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ACVIM Specialty Exam > Nephrology, Urology > Flashcards

Nephrology, Urology Flashcards

1
Q

Predisposing factors for proteinuria in dogs?

A

HAC, hyperlipidemia, pancreatitis, GB mucocele

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2
Q

What are the roles and effects of fibroblast growth factor (FGF)-23?

A

Phosphaturic hormone associated with CKD-mineral bone disorder (MBD).
Released from osteocytes in response to increased serum phosphorus & calcitriol concentrations  promotes PO4 urinary excretion by downregulation of Na-PO4 co-transporter in renal PT cells & inhibition of calcitriol synthesis.
Binds to FGF receptor-α-klotho complex (klotho = co-factor).
Circulating FGF-23 concentrations increase with advanced CKD stages in cats & dogs. Mechanisms: decreased FGF-23 clearance due to decreased GFR, compensation for phos accumulation in the body and for decreased klotho protein concentrations.

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3
Q

Creatinine - filtered or secreted?

A

Creatinine is freely filtered by the glomeruli. 10%–30% is secreted by the PCT in the basal state. Under normal circumstances, the rates of creatinine production and excretion are fairly constant.

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4
Q

Describe what disturbances of calcium homeostasis occurs after initiating a phosphate-restricted diet in cats with CKD, and its adverse effects?

A

xxx
After initiating a phosphate-restricted diet, hyperCa-enhanced renal Ca excretion acts as a compensatory mechanism - but extent of compensation is inadequate to prevent increments in plasma [Ca].

HyperCa –> reduction in GFR

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5
Q

Mechanisms of hyperCa, and which is applicable to CKD?

A
  • Decreased urinary excretion
  • Increased intestinal absorption
  • Increased bone resorption
    (can be a combo)

CKD: impaired calcium
excretory function.

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6
Q

Familial proteinuric kidney disease - which breeds & pathomechanism?

A

Underlying gene mutations often unknown.
Defects in the production or assembly of collagen IV (Alport syndrome).
Bull Terrier, Dalmatian, English Cocker Spaniel, Samoyed.

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7
Q

Hereditary focal segmental
glomerulosclerosis is overrepresented in which breed? Concurrent with what other condition?

A

Soft Coated Wheaten Terriers
PLE

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8
Q

Juvenile nephropathy (<3yo) - which breeds?

A

Dogue de Bordeaux, Rottweiler, Gordon Setter

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9
Q

Familial renal amyloidosis - which breeds (D/C)?

A

Shar-Pei, Beagles, English Foxhounds, Bracchi Italiani
Abyssinians

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10
Q

Why is serum P concentration unreliable when clinically assessing cats with CKD?

A

Many regulatory mechanisms occur with progressive CKD. So many measures of renal function (GFR, US, sCr, FGF-23, PTH) may be altered prior to increase in serum P in CKD.

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11
Q

What association has been observed between FGF-23 & SDMA in cats with CKD?

A

In geriatric cats with early CKD but not azotemia, FGF-23 concentration is associated with SDMA (indicative of decreased GFR).

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12
Q

SDMA
- What does it stand for?
- Origin?
- Diagnostic utility?
- What extra-renal factors cause an increase in SDMA?

A
  • Symmetric dimethylarginine.
  • Methylated arginine. Derived from intranuclear methylation of L-arginine by protein-arginine methyltransferase –> released into circulation after proteolysis.
  • Primarily eliminated by renal excretion, so highly correlated with GFR - useful as early indicator of renal dysfunction than sCr.
  • Factors: thyroid dysfunction (e.g. hypoT post I131), psychogenic polydipsia (dogs), skin disease (dogs) - unknown mechanism, breed (Greyhounds have higher SDMA)
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13
Q

When performing US-guided renal biopsies:
- What biopsy evaluation techniques are used?
- What is the recommended no. of glomeruli for diagnostic quality samples?

A
  • Min 10 glomeruli per sample, prefer 15-20 for LM
  • Light microscopy, immunofluorescence, TEM
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14
Q

Ammonium urate urolithiasis - what 2 disease entities?
Predisposed dog & cat breeds?

A

1) Hepatic portovascular anomalies
- Yorkies, cats with PSS

2) Inherited defect of hepatic uric acid transporter (SLC2A9 gene mutation). Lack of uric acid degradation to its more soluble metabolite (allantoin) > increased urinary excretion of uric acid > hyperuricosuria. NOT X-linked, homozygous recessive.
- Dalmatians (all secrete lots of uric acid but only 5% stone formers), almost all male (9:1), Eng Bulldogs, Black Russian Terrier

3) Unknown (cats) - Egyptian Mau, Siamese, Birman

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15
Q

Cystine uroliths - types, gene mutation, breeds?

A

Gene mutations associated with cystine tubular malabsorption.

Type Ia: SLC3A1 gene, autosomal recessive. Big dogs - Newfoundlands, Labs, Landseers

Type IIa: SLC3A1 gene, autosomal DOMINANT with incomplete penetrance. Active dogs - ACD, Border Collies

Type III: sex linked, androgen dependent. Intact males (esp Mastiffs, Eng & French Bulldogs)

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16
Q

Radiolucent uroliths?

A

Xanthine
Cystine (can be radioopaque)
Urate
(can’t see you)

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17
Q

Extra-renal factors that can affect SDMA?

A

DM (cats) - reduce SDMA

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18
Q

What no. of colony forming units is associated with a significant UTI?

A

> 10^5 CFU/ml

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19
Q

What are the challenges in diagnosing Corynebacterium urealyticum UTI?

