously, usually when they start their daily activity.3 Elimination occurs every 3–10 days. The bladder of a sloth can hold up to 1.5 L and sloths generally expel anywhere from 800–1200 ml of urine at a time.2,4,6 Sloth urine tends to be dilute and alkaline based on limited urinalyses results currently available.

The causes of nephrolith and urolith formation in the sloth are likely multifactorial. Uroliths composed of calcium, magnesium, ammonium, phosphorous, magnesium phosphate hydrate, and carbonate apatite are associated with an alkaline urine and appear to be the predominant stone type documented in this species.5

Bacterial cystitis may contribute to urolith and nephrolith formation as it increases organic debris available for stone formation. Urease positive bacteria such as Staphylococcus sp., Streptococcus sp., Klebsiella sp., and Proteus sp. can contribute to formation of struvites.5 Urinary tract infections were reported frequently in the retrospective study.6 Little information regarding results of urine cultures in this species exists. Klebsiella sp. was cultured from a two-toed sloth with struvites.8 Further studies of sloth culture results as correlated with urinary tract infection and stone formation are needed.

Diets offered to captive sloths may also contribute to the development of stone formation and kidney disease. Dietary protein and mineral levels may be important concerns for sloths as high protein diets are believed to contribute to stone formation and kidney disease in companion animals.5 Commercially produced low protein diets have been instrumental in reducing the occurrence of both diseases.5

Current domestic animal research is also directed at determining if foods high in magnesium and phosphorus predispose dogs and cats to uroliths and renal failure.1,7 Most commercially produced low protein diets are also lower in phosphorus, magnesium, and calcium. Foods highest in phosphorus content are proteins like meat. Legumes such as squash, zucchini, broccoli, mustard greens, cabbage, and asparagus also have a high phosphorus level.1,7

In the wild, studies indicate sloths eat primarily foliage including leaves, blossoms, shoots, green stems, and fruit.4 Speculation exists that sloths eat animal matter when it is easily available, yet this practice has not been documented.3,6

Captive sloths have proven to be fairly indiscriminate as regards dietary preference. They are fed a combination of fruits, vegetables, and greens in varying amounts, as well as some source of protein such as a feline diet, dog kibble, eggs, primate canned diet and/or biscuits.2-4,6,9

Two sloths presenting with cystic calculi underwent cystotomy for stone removal and were placed on a different diet such that their intake of protein, phosphorus, and magnesium was reduced.8 Their original canned primate diet (ZuPreem Primate Diet and ZuPreem Marmoset Diet, Mission, KS, USA) was replaced with Hill’s S/D (Hill’s Pet Products, Inc., Topeka, KS, USA) and stones did not reoccur. A study on the correlation between the amount or type of protein and minerals in the diet as it relates to renal disease and stone formation in the two-toed sloth is being pursued at this time.

This case demonstrates the need for performance of regular physical exams and clinical diagnostic tests to detect urinary tract disease in sloths. As seen in this case, two-toed sloths can quickly become ill and die before underlying renal disease is detected. It can be difficult to note a change in activity such as lethargy in these animals because they are sedentary by nature and are often in exhibits where they are not easily observed. Regular evaluation of changes in routine urine results including pH, protein levels, bacteria levels, and the amount of crystals in the urine may illuminate an animal’s predilection towards urinary tract infections, stone formation, and subsequent kidney problems. Sloths can be difficult to catheterize yet cystocentesis can be performed with relative ease. Free catch urine samples may be collected regularly for analysis of basic parameters and trends in urine composition.

Yearly blood chemistry values may reveal azotemia although this abnormality is not consistently seen in this species, as was the case with this sloth. Regular radiographs may reveal such abnormalities as visceral mineralization as has been documented for end-stage renal disease.6

Therapeutically, urine acidifiers may be considered to address urinary tract disease in sloths although there is no published information regarding their use in this species. The fact that two-toed sloths have a rumen-like gastrointestinal system might affect the viability of these acidifiers.


I would like to thank Laura Arriaga, the veterinary technician at the Potawatomi Zoo, for performing the necropsy and taking the pictures for this presentation. Thanks also to Dr. Ivan Rubiano, Dr. Deidre Fontenot, Dr. Rudy Wedlarski, Dr. Vicki Clyde, Judy Aviarios, Dr. Jackie Gai, and Dr. Beth Hammond for contributing the diet information from their respective institutions.

Literature Cited

1.  Allen, T.A., D.J. Polzin, and L.G. Adams. 2000. Renal disease. In: Hand, M.S., C.D. Thatcher, R.L. Remilliard, and P. Roudebush (eds.). Small Animal Clinical Nutrition, 4th ed. Mark Morris Institute, Topeka, Kansas. 563–604.

2.  Diniz, L. and P.M.A. Olivera. 1999. Clinical problems of sloths (Bradypus sp. and Choloepus sp.) in captivity. J Zoo Wildl Med. 30:76–80.

3.  Gillespie, D. 2003. Xenarthra: Edentata (Anteaters, Armadillos, Sloths). In: Fowler, M.E. and R.E. Miller (eds.). Zoo and Wildlife Medicine, 5th ed. WB Saunders, Philadelphia, Pennsylvania. 397–407.

4.  Goffart, M. 1971. Function and Form in the Sloth. Pergamon Press, Ltd. Oxford.

5.  Grauer, G. 1998. Urinary tract disorders. In: Nelson, R.W. and C.G. Couto (eds.). Small Animal Internal Medicine, 2nd Ed., Mosby, St. Louis, Missouri. 638–669.

6.  Moore, T.A. and N. Lamberski. 2001. Retrospective study of morbidity and mortality in the two-toed sloth (Choloepus hoffmanni and Choloepus didactylus). In: Proc Am Assoc Zoo Vet Annu Meet. 314–320.

7.  Osborne, C.A., J.W. Bartges, J.P. Lulich, D.J. Polzin, and T.A. Allen. 2000. Canine urolithiasis. In: Hand, M.S., C.D. Thatcher, R.L. Remillard, and P. Roudebush (eds.). Small Animal Clinical Nutrition, 4th Ed. Mark Morris Institute, Topeka, Kansas. 605–688.

8.  Rappaport, A.B. and H. Hochman. 1998. Cystic calculi as a cause of recurrent rectal prolapse in a sloth (Choloepus sp.). J Zoo Anim Med. 19:235–236.

9.  Wallace, C and Y. Oppenheim. 1996. Hematology and serum chemistry profiles of captive Hoffman’s two-toed sloths (Choloepus hoffmanni). J Zoo Wildl Med. 27:339–345.


Speaker Information
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Julia E. Napier, DVM
Potawatomi Zoo
South Bend, IN, USA

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