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Which mutation is responsible for autosomal dominant polycystic kidney disease (PKD) in Persian cats?

A
B
C
D
to track
2026 Statistics

Key Facts: ACVNU Exam

AVMA RVSO

Provisional 2022

Newest vet specialty board

IRIS

CKD Staging

Stage 1-4 by Cr + UPC/BP substaging

SUB

Cat Ureteral Obstruction

Subcut ureteral bypass

SDMA

Early CKD Marker

Less affected by muscle than Cr

ACVNU is the newest AVMA-recognized vet specialty board (provisional 2022) for nephrology and urology. Master IRIS CKD staging (G1-G4 by Cr; substaging by UPC + BP), SGLT2i (DAPA-CKD/EMPA-KIDNEY) + finerenone for diabetic CKD, ethylene glycol (4MP fomepizole), feline ureteral obstruction (subcut ureteral bypass SUB), ISCAID 2019 UTI guidelines, and Persian cat PKD1 mutation screening.

Sample ACVNU Practice Questions

Try these sample questions to test your ACVNU exam readiness. Each question includes a detailed explanation. Start the interactive quiz above for the full 100+ question experience with AI tutoring.

1A 4-year-old Labrador presents 6 hours after suspected ethylene glycol ingestion. Which antidote is the treatment of choice in dogs?
A.N-acetylcysteine
B.Fomepizole (4-methylpyrazole)
C.Atropine
D.Vitamin K1
Explanation: Fomepizole (4-MP) is the antidote of choice for ethylene glycol toxicity in dogs because it competitively inhibits alcohol dehydrogenase, preventing metabolism of ethylene glycol to its toxic metabolites (glycoaldehyde, glycolic acid, glyoxylic acid, oxalic acid). Ethanol is a second-line option when fomepizole is unavailable. Early administration (within 8 hours in dogs) prevents the development of severe AKI from calcium oxalate crystal deposition in renal tubules.
2Which plant is the most common cause of acute kidney injury in cats following ingestion?
A.Sago palm
B.Lily (Lilium and Hemerocallis spp.)
C.Oleander
D.Foxglove
Explanation: True lilies (Lilium spp.) and daylilies (Hemerocallis spp.) cause acute tubular necrosis in cats. Even small exposures (chewing leaves, ingesting pollen, drinking vase water) can produce severe AKI within 24-72 hours. The exact nephrotoxin remains unidentified. Aggressive decontamination and IV fluid diuresis within 18 hours of exposure offer the best prognosis. Cats are uniquely susceptible; dogs typically only develop GI signs.
3According to the IRIS AKI grading system, a dog with a serum creatinine of 2.8 mg/dL and oliguria for 8 hours would be classified as which grade?
A.AKI Grade I
B.AKI Grade II
C.AKI Grade III
D.AKI Grade IV
Explanation: IRIS AKI Grade III corresponds to creatinine 2.9-5.0 mg/dL or documented increase >0.3 mg/dL within 48 hours with oliguria/anuria. Grade I is non-azotemic AKI (Cr <1.6) with clinical/biomarker evidence. Grade II is mild azotemia (Cr 1.7-2.5). Grade IV is Cr 5.1-10.0. Grade V is Cr >10.0. The grading system also incorporates urine output and need for renal replacement therapy.
4Which serovar of Leptospira is most commonly associated with acute kidney injury in dogs in North America?
A.Icterohaemorrhagiae and Canicola only
B.Pomona and Grippotyphosa
C.Hardjo and Bratislava
D.Australis and Tarassovi
Explanation: In North America, Pomona and Grippotyphosa are now the most common serovars associated with leptospirosis-induced AKI in dogs, having largely supplanted the historically common Icterohaemorrhagiae and Canicola (which were targeted by older bivalent vaccines). Modern quadrivalent vaccines include all four serovars. Wildlife reservoirs (raccoons, skunks, deer) maintain Pomona and Grippotyphosa in the environment.
5A dog presents with acute oliguric AKI after ingesting raisins. Which is the suspected mechanism of nephrotoxicity?
A.Direct glomerular damage by anthocyanins
B.Tartaric acid causing proximal tubular injury
C.Oxalate crystal precipitation
D.Renal vasoconstriction by tannins
Explanation: Recent veterinary toxicology evidence implicates tartaric acid and its potassium bitartrate salt as the likely nephrotoxin in grapes and raisins for dogs. Affected dogs develop proximal tubular necrosis, oliguric or anuric AKI, and often require renal replacement therapy. Susceptibility appears idiosyncratic. Aggressive decontamination and fluid diuresis are the mainstays of treatment; the prognosis for anuric cases without RRT is poor.