A

Aerobic, non-spore forming, lipophilic G+ bacillus. Very slow growing and does not grow well after overnight incubation.
Enriched culture (e.g. with blood agar) for 72hrs+ is recommended, or risk false negative.

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20
Q

What is the microbiome composition of urine in healthy dogs? What findin was associated with bacterial communities in urine?

A

Low presence of bacteria and/or fungi, identified on next-generation sequencing molecular diagnostics but not routine culture.
Struvite crystals.

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21
Q

JVIM consensus: Describe the tiers for dogs diagnosed with glomerular disease?

A

Tier I persistent renal proteinuria.
- I-A: subclinical
- I-B: proteinuria + hypertension (+/- TOD)

Tier II renal proteinuria + hypoalb.
- II-A: proteinuria + hypoalb (+/- complications - oedema, TE)
- II-B: proteinuria + hypoalb (+/- complications) + hypertension

Tier III renal proteinuria + azotemia
- III-A: proteinuria + azotemia
- III-B: proteinuria + azotemia + hypertension
- III-C: roteinuria + azotemia + hypoalb +/- hypertension

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22
Q

ACVIM consensus:
Drugs associated with glomerulonephropathy & brief MOA?

A

PPA (hypertension), steroid (incr glomerular permeability), sulfonamides (crystalluria, tubular necrosis, interstitial nephritis, glomerular lesions as part of a vasculitis syndrome), TKI (VEGF over/underexpression + incr intraglomerular P > hypertension)

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23
Q

Infectious causes of renal proteinuria?

A

Parasitic - HWD
Bacterial - Ehrlichia (canis, chaffeensis, ewingii), lepto (usually tubular), Bb, Rickettsial/RMSF (acute), Bartonella, Anaplasma (phago, platys), Brucellosis, Mycoplasma
Viral - CAV-1
Fungal - Blasto
Protozoa - Hepatozoon, Leishmaniasis, Trypanosomiasis

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24
Q

ACVIM consensus
What 3 microscopic methods & special stains are used for renal biopsy evaluation?

A

1) Transmission electron microscopy (TEM; ultrastructural) - glutaraldehyde
2) Immunofluorescence (IF) - Michel’s medium
- Ab against IgG/IgM/IgA, C1q, C3, lambda & kappa light chains&raquo_space; detect immune-complex deposits.
3) Light microscopy (LM) - formalin fixed

Special stains:
- H&E
- Masson’s trichome (MT) for collagen & CT (amyloid looks mottled blue)
- PAS-hematoxylin for junction between tissue compartments
- Jones methenamine silver (JMS) for fine structures of glomerular BM (useful for immune complex deposits)
- Congo red for amyloid.

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25
Q

Requirements for diagnostic renal bx sample?

A

Ciancolo paper
3um sections, minimum 10 glomeruli.
16ga needle usually ok.

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26
Q

What immunopathological feature is useful to differentiate between reactive vs primary amyloidosis?
Limitation of trucut method of renal biopsies?
Comparisons in distribution of renal amyloidosis in dogs vs cats?

A

Congo red–stained amyloid deposits with reactive amyloidosis (amyloid A) lose their affinity for Congo red after K permanganate oxidation (decolourise). Whereas primary amyloidosis (amyloid L) is resistant to KP.

Trucut method obtains renal cortical biopsies, will miss medullary lesions.
Dogs - usually just glomerular involvement, cortical & medullary interstitium less involved. EXCEPT Chinese Shar Peis. Cats - renal amyloidosis usually medullary +/- glomerular.

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27
Q

ACVIM consensus statement
What is the 1st vs 2nd-line anti-proteinuric tx recommended in dogs?

When monitoring a patient receiving anti-proteinuric tx, what are the tolerable limits for parameters monitored?

A

1st line: ACE-I
2nd line: ARB

SCr: increase <30% (stage 1-2 CKD), <10% (stage 3), 0% (stage 4)
K+ <6.0mmol/L
SBP 120 to <180mmHg

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28
Q

ACVIM consensus statement
What is the benefit of O3FA supplementation in glomerular disease? What is the recommended ratio of O3 vs O6 FA dietary supplementation?

A

Renoprotective; suppresses glomerular inflammation and coagulation by interfering with production of proinflammatory prostanoids (derived from arachidonic acid via COX pathway), lowers intraglomerular pressure.
Recc ratio O6:O3 = 5:1

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29
Q

Explain the overfill vs underfill hypothesis in nephrotic syndrome? What are the differences in therapeutic management between overfilled vs underfilled dogs?

A

Hypothesis relates to vascular volume & hydration status.
**Overfilled dogs (volume expanded): **more ‘stable’, early dz. Alb still normal. Intrarenal Na retention&raquo_space; ECF volume expansion –> incr hydrostatic P. These dogs should have very conservative IVFT (if at all), shouldnt need IVFT for short procedures under GA (e.g. renal bx).

Underfilled dogs (volume contraction): late disease, progressive hypoalb&raquo_space; decr oncotic P in vessels&raquo_space; decreased circulating volume, renal blood flow&raquo_space; RAAS activation. +/- oedema/ascites. IVFT indicated esp if acute GI signs, worsening azotemia.

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30
Q

Indications for diuretic tx in glomerular disease?

A

Not indicated unless life-threatening oedema or ascites (e.g. impairing respiration etc.). Avoid too aggressive tx (» dehydration, worse azotemia, blood statsis > TE).
- Furosemide = 1st choice in dogs with pulmonary edema or hyperkalemia
- Spironolactone = 1st choice in dogs with pleural or abdominal effusion

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31
Q

Immune dysregulation in SCWTs may be associated with what type of renal lesions?

