Herp Nephrology & Urology Flashcards
What species of reptiles have well developed urinary bladders?
What reptile taxa have rudimentary bladders?
What taxa do NOT have urinary bladders?
What are the three parts of the reptile cloaca?
MARMS – 66. Urology
Anatomy:
Presence of Urinary Bladders, Table 66.1
- No urinary bladders: snakes, crocodilians, some lizard taxa (most monitors and tegus)
- Rudimentary urinary bladders: some lizard taza
- Well developed urinary bladders: chelonians, tuatara, some lizard taxa
- In species with bladders: urine enters via the urodeum of cloaca and urethra (not directly from uretersIn species without bladders: urine stored in distal dilated ureters or cloacocolonic region
Cloaca
- Coprodeum: anterior; waste from large intestine
- Urodeum: receives from ureters, urethra, and genital ducts (genital ducts and ureters fuse to enter in some species)
- Proctodeum: receives waste and urogenital products discharged through vent
Describe the renal anatomy of squamates and tuataras.
Where are the kidneys located in lizards? What is unique about the caudal poles of the kidneys? What vessels supply and drain the kidneys?
Where are the kindeys located in snakes? What vessels supply and drain the kidneys?
Are squamate kidneys lobulated?
What is the sexual segment of the kidneys? What does it produce?
Lizards:
- Kidneys: within or cranial to pelvis, paired, elongated, slightly lobulated, often flattened dorsoventrally (laterally in chameleons)
- Mature males: kidneys have hypertrophy of the distal convoluted tubules to produce seminal fluid
- Caudal poles of iguana kidneys are fused
- Portal venous supply: returning blood from tail (caudal v) and hind legs (iliac v) -> left and right afferent renal portal v to supply kidneys-> capillaries perfuse renal tubule cells -> venous blood drains into interlobular efferent v -> renal veins -> fuse to form postcaval v -> blood back to heart
- Pelvic v connect to iliac v before attachment to afferent renal portal v, can divert blood around kidneys into ventral abdominal v to liver
Snakes
- Boid kidneys: paired, flattened, elongated, 25-30 lobules (except dwarf and rough boas without lobules)
- Left behind right
- Renal position reported as position from snout to cloaca in boids, colubrids, elapids, and viperids; occupy 10-15% of snake’s body length
- Males: hypertrophy and pale sexual segment; kidneys closely associated with vas deferens
- Urine stored in distal colon or dilated distal ureters
- Similar blood flow except no iliac v (mesenteric v receives connections from renal portal v)
Tuatara
- Paired, single lobed, crescentic in outline, dorsal in pelvic canal
- Blood supply similar to lizards except no direct connection between iliac and abdominal v
Where are the kidneys located in chelonians?
Is that different in seaturtles?
What is unique about the bladder of chelonians?
What vessels supply and drain the kidneys?
Where are the kidneys located in crocodilians?
Are they the same size?
What vessels supply and drain the kidneys?
Chelonians
- Kidneys paired, retrocoelomic, caudodorsal coelom, flattened, lobulated
- Sea turtles - kidneys cranial to pelvic girdle
- Kidneys -> ureters -> urodeum -> urethra -> bladder (storage)
- Bladder: bilobed
- Small bilateral accessory bladders
- Two abdominal v found linked with a transverse anastomosis
Crocodilians
- Kidneys paired, lobulated, dorsal body wall near spinal column
- Left kidney may be larger than right
- Two abdominal v connect to an iliac v
- Mesenteric v originates from afferent renal v
Describe the microscopic anatomy of the reptilian kidney.
Do they have a renal pelvis?
What is the corticomedullary distinction like?
Is there a loop of henle?
How many nephrons do they have?
Describe the flow of urine through the nephron.
What part of the nephron is the sex segment?
