Renal Papillary Necrosis in Three Captive Bengal Tigers (Panthera tigris tigris) Treated with Nonsteroidal Anti-Inflammatory Drugs
American Association of Zoo Veterinarians Conference 2007
Arely G. Rosas-Rosas1, MVZ; Carles Juan-Sallés2, DVM, DACVP; Michael M. Garner3, DVM, DACVP; Ray Ball4, DVM; Freeland Dunker5, DVM
1Africam Safari, Puebla, Puebla, México; 2ConZOOlting Wildlife Management, Samalús, Barcelona, Spain; 3Northwest ZooPath, Monroe, WA, USA; 4San Francisco Zoo, San Francisco, CA, USA; 5Busch Gardens, Tampa, FL, USA


This paper describes three cases of renal papillary necrosis (RPN) in Bengal tigers (Panthera tigris tigris) from different facilities that were previously treated with nonsteroidal anti-inflammatory drugs (NSAIDs) (Table 1).

Table 1. Clinical history and treatment of three captive Bengal tigers (Panthera tigris tigris) with renal papillary necrosis



Age (years)

Weight (kg)

Motive of use of NSAIDs



Duration of treatment


1 (AS)a




Clinically healthy, treated with NSAIDs for minor surgical procedure

Flunixin meglumine (Finadyne®)

1 mg/kg

1 day (single dose)


2 (SFZ)b




Infected bite wounds, degenerative joint disease

Flunixin meglumine (Banamine®)

0.85 mg/kg

2 days (daily)


3 (BG)c




Vertebral osteoarthritis with medullar compression (two periods of treatment)

Etodolac (EtoGesic®)

5 mg/kg

7 days (with 3 days off)


6.4 mg/kg

5 days (daily)
2 days off
20 days (q 48 h)

aAS=Africam Safari Zoo, México
bSFZ=San Francisco Zoo, USA
cBG=Busch Gardens, USA
dF=female; M=male
e*Finadyne® (Schering Plough); Banamine® (Schering Plough); EtoGesic® (Fort Dodge)

Grossly, case 1 had multiple gastric ulcers, yellow discoloration of the renal papillae and dehydration. In case 2, the urinary bladder was filled with milky white urine, and focal areas of necrosis were detected in the renal pelvis/medulla. In case 3, the left kidney was firm and swollen and had black pigmentation of the pelvis.

Histologically, in all cases there was RPN. In case 1, there was also renal tubulointerstitial and gastric mineralization. The kidney in case 2 also had suppurative and necrotizing, tubulointerstitial nephritis in the medulla. Interestingly in case 3, the renal lesion was unilateral and was associated with infarction of the papillae.

In all cases, the renal lesions are consistent with ischemia of the papillae associated with the use of NSAIDs in mammals and contributed significantly to the death of these tigers. However, in case 2, a bacterial etiology may be involved based on the presence of scattered gram-negative bacilli. Immunohistochemistry and Warthin-Starry stain were negative for leptospirosis. RPN can occur in humans and animals treated with NSAIDs as a result of inhibition of cyclooxygenase and synthesis of prostaglandins.3 It is common in horses with prolonged treatments with phenylbutazone or flunixin-meglumine.4

Two of three tigers in this report were treated with flunixin meglumine. RPN has been previously documented in a tiger treated with this drug.5,7 The recommended dose for flunixin meglumine in cats is 0.25 mg/kg, although cats treated with 1 mg/kg during 7 days had no secondary/toxic renal or gastric effects in a study.6 In case 1, five other tigers treated with the same protocol at the same time did not show any signs of disease. This suggests an individual, possibly genetic factor, may be implicated in this animal. Case 3 was treated with etodolac that has not been associated with renal disease previously;2 it has been used successfully in tigers with osteoarthritis, but constant monitoring is recommended.1 Interestingly, there was no clinical indication of renal insufficiency at any time in this animal. Based on these three cases and a previous report of RPN in tigers, caution is recommended for the use of NSAIDs in felids, particularly tigers.

Literature Cited

1.  Ball, R.L., L. Weiner, and A. Richner. 2001. Etodolac as an adjunct to managing osteoarthritis in captive Bengal tigers (Panthera tigris). Proc. Am. Assoc. Zoo Vet. Pp. 137–139.

2.  Brater, D.C. 1990. Evaluation of etodolac in subjects with renal impairment. Eur. J. Rheumatol. Inflamm. 10:44–55.

3.  Bochelser P.N. and D.O. Slauson. 2002. Inflammation and repair of tissue. In: Slauson D.O. and B.J. Cooper (eds.). 2002. Mechanisms of Disease, 3rd ed. Mosby Inc., St. Louis, Missouri. Pp 210–214.

4.  Maxie M.G. The urinary system. 1993. In: Jubb K.V.F., P.C. Kennedy and N. Palmer. Pathology of Domestic Animals, 4th ed. Academic Press, Inc., San Diego, California. P 472.

5.  McCullagh, K.G., and V.M. Lucke. 1978. Renal papillary necrosis in the tiger. Acta Zool. Pathol. Antverp. 70:3–13.

6.  Taylor, P.M., Winnard, J.G., Jefferies, R., and Lees, P. 1994. Flunixin in the cat: a pharmacodynamic, pharmacokinetic and toxicological study. Br. Vet. J. 150:253–262.

7.  Wolf, D.C., S.D. Lenz, and W.W. Carlton. 1991. Renal papillary necrosis in two domestic cats and a tiger. Vet. Pathol. 28:84–87.


Speaker Information
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Arely G. Rosas-Rosas, MVZ
Africam Safari
Puebla, Puebla, México

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