A

PLN due to podocytopathy causing changes in glomeraular permselectivity, lesions resemble focal segmental glomerulosclerosis.
Unknown if role in development of PLE.

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32
Q

Updated IRIS 2023 guidelines
What disease in dogs & cats may cause an SDMA elevation without changes in sCr or GFR reduction?
What cat & dog breeds have higher serum SDMA?

A

Lymphoma
Birman cats (20% have higher sCr), Greyhounds

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33
Q

Contraindications for renal biopsy?

A
  • Severe azotemia (IRIS stage 4 CKD; sCr >440)&raquo_space; worsen nephron injury + incr bleeding risk
  • Other co-morbidities that cannot be mitigated: e.g. coagulopathy, structural renal dz (cysts, moderate/severe hydronephrosis), pyelonephritis/perirenal abscess, uncontrolled hypertension (SBP >160mmHg), severe anaemia. Lack of access to a renal diagnostic pathology center, or experienced staff.
  • When results of renal bx are unlikely to alter tx/prognosis** (small kidneys, chronic azotemia)**
  • If a rational presumptive diagnosis of AKI can be made noninvasively (e.g. toxins, recent hypotension)
  • Ethical or financial concerns
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34
Q

JVIM consensus
For which 2 dog breeds with hereditary/familial nephropathies may immunosuppressive therapy be beneficial?

A

SCWTs (podocytopathy), BMDs (membranoproliferative GN).
Otherwise IS therapy is contraindicated.

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35
Q

Indications for immunosuppressive therapy for glomerular disease w/o a pathological diagnosis?

A
  • Failure to respond to standard anti-proteinuric tx
  • sCr >265u/mol/L OR
  • Acutely severe and/or progressive azotemia (sCr >440) with no evidence of chronic dz
  • Severe hypoalb <2.0g/dL
  • Patient too unstable for renal bx but rapidly progressive glomerular dz
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36
Q

What is the recommended IS therapy for dogs with histologically proven IMGN?

A

Stable/slowly progressive dz
- Mycophenolate or chlorambucil alone, OR in combo with azathioprine on alternating days. (myco & aza have similar MOA)

Rapidly progressive dz
- Glucocorticoids (NOT as monotherapy due to AE). **Combo with mycophenolate **
– If using combo of GCS + slower acting drug, aim to taper GCS as quick as possible to LED.
- Consider as pulse tx: cyclophosphamide.

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37
Q

What were the 2 major complications (and incidence) in feline renal transplant recipients?
In renal transplant recipients with infection, what should be measured to ensure immunosuppression is not excessive?
What pre-operative treatment & monitoring could be considered in a donor if pyelonephritis or viral URTI is suspected?

A

Graft rejection most common.
Infection (14%) - bacteria most common (UT, feeding tubes, Mycobacteria, Nocardia), > viral (URT) > fungal, protozoal.
Blood cyclosporine levels - shouldn’t be too high or too low (latter could increase risk of graft rejection).

Cyclosporine challenge x7 days, then resubmit urine for culture. Positive cultures (even if subclinical) precludes donation.
Donors with previous UTI must have 2 negative post-treatment cultures.
Usually if fail cyclosporine trial, will develop CSx + positive urine culture within 48-72hrs of starting cyclosporine.

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38
Q

For hemodialysis, what should be the maximum total extracorporeal blood volume to minimize cardiovascular complications (hypovolemia, hypotension)?

A

<10% of patient’s total blood volume (can be calculated from BW)

Blood vol- Dogs 90ml/kg BW, cats 66ml/kg BW

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39
Q

What 2 formulas are commonly utilized to calculate efficacy of extracorporeal therapy? Which is preferred for CRRT & why?

A

1) Urea reduction ratio (URR) = [(pre-tx urea − post-tx urea)/pre-tx urea] × 100

2) Total solute removal per period of time = Kt/v
k = measurement of urea clearance (mL/min), t = time of tx (mins), V = Vd of urea (est 60% BW, in mL).

kt/V preferred for CRRT as more accurately reflects urea removed. URR disregards a) urea being generated by the body during the procedure (not so much of a concern for IHD but can be significant for CRRT) & b) urea that is convectively removed with excess bodily fluids (so underestimates urea removal in overhydrated patients)

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40
Q

What is the first line recommendations for immunosuppressant therapy to treat IMGN?

A

Mycophenolate mofetil or cyclophosphamide +/- short term glucocorticoids (limit to short-term therapy due to AE & worsening proteinuria).
Chlorambucil also an alternative.

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41
Q

Euglycemic glucosuria - causes?

A

Proximal tubular injury - e.g. RTA, drugs -aminoglycosides, toxins - ethylene glycol, hypoxia
cephalexin, enro - false positive

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42
Q

Prolonged ketonuria can lead to what electrolyte derangements?

A

HypoNa & HypoK (increased renal excretion)

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43
Q

What drug is started for canine renal transplant recipients pre-operatively and why?

A

Enoxaparin (up to 7d post op). Risk of thromboembolic dz
(also give morphine to cause ileus > reduce risk of intussusception)

44
Q

Where is FGF-23 produced & what’s its co-factor?
Effects of FGF-23 on phosphate, Ca/vit D & PTH?

A

Osteocytes, klotho.
FGF-23-klotho complex increases phos excretion, decreases calcitriol production (indirectly decr Ca absorption in GIT), decreases PTH production.

