Clinician's Approach to Renal Disease in Lizards
©1999 Stephen J. Divers, BSC, MiBiol, BVetMed, MRCVS, Proceedings of the ARAV, October 24-27, Sacramento CA
Key words: renal failure, kidney disease, lizard, squamata, green iguana, radiography, urography, endoscopy, fluid therapy
Urine produced by the kidneys flows down a ureter-like mesonephric duct to the urodeum of the cloaca, where it then passes into the bladder (if present) or cranially into the distal colon for storage prior to evacuation. Variable changes in urine concentration and electrolyte composition can occur within the bladder or distal colon. This means that bladder urine is not sterile and may not be a true osmotic/electrolyte representation of renal urine. A renal portal system is anatomically present but its functional significance is questionable. Nevertheless all potentially nephrotoxic or renally excreted drugs should be injected into the cranial part of the lizard.
History and Clinical
In cases of chronic renal disease, there will often be nutritional (high protein diets, excess vitamin D3 supplementation) or husbandry factors (low humidity, mild long term water deprivation) that may indicate potential renal compromise. Such animals tend to have a history of reduced appetite poor, weight gain or weight loss, and occasionally owners may notice increased drinking. They are usually of poor body condition, dehydrated and the kidneys may or may not be palpable. Unfortunately, most owners miss the initial signs associated with kidney disease, and so chronic cases will often be presented as emergencies just like the true acute renal failure case.
A thorough physical examination is essential but it is often necessary to resort to laboratory techniques and ancillary diagnostics to make a definitive diagnosis.
The calcium and phosphorus ratio is often a reliable indicator of renal disease, and is usually elevated before any other biochemical parameter. The solubility index is calculated as the product of Ca (mmol/L) x PO4 (mmol/L), and is normally less than 9. If the solubility index rises above 12 then healthy tissue will start to mineralize, while between 9 and 12 mineralization of diseased tissue (kidneys) occurs.
Urine samples, either freshly voided or obtained by cystocentesis, should be examined. Although lizard urine is not as clinically useful as mammalian urine, examination is warranted, particularly if obtained by cystocentesis. Microscopic examination may reveal blood, a high inflammatory cell presence or renal casts indicating active infection and acute disease. Normal bladder urine may not be sterile, but if a culture and sensitivity reveals a profuse growth of a single organism then that may be significant and worth acting upon.
Ultrasonography from the ventral mid line and just caudal to the vent can also be used to assess gross pathological changes.
There is increasing interest in the use of MRI (which is superior to CT scanning) but the limited availability and costs of such imaging techniques makes them practically obsolete for most clinicians.
The problems facing the clinician include making a definitive diagnosis, determining if it is acute or chronic, providing specific therapy and general support, and providing the owner with a prognosis. To this end the author has found that renal biopsy represents the most important diagnostic and prognostic tool when investigating renal disease.
Renal biopsies can be taken in four ways: major celiotomy approach, cranial tail cut-down approach, transcutaneous needle biopsy and endoscopic biopsy. The author prefers endoscopic biopsy because it enables visualization of both kidneys and ureters via a small laparoscopic (celiotomy) incision and the taking of 1-4 small biopsies (3 Fr) which are submitted for culture and histology. In the vast majority of cases biopsy provides the definitive diagnosis and helps give the owner a prognosis. The site of entry is in the paralumbar area, with the lizard in lateral recumbency; Air inflation aids visualization. The author's personal opinion is that as soon as the lizard is hydrated and stable for anesthesia, endoscopy and biopsy should be attempted.
Acute renal failure
Hydration status should be monitored using serial weight and PCV measurements. When correct hydration has been achieved, it is vital that over hydration is avoided and therefore a reduction in maintenance fluids to 2-10 ml/kg/d is required but hydration status must continue to be monitored. If over hydration does occur (pharyngeal edema, pulmonary edema) then the use of diuretics is advisable (furosemide, thiazides).
In cases where uric acid levels are significantly elevated (>750 mmol/l) the use of allopurinol (20 mg/kg p.o. q 24 hr) may reduce hepatic uric acid production, while the administration of anabolic steroids may reduce protein catabolism. In cases of pre-renal ARF, rehydration, restoration of circulatory volume and supportive therapy may be all that is necessary. In cases of post renal obstruction, renal stones and ureteral obstructions will often have to be surgically removed before urine flow can be reestablished. In cases of toxin induced nephropathy, identification and removal of the toxin from the environment and gastric lavage may be useful. In cases of suspected aminoglycoside toxicity all drug medication should stop and osmotic diuresis instigated to maintain renal perfusion once normal hydration status has been achieved. Acute hypercalcemia (from acute vitamin D3 overdose but not breeding females) can cause ischemic acute tubular necrosis through the development of nephrocalcinosis, and in such cases prednisolone, calcitonin and diuresis should be considered. Chronic renal damage can also lead to calcium salt deposition in soft tissues including the kidney due to an elevation in the solubility index. Acute renal disease due to infectious agents should be empirically treated with broad spectrum anti microbials until culture and sensitivity results are obtained. It is important to use drugs with a large safety margin as drug metabolism and excretion may be significantly affected.
If the lizard remains oliguric once hydration and any underlying causes have been addressed, then the i.v. Or i.o. administration of 20% dextrose may be used in an attempt to induce diuresis. Initially dextrose is given at 0.4-1.0 mI/kg/hr i.v. Or i.o. for 30-60 min, then the rate is reduced to 0.2-0.5 MI/kg/hr. If the lizard remains oliguric, then diuretics and coelomic dialysis may be attempted. The right lateral coelomic region just cranial to the right limb is prepared aseptically and a 18-23 g 25-50 mm Teflon catheter is introduced into the coelomic cavity and sutured to the skin. Warm (30-35 C) fluids (30-40 ml/kg) are injected into the coelomic cavity and left in situ for 1-2 hr before being removed. Balanced electrolyte and hypertonic 5% dextrose solutions are recommended, however due the relative insolubility of uric acid compared to urea, dialysis appears to be less effective in reptiles than mammals.
(From January 1995 to January 1996, the author has treated 11 cases of acute renal failure in lizards, 7 cases (64%) are known to have survived for longer than a year.)
Chronic renal failure
(From January 1995 to January 1996, the author has treated 23 cases of chronic renal failure in lizards, 5 cases (22%) are known to have survived for longer than a year.)
If, as clinicians, we fail to resolve acute renal failure or permit chronic renal disease to progress unhindered then the outcome will be gout (visceral and articular). Acute gouty episodes may be treated symptomatically but widespread visceral gout is the result of end stage kidney disease and the prognosis is usually hopeless .
1. Barten, S.L. (1996). Lizards. In: Reptile Medicine and Surg&y (Ed. D.R. Mader), p 47-61. WB Saunders, Philadelphia.
2. Divers, S.J., Redmayne, G. and Aves, E.K. (1996). Hematological and biochemical values of 10 green iguana (Iguana iguana). Veterinary Record 138:203-205.
3. Frye, F.L (1991). Comparative histology. In: Biomedical and Surgical Aspects of Captive Reptile Husbandry (Ed. FL Frye), p 488-501. Krieger, Malabar.
4. Mader, D.L. (1996). Gout. In: Reptile Medicine and Surgery (Ed. DR Mader), p 374-379. WB Saunders, Philadelphia. 5. Zwart, P. (1992). Urogenital systern. In: Manual of Reptiles (Eds. P.H. Beynon, M.P.C. Lawton and J.E. Cooper), p 117-120. BSAVA, Cheltenham.
Please see the Glossary if you need some help with the terminology and abbreviations.
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