Microscopic anatomy
- No pelvis or pyramids; not divided into medulla and cortex, no loop of Henle
- A few thousand nephrons (mammals have a million or so)
- Renal corpuscles in circular pattern in mid portion of each lobule
- Glomeruli less developed compared to birds
- Glomerulus -> neck segment -> proximal tubule ->intermediate segment -> distal tubule -> collecting duct -> ureter
- Ciliated cuboidal cells except distal tubule (no cilia)
-
Male squamates: distal tubule followed by sex segment - flat mucus cells that increase in height 2-4x in breeding season; Possible functions:
- Creation of copulatory plug against rivals
- Blockage of tubules during copulation to separate urine and seman
- Activate source of sustenance for sperm survival
- Ureter on ventromedial surface of kidney
- Nephron blood supplied by afferent arteriole forming glomerular capillary tuft surrounded by Bowman’s capsule; blood exits efferent arteriole supplying blood to tubule cells
- Venous blood mixes with arteriolar blood at start of proximal tubule
Describe the renal physiology of reptiles.
What are the primary nitrogenous wastes? How does that differ by species?
How does GFR compare with mammals and birds?
How is GFR regulated in reptiles?
What hormone decreases GFR? what hormone increases GFR?
Water, sodium, and potassium are reabsorbed where in the filtration process? How is that different from mammals?
What effect does the renal portal system have clinically?
Physiology
- Nitrogenous waste from proteins/amino acid metabolism includes ammonia, urea, or uric acid
- Ammonia: aquatic turtle species, crocodilians (66% in nile crocodile)
- Urea (40,000 x more soluble than uric acid): more common in aquatic species (80% in snappers), terrestrial chelonians
- Uric acid: water conservation (lack loop of henle)
- Decreased GFR (assists with water conservation)
- Reptiles 5-25 ml/kg/hr
- mammals/birds 100-200 ml/kg/hr
- Decreases during dehydration and increases with water loading
- Not many studies with effect of temp on GFR - may increase with large temperature change, but MAP and GFR seemed independent of temp within optimal zone
- GFR appears to be mediated by changes in the number of filtering glomeruli, rather than variation in nephron filtration rates
- Renal portal blood supply continues to perfuse the tubules despite low GFR - prevents ischemic necrosis - more blood shunted through kidneys during times of water deprivation
- Posterior pituitary releases arginine vasotocin (AVT) causing vasoconstriction of the afferent glomerular arteriole, which decreases GFR
- AVT may also stimulate dilution of urinary fluid in intermediate segment to facilitate water reabsorption
- High doses of oxytocin can decrease GFR (may be mediated by BP)
- Prolactin increases GFR (may be mediated by systemic arterial BP)
- Tubular function - regulation of water, sodium, potassium, hydrogen ions, calcium, phosphorus, and nitrogen compounds
- In mammals, proximal tubules absorb 60-80% of filtered water. Only 30-50% in reptiles, but rest is absorbed in distal tubules, colon, cloaca and bladder if present
- Failure to excrete urate -> hyperuricemia -> gout -> death
- Sodium and potassium freely filtered by glomerulus, but in many species the colon, cloaca and bladder are more important sites for regulation of sodium excretion/water reabsorption
- AVT, aldosterone and temperature can affect sodium and potassium regulation
- Studies on furosemide indicate that it exerts diuretic effects (increases sodium, chloride, potassium, and water losses) despite the lack of a loop of Henle
- Vitamin C synthesis occurs in kidney
- Renal portal system and drugs in caudal body
- Possibility of high dose first pass effect for renal toxicity (aminoglycosides)
- Effect on plasma drug concentrations has not been proven to decrease clinical efficacy
What findings on anamnesis and examination may indicate renal disease?
How does it vary in acute renal failure rather than chronic renal failure?
History and PE
Acute
- Acute onset of depression, anorexia, sometimes cessation of urine/urate output -> often in poorly managed conditions
- Exposure to nephrotoxins (aminoglycosides, high D3 doses)
- Water deprivation, severe dehydration, hemorrhage - > poor perfusion -> acute failure
- Good/better body condition compared to chronic
Chronic urinary tract disease
- Long term poor husbandry: high protein diets (canned dog or cat food), inadequate humidity or water access, substituting oral D3 for broad spectrum UVB lighting (nephrocalcinosis)
- History of secondary nutritional hyperparathyroidism - chronic renal damage, PTH cytotoxic effects
- Deteriorating body condition, decreased appetite and activity over weeks or months
- Usually dehydrated and emaciated; pu/pd rarely reported
- Severe renal compromise - depressed, weakened
Additional things to look for
- Pharyngeal edema not uncommon
- Lizards can have bilateral exopthalmia and/or increased scleral vascularity
- Palpation of enlarged kidney (species dependent)
- Constipation
- Cloacal prolapse
What changes may be noted on biochemistry panels in reptiles with renal disease?
