Pigmenturia and Toxicants that Affect the Urinary Tract LA

Question 1

what are 4 causes of pigmenturia?

Answer 1

1. hemorrhage
2. hemoglobin
3. myoglobin
4. bilirubin

spin down the sample (if clear supernatant = red cells)

hemoglobin versus myoglobin: ammonium sulfate precipitation test

need to differentiate true pigmenturia from oxidizing agents or drugs
-plant compounds (pyrocatechines; when seen only in shavings/bedding)
-rifampin and phenazopyridine

Question 2

describe pigmenturia workup

Answer 2

1. start with signalment!
   -young small ruminant, water fed from a bottle causes osmotic hemolysis

-any age or species:
rule out oxidizing agents, toxins, overexertion
–seen only in shavings/bedding: harmless pyrocatechans
–overexertion: rhabdomyolysis = myoglobin in urine (brownish red)

2. them move on to PE
   -anemia?
   -icterus: hyperbilirubinemia so could be bilirubinuria too
   -brown discolored membranes: methemoglobin
3. spin down blood: cells spin out pigment will not
   -clear supernatant = hemorrhage, not clear = move on to blood
   serum brown/yellow: bilirubin
   serum clear: myoglobin
   serum red/pink: hemoglobin
4. minimum database:
   -complete cell count/fibrinogen: anemia (hemolysis), systemic disease (infection)
   -serum/plasma biochem: liver or muscle disease
   -UA/sediment: casts, dipstick can’t differentiate myoglobin versus hemoglobin (ammonium sulfate precipitation if can’t distinguish Hgb from Mgb)

Question 3

describe pigmentary nephropathy

Answer 3

1. due to hemoglobin and myoglobin
   -direct toxicity to renal tubular epithelial cells = oxidative damage
2. results in cast formation, tubular obstruction, altered renal blood flow
3. can cause ACUTE KIDNEY INJURY and result in ACUTE RENAL FAILURE

-bilirubin can also be nephrotoxic! bile cats nephropathy

pigmenturia is NOT BENIGN!!!!

Question 4

describe treatment of pigmenturia

Answer 4

1. treat underlying disease
2. judicious isotonic intravenous fluid diuresis
3. pain management: consider renal excretion!!
4. supportive care

Question 5

describe toxins that cause renal failure in terms of their mechanism of action

Answer 5

1. directly toxic to renal tubular cells: aminoglycosides, pigmenturia
2. obstruction of renal tubules: oxalates, ethylene glycol
3. ischemic or vasomotor nephropathy: inadequate renal blood flow

Question 6

describe oak (quercus sp.) as a toxicant that causes renal failure

Answer 6

1. cattle and sheep most commonly affected, need to eat a lot over several days
2. goats: need to/can adapt if slow exposure; toxicosis possible if overwhelming amount in short period of time
   -young goats less likely to develop tolerance
3. toxic principle: tannins
   -young green seedlings and green acorns MORE CONCENTRATED toxic principle
4. clinical signs:
   -anorexia
   -constipation- often missed in cattle
   -red brown urine- often missed in cattle
   -progress to develop peripheral edema and bloody diarrhea
5. post-mortem:
   -nephritis and perirenal edema with hemorrhage
   -pale cortex
   -diffuse tubular necrosis
   -fibrosis in chronic cases
6. other: in horses: severe GI pain +/- hemorrhagic colitis
7. prevention if can’t limit exposure!
   -add calcium to diet
   -alfalfa based or calcium hydroxide (lime) binds tannins

Question 7

describe pigweed (amaranthus spp.) as toxins that cause renal failure

Answer 7

(bovine, sheep, goat, pig) horses very uncommon!

pigweed produces oxalates and other unknown nephrotoxins

1. renal tubular necrosis and perirenal edema
2. animals die from acute renal failure, hyperkalemia, and cardiac arrest
3. animals must eat the plant for days

other: pigweed is also a nitrate producing plant!
-nitrate toxicosis is more common than renal effects
-nitrite-hemoglobin = methemoglobinemia: lack of oxygen results in blue to brown mucous membranes, chocolate brown blood, respiratory distress, come, and death
-IV methylene blue is antidote but expensive!

Question 8

describe hypervitaminosis D

Answer 8

can cause hypercalcemia and hyperphosphatemia, resulting in anuric renal failure and mineralization of soft tissues

can be due to
-rodenticides
-day blooming hessamine/jasmine
-iatrogenic: oversupplementation

Question 9

describe vasomotor nephropathy

Answer 9

NSAIDs: phenylbutazone and flunixin meglumine, firocoxib (COX-2 selective)

can result in renal papillary necrosis:
-reduces blood flow to kidney due to constitutive (house-keeping) prostaglandin blockade

clinically: acute kidney injury (azotemia and evidence of blood in urine)

AVOID NSAIDs in these patents!!! restore volume and circulation

administer misoprostol (synthetic protsglandin E2): probs more useful for GI effects of NSAID tox

Question 10

remember aminoglycosides

Question 11

what toxin causes renal effects AND cystitis? describe

Answer 11

cantharidin (blister beetle) toxicosis
-need to consume approx 100-150 beetles

clinical signs:
-circulatory shock
-INTENSE PAIN
-colic
-bruxism
-ptyalism
-HYPOSTHENURIA in the face of dehydration

toxic principle: cantharidin
-absorbed through skin and mucous membranes
MOA: protein phosphatase inhibition, causes mucosal irritation via acantholysis and ulceration, and causes hyposthenuria by interfering with the action of vasopressin on Na-K-ATPase in cortical collecting ducts

IMPORTANT:
-GI signs, renal signs, increased CK, cardiovascular effects
-electrolyte derangements, urinary and GI loss can cause profound ionized hypocalcemia and hypomagnesemia

Question 12

describe cantharidin toxicity management and prognosis

Answer 12

1. eliminate ingestion/exposure
2. prevent absorption: bind toxin
   -activate charcoal or biosponge
   -avoid mineral oil
3. pain control
4. fluid therapy:
   -restore volume, diuresis, correct electrolyte abnormalities
5. GI mucosal protection

prognosis: fair to good with early diagnosis and aggressive management