45
Q

Acute/chronic prostatitis
- Recommended empirical abx choices
- Abx selection should be based on …..breakpoints
- Duration of abx treatment
- Monitoring recommendations

A

2019 ISCAID guidelines
- TMPS (good vs aerobes but NOT anaerobes), FQs (good vs G- & aerobes but NOT anaerobes). Drugs that can cross the blood-prostate barrier (high pKa, weakly alkaline, lipophilic). NOT clindamycin or macrolides (good prostate penetration but ineffective vs G- e.g. Enterobactericae, good for G+; use only if C&S shows G+ with susceptibility). Chloramphenicol (good for anaerobes; highly protein-bound so high doses needed).
- Serum/soft tissue breakpoints (not urine)
- Acute 4 wks, chronic 4-6 wks, longer if castration not performed, abscessation
- Monitoring: not with C&S of prostatic fluid, imaging to monitor prostatic size/structure + clinical response.

46
Q

In which 4 situations may urine culture be considered in dogs & cats lacking LUT signs?

A
  1. Suspected pyelonephritis
  2. Investigating bladder as a source of bacteremia/septicemia
  3. Patients undergoing a surgical or minimally invasive procedure that involves entry/transection of the urinary tract
  4. Suspected struvite uroliths
47
Q

List 3 patient characteristics & 2 stone characteristics that fulfill the crtieria for lithotripsy urolith removal in dogs 7 cats.

A
  1. Patient size - any female dog/cat, male dogs >7kg
  2. Female easier than males (for voiding urohydropulsion)
  3. Location - urethral easier than bladder (to evacuate stone fragments)
  4. Stone diameter <2-3cm (females), <1cm (males)
  5. <5 stones in females

If don’t fulfill criteria, consider PCCL

48
Q

What is a major factor contributing to persistent incontinence in dogs following laser ablation of intramural ectopic ureters? What other common post-procedural complication should be evaluated & addressed?

A

Concurrent USMI in 75-90% dogs with EU, impt to treat concurrently. 47% continence rates post-laser, increased to 77% with concurrent USMI tx. Males higher success than females.
Berent VNCA 2016 - application of hydraulic occluder increases continence rate to 92%.
LUTI within 6mths of procedure in 30% dogs - perform regular urine cultures

49
Q

What type of urolith is resistant to extracorporeal shockwave lithotripsy (ESWL) ? Why is this also not a feasible option to remove nephroliths in cats?

What is the response/outcome in dogs undergoing ESWL for nephrolith removal?

A

Cystine uroliths - if removal indicated perform endoscopic nephrolithotomy instead

Feline ureter is only 0.3 mm in diameter, vs a typical nephrolith fragment after ESWL has a diameter of ≈1 mm –> so very likely to cause ureteral obstruction. Also higher risk of haemorrhage in cats. Feline CaOx uroliths also more resistant to fragmentation.

Berent VCNA 2016
In dogs, treatment is successful - 85% success, <1% mortality rate. Disadv/complications - 30% require 1+ tx, 10% develop transient ureteral obstruction (can take weeks for all stone fragments to move into the bladder). Not recc if stones >1-1.5cm. Can place prophylactic ureteral stent to minimize risk of ureteral obstruction (passive ureteral dilation).

50
Q

What treatment options are available for idiopathic renal hematuria in dogs and what are the success rates?

A
  1. Medical management - ACE-I or ARB - Kortum JSAP 2021 - complete resolution of haematuria 42%, partial improvement 26%, no improvement 31%.
  2. Renal sclerotherapy with silver nitrate - >80% resolved hematuria (median 6hrs to 7d post-op).
  3. Ureteroscopy with endoscopic electrocautery - if failed sclerotherapy, for dogs >20 kg, and preferably performed after a ureteral stent has been in place for at least 1-2 weeks to allow for passive ureteral dilation, which makes navigation in the ureter and renal pelvis easier
  4. Ureteronephrectomy - not recommended.
51
Q

What can be used to dissolved mineralisation in SUB devices and how does it work?

What % of SUB devices develop mineralisation, and how many require device exchange?

A

EDTA (usually 2% tEDTA solution). Metalloprotease inhibitor which acts as a chelating agent, forms stable complexes in solution with multiple ions such as Mg, Ca, strontium, barium. Can dissolve CaOx crystals (main stone composition in cats).

Indicated if causing ureteral obstructions (some patients have mineralised devices but not clinical, don’t recommend interventions in these cases)

25% mineralisation ~1 year post-op. 13% exchange required from re-obstruction.

52
Q

What concurrent condition is associated with 20% of obstructive ureteroliths in cats? What clinical implications does this have?

A

Ureteral stricture. Reduces likelihood of medical management being successful. Feline ureteral internal diameter of 0.3-0.4mm makes even 1-2mm liths unlikely to pass, so worse with stricture.

Medical management is really only appropriate for partial obstructions with minimal loss of renal function, no/controlled pain, and no infection or progressive ureteral/pelvic dilation. Trial for 24-48h. Closely monitor imaging, renal function, and for complications.

53
Q

How does the chronicity of ureteral obstruction impact irreversibility of renal function?

A

Obstructions that persist for 7 days are expected to permanently reduce renal function by 1/3. After 40 days, no return of function is expected.

54
Q

Most common urolith types in dogs vs cats?

A

Dogs: 50-60% struvite (usually infection-associated)
Cats: 92% CaOx, 8% dried solidified blood stones. (Struvite uncommon but usually sterile).

55
Q

What mechanisms may contribute to CaOx urolithiasis, and which is thought to predominate in dogs?