What is the best method for measuring nitrogenous waste products?
What elecrolyte disturbances may be present?
How may protein be affected?
Serum biochemistry
- Azotemia, hyperuricemia, uremia -> majority of renal function lost, renal failure
- Creatinine is poor indicator of renal disease - low production, variable excretion
- Squamates: uric acid is principle nitrogenous metabolite to measure
- Many chelonians and crocodilians: urea and ammonia quantification may be important
- Proportions of ammonia, urea and uric acid vary with hydration status, postprandial effects and hepatobiliary disease
- Serial measurements of nitrogenous wastes are recommended for clinical value and reliance on UA alone is flawed
- Ammonia must be collected in cold heparinized syringes, kept on ice, and analyzed in an hour
- Ca/P ratios may be inverted (green iguana), but not in all cases of renal failure
- Hyponatremia and hyperkalemia: dysfunction of distal tubules, cloaca, colon, bladder or salt glands
- AST, CPK, LDH may be elevated, but not specific to renal damage
- Hypoalbuminemia: severe glomerular disease may increase urinary loss of albumin, however accurate ALB determination requires electrophoresis
- Chronic disease may lead to renal secondary hyperparathyroidism; commercially available 1,25-dihydroxycholecalciferol test (reference ranges unavailable)
- Biochemical values affected by gender, season, nutrition and management
- Interpret reference ranges with caution
- Obtaining serum chemistry values from clinically healthy patients recommended during routine wellness checks to serve as baseline
What hematologic changes may occur in a reptile with renal disease?
What changes may be found with the red cells? What about the white cells?
Hematology
- Elevated PCV: dehydration
- Chronic renal disease ->nonregenerative anemia -> masks dehydration
- Acute infection (without immunosuppression): heterophilia and/or azurophilia
- Chronic renal disease: decreased, normal, or mildly increased WBC; monocytosis common
- Reptiles that have been kept inappropriate (colder) temperatures may fail to show appropriate leukocyte response even with overwhelming infection (immunocompromised)
- Interpret reference ranges with caution
Describe the evaluation of urinalysis in reptiles?
Is USG useful?
Is reptile urine sterile?
What are some of the more common collection techniques?
What does green urine indicate?
What are some typical reptile urine pH?
How does protein change with illness?
Urinalysis
- Reptiles don’t concentrate urine, so USG is not helpful
- Urine passes through urodeum before entering the bladder and is not sterile
- Free catch - some individuals may not void with handling or stimulation of cloaca, additional contamination from surfaces
- Cystocentesis - bladder wall is thin with potential for leakage and coelomitis, changes can occur in cloaca and bladder so it may not represent renal urine
- Chelonians: left prefemoral approach preferred (liver on right); rotate to allow bladder to fall
- 22-25 g needle
- Ultrasound recommended
- Catheterization is challenging; endoscope guided urethral catheter placement allows for repeated acquisition of samples
- Urine evaluation ideally immediately after obtaining sample (pH and bacterial changes, cell lysis, crystal precipitation)
- Gross evaluation: starvation and hepatic disease promote biliverdin production -> lime green color
- Dipsticks not validated but can be useful
- pH
- unpublished studies: herbivorous tortoise urine normally alkaline, box turtle urine slightly acidic
- Desert tortoises: mean urine pH 5.6-7.3
- Red-eared sliders: 6.7
- Hawksbills: 5.9-6.2
- Herbivorous tortoises: acidic in drought, high protein diets, near the end of hibernation, prolonged anorexia -> returns to normal after a few weeks of foraging
- Acidic urine and dehydration may be predisposing factors for urate crystals and uroliths
- Alkaline urine could indicate UTI from urease positive bacteria (based on mammal medicine)
-
Protein:
- Dip sticks primarily respond to albumin; false positives (hematuria, pyuria, reproductive secretions)
- Unpublished data: >30 mg/dL during hibernation or illness of tortoise and box turtles
- Glucose: not normally present in significant amounts; better documentation needed
- Occult blood: hemoglobin (transfusion reactions, hemolytic anemias, DIC, heat stroke), myoglobin (severe rhabdomyolysis in crushing injuries), erythrocytes; verify with sediment
- Ketones:
- largely unstudied
- most dipsticks do not respond to B-hydroxybutyrate, which may be a relevant ketone in desert tortoises
- color can cause false positive
- trace found in tortoises emerging from hibernation
- Leukocyte esterase reaction: poor sensitivity in dogs and cats, not evaluated in reptiles
- Nitrite: significance unknown, validated in humans
- Urobilinogen and bilirubin:
- Role in reptiles unclear, mostly useless
- Only snakes appear capable of producing significant quantities of bilirubin
Describe the evaluation of urine sediment in reptiles?