6Which class of drugs causes AKI primarily through hemodynamic alteration of renal blood flow rather than direct tubular toxicity?
A.Aminoglycosides
B.Amphotericin B
C.NSAIDs
D.Cisplatin
Explanation: NSAIDs cause AKI by inhibiting cyclooxygenase-mediated prostaglandin synthesis, which normally maintains afferent arteriolar vasodilation under conditions of decreased renal perfusion (dehydration, anesthesia, heart failure). Loss of prostaglandin support causes ischemic injury. Aminoglycosides, amphotericin B, and cisplatin all cause direct proximal tubular cell toxicity through different mechanisms (cellular uptake/lysosomal accumulation, membrane disruption, and DNA crosslinking, respectively).
7Which urine sediment finding is most suggestive of ethylene glycol toxicity?
A.Struvite crystals
B.Calcium oxalate monohydrate crystals
C.Ammonium urate crystals
D.Bilirubin crystals
Explanation: Calcium oxalate monohydrate crystals (picket-fence or dumbbell-shaped) appearing in the urine within 3-6 hours of ingestion are highly suggestive of ethylene glycol toxicity. They form when glycolate is further metabolized to oxalic acid, which complexes with serum calcium and precipitates in renal tubules. Calcium oxalate dihydrate (envelope-shaped) crystals can occur in normal urine, so monohydrate crystals carry more diagnostic weight.
8Which classification best describes acute kidney injury caused by ureteral obstruction with hydronephrosis?
A.Pre-renal AKI
B.Intrinsic renal AKI
C.Post-renal AKI
D.Functional AKI
Explanation: Ureteral obstruction is a classic cause of post-renal AKI. Backpressure from obstruction reduces glomerular filtration and ultimately damages the renal parenchyma. Pre-renal AKI results from decreased renal perfusion (hypovolemia, hypotension). Intrinsic AKI involves direct parenchymal injury (toxic, ischemic, infectious). Prolonged post-renal obstruction can become intrinsic AKI as nephrons are destroyed.
9Which biomarker is considered the earliest detectable indicator of decreased GFR in dogs and cats?
A.Serum creatinine
B.BUN
C.SDMA (symmetric dimethylarginine)
D.Serum phosphorus
Explanation: SDMA (symmetric dimethylarginine) increases when GFR has declined by approximately 25-40%, often months to years before creatinine rises above the reference range. SDMA is less affected by extra-renal factors such as muscle mass, making it especially useful in cats with sarcopenia. Creatinine typically does not exceed reference range until ~75% of nephron mass is lost. BUN is influenced by diet, hydration, and GI bleeding.
10A dog with anuric AKI fails to respond to fluid challenge and a furosemide trial. Which intervention should be considered next?
A.Empiric corticosteroids
B.Mannitol bolus regardless of volume status
C.Renal replacement therapy (hemodialysis or CRRT)
D.High-dose dopamine infusion
Explanation: Anuric AKI unresponsive to fluid resuscitation and diuretic challenge is an indication for renal replacement therapy (intermittent hemodialysis or CRRT). RRT supports the patient while tubular regeneration occurs. Mannitol in volume-overloaded anuric patients risks pulmonary edema. Low-dose 'renal' dopamine has no proven benefit and is no longer recommended. Steroids are not first-line for AKI without specific immune-mediated etiology.

About the ACVNU Exam

AVMA-recognized (provisional 2022) veterinary specialty board for nephrology and urology. The newest vet specialty board with first diplomates conferred recently. Covers acute kidney injury (AKI workup, IRIS staging, ethylene glycol/lily/lepto), chronic kidney disease (IRIS stages 1-4, substaging by proteinuria/BP, SGLT2/finerenone), glomerular disease (lupus, IgA, MN/PLA2R, ANCA), urolithiasis (calcium oxalate, struvite, urate, cystine), UTI/pyelonephritis (ISCAID 2019 guidelines), renal replacement therapy (HD/CRRT/PD/transplant), feline nephrology (PKD, ureteral obstruction with SUB), and canine urology (BPH, ectopic ureter).