A
  1. Hypercalciuria
    - Ca hyperabsorption in the GIT predominant mechanism in dogs
    - Resorptive – increased bone turnover - not proven
    - Renal leak – decreased renal Ca resorption
    - Idiopathic hyperCa (cats)
    - Meds & dietary factors – loop diuretics, corticosteroids, urinary acidifiers, increased dietary Ca, increased intake of vitamins C & D, low B6.
  2. Hyperoxaluria
    - Decreased degradation of dietary oxalate secondary to decreased enteric Oxalobacter formigene
56
Q

What is the most common location of ectopic ureters in female vs male dogs? What about most common EU type in cats?

A

Female dogs - 45% distal urethra
Usually bilateral
Male dogs - 36% preprostatic urethra

Cats - extramural, 50:50 bilateral/unilateral

57
Q

Which of the following is prognostic for return of renal function: renal pelvic size, degree of renal parenchyma visible, severity of RP dilation, and chronicity?

A

None of the above. (Acute/chronic ureteral obstructions can have a severely dilated renal pelvis (>3 cm) with minimal visual parenchyma, and after decompression the kidney can return to looking normal within days)

58
Q

Compare & contrast procedural considerations & outcome of ureteral stenting in dogs vs cats?

A

Cats - usually sx placed (10-15% endoscopically placed). 95% improved azotemia, peri-op mortality 7.5% (none related to stent complications/persistent ureteral obstruction). Most common post-stent complications: dysuria 38%, reocclusion requiring stent exchance 25%.

Dogs - 90-95% endoscopically placed. >90% success rate. Mortality <2%. Most common post-stent complications: recurrent UTI 15-59% (not likely related to stent, but to urolith/pyelonephritis/urethral incompetence/host immune dysfunction), stent occlusion <10%, migration/encrustation <10%, UVJ proliferative tissue dvpt.

59
Q

What treatments are available for idiopathic detrusor-urethral dyssynergia in dogs?

A
  • Medical management (alpha blockers etc.)
  • Botulinum-A toxin injections into urethral muscle trialled, some success (case reports)
60
Q

Proteins that are filtered through the glomerulus are effectively reabsorbed via ….. in the proximal tubules, accounting for minimal proteinuria in health.

A

Megalin/cubulin-mediated endocytosis

61
Q

Feline renal transplant recipients are at 6-fold risk of developing….. post transplantation.

What is the survival outcome of cats post renal transplantation?

A

Lymphoma, most commonly mid-high grade, diffuse large B-cell. MST 2-15d.

6-month survival: 60-65%, 3-year survival: 40%.

62
Q

Complications associated with uremia?

A
  • Reduce RBC lifespan
  • Thrombocytopathia (prolonged BMBT but normal coags) - abnormal platelet adhesiveness & aggregation, decreased clot retraction, decreased TXA production by platelets
  • Immune suppression > 2’ infections (25% in hemodialysis patients)
  • Pericarditis
  • Pneumonitis
  • Gastropathy (uremic gastritis with ulceration dogs; gastric fibrosis & mineralization cats)
  • Stomatitis (oral ulcerations)
  • Impaired ADH responsiveness (impairs ADH-stimulated adenyl cyclase activity) & thus water permeability in the DT/CDs > PUPD
  • Met acidosis (reduced renal NH4+ excretion + reduce acid/H+ secretion)
  • V+ (stimulation of CTZ receptors in emetic centre)
63
Q

Beneficial mechanisms of AT-II inhibition (e.g. ACEI, ARBs)?

A
  • Reduction in efferent arteriolar resistance > anti-proteinuric.
  • Also anti-hypertensive (10-15% reduction in BP)
  • Inhibition of glomerular mesangial growth and glomerular hypertrophy and subsequent fibrosis.
  • Reduced loss of glomerular heparin sulfate > hypercoagulability.
  • Decreased size of glomerular capillary endothelial pores.
  • Improved lipoprotein metabolism.
  • Slowed glomerular mesangial growth and proliferation.
  • Inhibition of bradykinin degradation.
64
Q

Failure to reabsorb which other AA may occur concurrently in dogs with cystinuria? What is the role of this AA? What implications does this have for treatment?

A

Carnitine. Enzyme cofactor necessary to transport energy-generating FAs from cytosol to the mitochondrial matrix.
High fat, low protein diets recommended for cystinuria, but may exacerbate carnitinuria > chronically may cause carnitine deficiency > DCM

65
Q

What treatments are recommended for dogs with urate urolithiasis and how do they work?

A

Address PSS or hepatic dz if identified.

For dogs w/o PSS/hepatic dysfunction:
1. Dissolution with purine-restricted diet 1st-line (e.g. Hills u/d). Target urine pH 7-7.5.
2. Urinary alkalinization
- Reduces renal tubular production of NH3 & thus NH4+ that complex with urate to form calculi.
- If refractory/persistent aciduric urine despite diet > add K citrate or NaHCO3
2. Allopurinol - XO inhibitor.
- MUST be given with low-purine diet (otherwise risk of xanthine urolith formation). NOT for cats.
- NOT for liver dz dogs (also need enough liver function to convert allopurinol to oxypurinol)
3. Urolith removal if causing LUT signs, refractory to med management etc. Minimally invasive > sx.

66
Q

List mechanisms that predispose Dalmatians to urate urolithiasis.

A

Inherited defect of uric acid membrane transporter (SLC2A9 gene mutation) - autosomal recessive > leads to differences hepatic & renal management of uric acid:
- Normal uricase enzyme [ ] but abnormal uric acid transport across hepatic membranes > limits uric acid metabolism
- Decreased uric acid PT reabsorption
- Increased uric acid active secretion in DTs

67
Q

Which breeds have primary renal glucosuria been reported in?