How should it be prepared?
What cells are typiclaly normal to see?
Is bacteria normal or abnormal?
What protozoan parasites may be seen?
Urine sediment evaluation
- Centrifuge 1000-1500 rpm for 5 minutes; examine stained and unstained
- Clinically healthy tortoises: small numbers of leukocytes and epithelial cells (some ciliated), but mostly acellular
- Erythrocytes not routinely seen unless with catheterization or cystocentesis
- Urodeum of cloaca involves some degree of bacterial contamination and mixed population of rods and cocci may be normal
- Huge number of monomorphic bacteria or yeast is of concern, especially with prominent inflammatory response -> urine culture
- Protozoan or metazoan renal parasites
- Hexamita: chelonians, flagellated protozoan
- Myxidium, Myxobolus: Myxozoan parasites reported in aquatic turtles
- Snakes and crocodilians (urine stored in dilated distal ureters and/or colon, so may be useful fecal substitute in animals not producing feces
- Casts and crystals: caution with interpretation; urate crystals can be seen (as well as others)
What imaging modalities may be useful in diagnosing renal disease in reptiles?
Describe renal aspiration and cytology in these speices?
Imaging
- Radiography: renomegaly, radiopaque uroliths, soft tissue mineralization, chronic mineralized gout, constipation
- IV urography (800-1000 mg/kg iohexol) - identify masses (abscesses, neoplasia, calculi), ureteral damage or obstruction, GFR
- Ultrasonography: assist with biopsy, cystocentesis; appreciate mineralization, cysts; consider transcloacal imaging in giant reptiles
- Scintigraphy: technetium useful to evaluate renal function in green iguanas; generally impractical
- CT, MRI, endoscopy are great advanced imaging options
- Endoscope guided FNA or biopsy are preferred over surgery
Needle aspiration and cytology
- Transcutaneously or with ultrasound guidance
- Small amount of diagnostic material and lack of tissue architecture
- Culture and cytology
Describe renal biopsy in reptile species.
What are some important risks to consider?
What are the advantages of endoscopic versus surgical biopsy?
Describe the various surgical approaches to the biopsy.
What unique approach is needed for iguanids? Why?
Renal biopsy: gold standard diagnostic, anesthesia recommended
- US guided possible in squamates, risky (hepatic needle biopsy in squamates resulted in gi perforation (6%) or hemorrhagic death (12%); Caution…
- Endoscopic biopsy
- Evaluate renal size, shape, color, locate abnormal areas
- Rapid, safe, effective
- Endoscopic scissors and biopsy forceps
- Less risk to surrounding structures
- Surgical biopsy allows for larger sample collection and completely evaluate other structures; increased anesthesia and surgical exposure are risks
- Hemorrhage expected
Renal Biopsy
- Determine pathology of renal dysfunction/disease, neoplasia
- Weigh possible complications (hemorrhage) and whether results will change current treatment
- Evaluate clotting times prior to surgery
- Endoscopic biopsy is safe, effective, minimally invasive and preferred over surgical approaches (chapters 64 and 66)
- Traditional Coeliotomy - collect larger samples and evaluate other structures
- Ventral coelomic approach - difficult to access dorsal kidneys, good retraction and packing required
- Lateral coelomic approach may be easier
- Collect biopsies with sharp dissection using scalpel blade; avoid radiosurgical and laser devices due to thermal artifact; avoid crushing
- Hemorrhage common - radiosurgery, laser, gelfoam
- Intrapelvic kidneys in iguanids:
- Cranial tail cut-down, small longitudinal incision in lateral midline just below lateral processes of the coccygeal vertebrae at the tail base (1-3 cm, starting just behind the hind limb)
- Blunt dissection between dorsal and ventral coccygeal muscles to expose caudolateral aspect of kidney
- Valuable technique when kidneys not enlarged, intrapelvic approach difficult or endoscopy not available
- Limited to unilateral biopsy or bilateral cut-down
- Best for diffuse diseases that involve caudal kidney
How is GFR measured in reptiles?