Questions

100 scored questions

Time Limit

Per ACVNU

Passing Score

Per ACVNU

Exam Fee

Per ACVNU (ACVNU)

ACVNU Exam Content Outline

20%

CKD & IRIS Staging

IRIS stages 1-4, substaging by proteinuria + BP, SGLT2i, finerenone, phosphate binders

15%

AKI

AKI causes (ethylene glycol, lily, lepto), IRIS AKI grading, RRT indications

15%

Glomerular Disease

PLN, immune-complex GN (lupus, MN PLA2R), amyloidosis, renal biopsy interpretation

15%

Urolithiasis

Ca-oxalate, struvite, urate (Dalmatian/PSS), cystine; medical/surgical management

10%

Feline Nephrology

CKD in cats, PKD1 mutation Persian, ureteral obstruction SUB, telmisartan ARB

10%

UTI & Pyelonephritis

ISCAID 2019 guidelines: sporadic vs recurrent, complicated, pyelonephritis 4-6 wk

10%

Renal Replacement Therapy

IHD, CRRT, peritoneal dialysis, kidney transplantation (cyclosporine + pred)

5%

Canine Urology

BPH, prostatitis, ectopic ureter, hormone-responsive incontinence (PPA, estriol)

How to Pass the ACVNU Exam

What You Need to Know

  • Passing score: Per ACVNU
  • Exam length: 100 questions
  • Time limit: Per ACVNU
  • Exam fee: Per ACVNU

Keys to Passing

  • Complete 500+ practice questions
  • Score 80%+ consistently before scheduling
  • Focus on highest-weighted sections
  • Use our AI tutor for tough concepts

ACVNU Study Tips from Top Performers

1Master IRIS CKD staging (G1-G4 by Cr) and substaging by UPC + BP — drives treatment decisions
2Memorize new diabetic CKD pillars: ACEi/ARB + SGLT2i + finerenone + GLP-1
3Drill feline-specific: Persian PKD1 mutation, ureteral obstruction SUB, telmisartan-approved ARB
4Know ethylene glycol treatment: 4MP (fomepizole) dogs first-line; ethanol if 4MP unavailable; dialysis for severe
5Apply ISCAID 2019 UTI: sporadic = amox/TMP-S 3-5d; recurrent → urine culture + investigate; pyelonephritis 4-6 wk

Frequently Asked Questions

What is the IRIS CKD staging system?

IRIS (International Renal Interest Society) stages CKD by stable creatinine: Stage 1 (Cr <1.4 mg/dL dogs / <1.6 cats), Stage 2 (1.4-2.0 / 1.6-2.8), Stage 3 (2.1-5.0 / 2.9-5.0), Stage 4 (>5.0). SDMA (symmetric dimethylarginine) used for early CKD detection. Substaging: proteinuria (UPC <0.2 nonproteinuric, 0.2-0.5 borderline, >0.5 proteinuric) and blood pressure (<140 normal, 140-159 mild, 160-179 mod, ≥180 severe risk). Substaging guides ACEi/ARB and antihypertensive therapy decisions.

How is feline ureteral obstruction managed?

Cat ureteral obstruction (most often calcium oxalate) is increasingly managed with subcutaneous ureteral bypass (SUB) device — a port system bypassing the ureter from kidney to bladder via SC tubing and access port. Allows long-term flushing/maintenance. Alternatives: ureteral stent (per-renal or surgical placement), traditional open ureterotomy/ureteroneocystostomy (higher complication rate). SUB has improved 1-yr survival to ~75-90% in obstructed cats.

What new drugs are pillars of diabetic CKD therapy?

Following landmark trials in human nephrology now applied to dogs/cats: (1) ACEi/ARB — proteinuria reduction (benazepril dogs, telmisartan ARB approved cats); (2) SGLT2 inhibitors — dapagliflozin DAPA-CKD, empagliflozin EMPA-KIDNEY trials demonstrated CKD progression slowing in humans, increasing veterinary use; (3) Finerenone — non-steroidal MRA (FIDELIO-DKD, FIGARO-DKD); (4) GLP-1 agonists. Veterinary-labeled SGLT2i now available (e.g., bexagliflozin for diabetic cats).

How should I study for ACVNU?

Plan 600-1,000+ hours. Master Bartges & Polzin Nephrology and Urology of Small Animals (current edition) cover-to-cover — primary reference. Read IRIS Guidelines (CKD, AKI), ISCAID 2019 UTI guidelines, ACVIM consensus statements (proteinuria, hypertension). ACVNU is provisional (2022) — exam blueprint still maturing; verify candidate guide directly from acvnu.org before sitting. Case logs and publications required.