A

Scottish Terriers, Basenjis, Norwegian Elkhounds, mixed-breeds
Can be first sign of Fanconi’s syndrome in dogs

68
Q

List causes of Fanconi syndrome in dogs.

A

Primary - 10-30% Basenjis
Idiopathic - Norwegian Elkhound, Labs, Shetlands, Mini Schnauzer.
Acquired - chlorambucil (cats), expired tetracyclines, toxicosis causing acute tubular necrosis, copper, primary hypoPTH, gentamicin, chicken jerky treats

69
Q

What contributes to hypertonic medullary interstitium in the kidneys?

A
  1. Urea recirculation 40-50%
    - UT-A1 & UT-A3 (via ADH) facilitate diffusion of urea out of the medullary collecting ducts into the MI
    - UT-A2 facilitates urea excretion into the thin descending LOH
  2. Ascending LOH - solute (Na > K, Cl) actively transported into MI (while being impermeable to H2O)
  3. Small amt of H2O leaving thick/thin descending LOH
  4. Vasa recta - counter current exchange (Hairpin configuration + slow medullary blood flow) prevents solute washout from MI
70
Q

How do the following causes contribute to nephrogenic DI?
- HyperCa
- HypoK
- Bacterial endotoxins (E coli)

A
  • HypoK: downregulates aquaporin-2 channels, reducing ADH responsiveness of the terminal nephron
  • HyperCa: inhibits ADH binding to its receptors, damages renal tubular ADH receptors, inactivates adenylate cyclase, and/or decreases NaCl transport into the MI
  • Endotoxins: competitive binding at ADH receptor sites > reversible tubular ADH insensitivity, interference with insertion of aquaporin-2 channels in renal tubular cells
71
Q

List some differences in clinical manifestations of renal amyloidosis in Chinese Sharpeis vs other dog breeds?

A

CSPs - mostly renal medullary lesions > so causes interstitial more than glomerular dz, nephrotic syndrome uncommon, lower degree of proteinuria (but higher azotemia) cf other breeds. Also typically have extra-renal amyloidosis (spleen, liver, adrenal, GIT, myocardium etc.)

72
Q

What signalment in dogs is predisposed to ectopic ureters?

A

Huskies, Labs, GRs, WHWTs, Newfies, Eng Bulldogs, Fox Terrier, Skye terrier, border terrier, griffon, mini/toy Poodle, Entlebucher mountain dog

Females

72
Q

Ureteral peristalsis is subject to neurogenic control (T/F).

A

False - myogenic in origin (s.m.) –> so persists with implantation.

Has SNS (A1-R&raquo_space;> A2, beta receptors) & PS (muscarinic) which mediate ureteral spasms during obstruction & inhibit normal peristalsis.

73
Q

What % of dogs with EUs have a history of LUTI?

A

2/3 cases (consider bladder wall bx culture)

74
Q

According to the 2023 IRIS CKD guidelines, what are the risks of feeding renal diets in cats with phosphate within target range (1.5mmol/L)? What clin path criteria warrants dietary phosphate restriction in these cats, and what monitoring is recommended?

A

Increased risk of hyperCa.
FGF-23 >400pg/mL in the absence of hyperCa, anemia or marked inflammatory disease = indication for dietary phosphate restriction.

Monitor tCa, if >12 mg/dl (3 mmol/l), switch to a less phosphate-restricted diet.

75
Q

In stage 3 CKD cats, what is the target PO4 range? How may serum FGF-23 measurement help in therapeutic monitoring in these cats?

A

> 0.9 to <1.6mmol/L
Once serum phosphate is within target range, serum FGF-23 measurement may help determine if further PO4 restriction would be beneficial. If FGF-23 >700pg/ml (w/o hyperCa, severe inflammatory dz or marked anemia), indication for further PO4 restriction (increase phosphate binder dose).

76
Q

What are the advantages of darbopoitein over epoietin to address anemia in CKD? AE?

A

DPO = hyperglycosylated so 3x T 1/2 cf EPA > less frequent dosing.
Less incidence of PRCA (<10%) cf EPA (25-30%)
Other AE - hypertension, iron def (supplement Fe concurrently), pyrexia, seizures (hypertensive encephalopathy), polycythemia > hyperviscosity syndrome, arthralgia

77
Q

What are the roles of alpha-klotho? Where is it expressed and what factors upregulate and/or downregulate it?

What is its utility in CKD dogs?

A

Co-factor for FGF-23.
Expressed mostly in kidneys & parathyroids.
Reduces serum PO4, PTH, calcitriol (thus iCa).
Soluble alpha-klotho helps Ca rebsorption in DTs

Upregulate - calcitriol
Downregulate - ATII

Urinary a-klotho may be useful as dz progression marker - decreases with CKD.

78
Q

Describe treatment options for USMI?

A

Medical:
- Phenylpropanolamine - non-selective A1 & A2 agonist. SE hypertension, tachy/bradyarrhythmias,
- Estrogen compounds - increase sensitivity of A1 receptors in urethra to NE.
* Incurin (estriol) = short acting; 82-92% improved/complete continence. May be synergistic with PPA.
* DES = synthetic; 65% complete, 23% improved continence.

  • Submucosal urethral bulking agent (collagen inj): may require multiple tx esp younger dogs. 80% continent after 1-2 tx, 90% with PPA.
  • GnRH analogue - Leuprolide. Downregulates pituitary expression of GnRH receptors > suppress LH & FSH pdtn. Complete continence in >50% cases that fail traditional medical tx. Effects 3mths+, repeat PRN

Sx:
- Colposuspension
- Urethral occluder placement (proximal 3rd of urethra)

If detrusor hyperreflexia
- Anti-muscarinic & anti-spasmodic: oxybutynin, propantheline

79
Q

What disease is associated with detrusor instability in cats?