Renal function (GFR)
- Iohexol excreted with glomerular filtration
- Plasma iohexol concentration over time after a single IV injection
- Rate of clearance used to estimate GFR by dividing the iohexol dose by the area under the curve
- 3 small blood collections over 24 hours
- No urine collection required
- Practical for smaller reptiles (300 g)
- Protocol is on table 66.4, page 641
- Validated in green iguanas and Kemp’s ridley sea turtles
- Prognostic determination, euthanasia decisions
- Cold stunned Kemp’s: 75% decreased function even after several days of hospitalization
Describe the mainstays of kidney disease in reptile species.
Treatment:
- Fluid therapy
-
Allopurinol
- Xanthine oxidase inhibitor
- 25 mg/kg q24h po is shown to decrease UA levels by 45% in green iguanas
-
Good husbandry
- Access to sunlight or at least UVB lighting
- Low protein diet: select pyrimidines over purines
- Potassium rich items may help (based on human med)
- Chart on p.642
If indicated
- Antibiotics if infection is demonstrated
- Calcium supplementation
- Oral recommended – calcitriol
- Injectable - may precipitate into soft tissue mineralization (hyperphosphatemia common)
- If immediate treatment is needed for stabilization, IV or IO to effect is recommended with phosphate binders
- Oral phosphate binders
- Oral aluminum hydroxide
- Between meals - can interfere with calcium absorption
- Questionable efficacy
- Probenecid
- Sulfinpyrazone
- Inhibit UA reabsorption from proximal tubule, but little to no reabsorption occurs in reptiles
- Diuretics (lasix, ethacrynic acid) - may increase urine volume and electrolyte excretion
- Furosemide
- 2 and 5 mg/kg
- No changes in BP, HCT, electrolytes, GFR
- Sodium excretion increased 20 fold, chloride and potassium excretion increased 12 fold
- Dehydration has been reported in sea turtles during treatment of brevetoxicosis (withholding fluid therapy)
- Suspect it may work on tubules, no loop of henle
Describe gout in reptile species.
What is it caused by?
What are the three forms?
What dietary deficiency may be a predisposing factor?
What are the typical clinical signs?
What is the prognosis?
How is it treated?
Gout
- Overproduction or underexcretion of uric acid causing hyperuricemia and deposition of insoluble monosodium urate (MSU) crystals in tissues
- Visceral, articular, periarticular
- Purine (adenine, guanine) degradation can produce significant quantities of uric acid in squamates and some chelonians; xanthine oxidase is required for formation of UA, UA cleared by glomerular filtration
- Dehydration can lead to blockage of renal tubule with UA
- Crystallization in synovial fluid -> acute, painful inflammation of joint (gouty arthritis)
- Gout usually involves chronic renal failure and/or dehydration
- Hypovitaminosis A suggested as predisposing factor in crocodile hatchlings (reduced UA secretion from squamous metaplasia of tubular cells)
- True gout has monosodium crystals vs pseudogout with any other precipitate (calcium hydroxyapatite, calcium pyrophosphate dihydrate)
- Primary gout is from overproduction of UA. Secondary gout occurs when hyperuricemia is from chronic disease or interfering drug
- MSU tophi can deposit in pericardial sac, kidneys, liver, spleen, lungs, sq and other soft tissues
- CS: anorexia, lameness, joint swelling, organ dysfunction
- Definitive diagnosis - crystals in affected joints/issues by cytology or biopsy
- Grave prognosis; cases can be maintained for short period with supportive care
- Prevention - good husbandry
- Treatment
- Lower blood UA levels (allopurinol)
- Promote urate excretion by diuresis
- Manage localized inflammatory tophi - surgical removal, antiinflammatories (colchicine, corticosteroids) and pain control (opioids, NSAIDs)
- Removal of crystals from joint is possible, but permanent arthropathy present, amputation or long term allopurinol therapy should be considered
- The authors of this chapter do not recommend NSAIDs if renal is questionable