A

FeLV infection

80
Q

What are the potential benefits (and considerations) of the following treatments in dogs with CaOx urolithiasis?
- K citrate
- Hydrochlorothiazide
- Vit B6

Deficiency in which bacteria may contribute to hyperoxalauria as a risk factor for CaOx urolithiasis?

A

ACVIM consensus
1. K citrate: urinary alkalinizer
2. Thiazide diuretics
- Enhance reabsorption of filtered Ca in DCTs > decrease urinary CaOx relative supersaturation. Monitor for hyperCa. +/- add K citrate if urine pH <6.5 (thiazides acidify urine).
3. Vit B6
- Only if B6 deficient diet. Favours conversion of oxalate precursors to glycine, minimizing oxalate production.

Oxalobacter formigenes = intestinal bacterium that ingests oxalate as its sole nutrient.

81
Q

What is the significance of struvite crystalluria in dogs without evidence of LUT infection?

A

Not clinically significant. As urease-producing bacteria are usually required for struvite urolith formation in dogs.

82
Q

Which uroliths are amenable to medical dissolution?

A

Struvite (+ tx infection)
Allopurinol-induced xanthine uroliths

83
Q

Treatment recommendations & goals for cystine urolithiasis?

A

Neutering
Target urine pH >6.5-7.0, USG </=1.020 (dogs), </=1.030 (cats)
Diet - decreased protein (methionine & cysteine) but enough carnitine & taurine; high moisture, avoid high Na (incr cystine excretion)
Aim 25% reduction in uCys: crea ratio
+/- urine alkalinizers if urine pH <7.5 - K citrate

Thiola (2-mercaptopropionylglycine or 2-MPG) for refractory cases to diet & neuter. Forms disulfide bond with cysteine molecules > forms thiol-cysteine complex 50x more soluble cf cystine. NOT in cats. SE: blood dyscrasias, cutaneous eruptions, proteinuria), lymphadenopathy.

84
Q

How can urine nitroprusside test & urine cystine:creatinine ratio be used for therapeutic monitoring of cystine urolithiasis in dogs?

A

Urine nitroprusside test
- Measure at baseline & 3-6mths to determine if tx reduces cystine excretion.

Urine cystine:creatinine ratio
Cystinuria = >75-125mg cystine/g creatinine
- Variable magnitude of cystinuria associated with stone formation (between 100 and 10,000umol/g creatinine)
- Used to determine if castration is beneficial in reducing cystinuria. Measure baseline & 2mths post. If WRI at 2mths > indicates castration was beneficial, and the risk for stone formation is likely eliminated. If increased at 2mths, recheck at 4mths > persistently positive result = likely non-androgen dependent dz, risk of recurrence & additional tx needed (diet, K citrate, 2-MPG).

85
Q

Hereditary xanthinuria has been reported in which breeds?
What are the 2 types of genetic mutations identified as cause for this?

A

CKCS, Dachshund.

Type 1 (xanthine dehydrogenase (XDH) deficiency)
- Increased urinary hypoxanthine & xanthine excretion.

Type 2 (molybdenum cofactor sulfurase (MOCOS) deficiency)
- Toy Manchester terriers, Eng Cocker Spaniels, CKCS, Dachshunds
- MOCOS converts the molybdenum cofactor of XDH from the oxo- form to the sulfide- form, which is necessary for XDH activity

86
Q

What sonographic features of the kidneys/ureters support a diagnosis of ureteral obstruction?

A

Dx of UO can be made if hydronephrosis & associated hydroureter proximal to an obstructive ureterolith regardless of degree of renal pelvic dilatation.
1 study - 100% cases with RP >13mm had UO, RP >7mm more likely associated with UO.
Caveats: >20-25% cats have ureteral stritures so may not see ureteroliths/RP dilation on AUS even if UO - need radiographs or ureteropyelography.

87
Q

What is Febuxostat’s MOA and potential benefits?

A

Newer selective xanthine oxidase inhibitor. But unlike allopurinol, is not a purine analog & doesn’t require hepatic metabolism to extend DOA.
MOA - non-competitively blocks the molybdenum pterin center = active site of xanthine oxidase enzyme > reduces oxidation of hypoxanthine > xanthine > uric acid.
For urate urolithasis

88
Q

What is a risk factor for emphysematous cystitis? What are causal pathogens?

A

Glucosuria (DM patients).
E coli, Clostridium - ferment glucose (+/- albumin) to gas products;

89
Q

Common pathogens implicated in LUTI in cats?

A

E coli > Enterococcus faecalis, Staph felis

90
Q

Which antimicrobial peptide expressed in the LUT functions to prevent bacterial access to important mineral stores?

A

VCNA UTI 2019 review
Lipocalin 2

91
Q

Membranoproliferative glomerulonephropathies (MPGN)
Which breeds & causal gene mutations?

A

Eng Cocker Spaniels (COL4A4) – autosomal recessive, type IV collagen defect (BM splitting)
Samoyeds (COL4A5) – X linked, type IV collagen defect (BM splitting)
Bull Terriers, Dalmatians – autosomal dominant.
Brittany Spaniels - complement III deficiency, autosomal recessive
BMD - autosomal recessive (often assoc with lyme)
SCWTs (assoc with PLE, abnormal processing of dietary Ag)

92
Q

What is the pathogenesis of overfilled vs underfilled hypothesis with glomerular disease?

A

Early disease = ‘overfill’. Low circulating vol > RAAS activation > intrarenal Na retention. Serum albumin concentration & intravascular COP are adequate.

Progressive dz = ‘underfill’. Incr urinary loss of albumin + incr hepatic synthesis of albumin. But RAAS activation in attempt to restore circulating volume is unsuccessful because hypoalbuminemia and decr IV COP prevent H2O retention in circulation despite compensatory mechanisms.

93
Q

Describe how hyperlipidemia occurs in nephrotic syndrome?

A

Decr plasma COP (hypoalb) + incr urinary loss of regulatory factors for lipid metabolism (especially orosomucoid glycoprotein
–> incr hepatic synthesis of lipoproteins + decr peripheral catabolism of lipoproteins
–> Liver diverts sugar intermediates to replace the lost orosomucoid –> decreased production of heparin sulfate, which is a co-factor required for normal lipoprotein lipase function –> affects hepatic catabolism of lipoproteins.
–> Orosomucoid also has an impt role in maintaining normal glomerular permselectivity –> loss worsens proteinuria

–> Large-MW, cholesterol-rich lipoproteins (not easily lost through damaged glomerular capillary walls) accumulate, while smaller MW proteins e.g. albumin and AT lost in urine
–> hyperchol/hyperlipidemia with progressive hypoalb

94
Q

Total Ca:P product greater than …. has been associated with increased mortality in CKD dogs. Consequences include ….

A

70mg2/dl2
Soft tissue mineralisation, vascular calcification (reported in people)

95
Q

FGF-23 binds to …. and acts directly on renal tubules to increase phosphate excretion by inhibiting ……… in the …..

A

alpha-klotho (co-factor)
Inhibiting NaPi co-transporters (type 2a & 2b) in the proximal tubules.

96
Q

All phosphate binders except …. act by inhibiting dietary phosphate absorption in the GIT. How does this drug work?

A

Niacinamide/nicotinamide (Vit B3, also immunomodulatory drug used for autoimmune skin dz in dogs)
MOA: inhibits Na/P co-transporters in both renal tubules (Na/Pi2a) & intestinal brush borders (Na/Pi2b) to reduce P reabsorption. Only used in people not vet med.

97
Q

What complication may occur when using >1 phosphate binder (AlOH & Ca-based products) in a hypoCa, hyperphos CKD patient? What treatment strategies can be employed to address this complication?

A

Ca-based phos binders (esp citrate) increase intestinal Al absorption, so may predispose to Al toxicity (see microcytosis, neuro signs).

Chelation therapy (deferoxamine), extracorporeal therapies (hemodialysis)

98
Q

Sevelamer hydrochloride/carbonate
- MOA
- Complications/AE

A

Synthetic hydrogel of cross-linked poly-allylamine; phosphate binder.

AE: metabolic acidosis from gastric CO2 production, GI signs (less for carbonate), iatrogenic hypoT (interfere with levothyroxine absorption in people), drug interactions (bind & reduce GI absorption of frusemide & cyclosporin)
NB: reduces serum cholesterol by 20-30%

99
Q

Lanthanum
- MOA
- AE

A

Rare metal, forms insoluble complexes with P in GI lumen. Greater capacity to bind P cf Ca compounds & sevelamer, comparable to AlOH. Hepatic excretion.
AE: GI (generally well tolerated).

100
Q

Is hemodialysis effective in addressing hyperphosphatemia in CKD patients? Why or why not?

A

To a limited extent. P has low MW but behaves like Phosphorus behaves as a middle MW solute - serum [ ] decreases markedly in 1st hr of dialysis then maintained at reasonable levels even with long dialysis sessions. Almost all patients will still need phos binders. Also long dialysis sessions not an option for vet patients.

101
Q

What phosphate binder is recommended for CKD patients that are hyperphos & hyperCa? How does it drugs work?

A

Cinacalcet (calcimimetic)
Potent PTH suppressor, decreases serum phos & iCa.
Acts directly on the Ca sensing receptor (CaSR) in the PT glands to reduce PTH secretion. Peak [ ] 2-6hrs, rapid absorption. Start low dose & monitor iCa/phos 1-2 wks after. (in people monitor PTH 12hrs post dose)
Well tolerated in people, AE: GI

102
Q

How may excessive dietary phosphate restriction precipitate hyperCa and hypercalciuria in CKD patients?

A

Low P intake –> decreased FGF-23 –> increased 1-alpha hydroxylase activity –> increased calcitriol –> increases intestinal Ca absorption + exacerbates hypercalciuria.

103
Q

What adverse renal changes may hyperCa cause?

A

Functional:
- Impairs responsiveness of CDs to ADH + direct interference with ADH receptor binding > nephrogenic DI
- Medullary washout (decreases urea permeability of CDs due to ADH interference + hyperCa increases renal medullary blood flow)
- Predispose to bacterial UTI (renal insufficiency, dilute urine, uroliths as nidus)

Structural
- Renal vasoconstriction, decreases RBF & GFR > may cause acute tubular necrosis
- Nephron loss, nephrocalcinosis (if Ca:PO4 >50), tubulointerstitial inflammation, interstitial fibrosis.
- Ca containing urolithiasis

104
Q

X-linked hereditary nephropathy (XLHN): what are clinical manifestations observed in males vs female dogs?

A

Males - gene mutations encoding glomerular type IV collagen > develop proteinuric end-stage KD between 6-18mo.
Females - heterozygotes develop juvenile proteinuria, but most have sufficient normal glomerular BM to maintain structural and functional integrity. Subclinical, normal USG, normal sCr levels until ~5yo.

ACVIM Specialty Exam (20 decks)

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