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!Small Animal Medicine > Chronic and Acute Kidney Dz > Flashcards

Chronic and Acute Kidney Dz Flashcards

1
Q

Chronic kidney dz

A

Persists of >3m
Creat >1.5 and BUN >33
USG: 1.008 -1.030 (inappropriate, not actively diluting or concentrating urine)

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2
Q

Non-azotemic kidney dz

A

Proteinuric (glo and tubular)
Structural (dysphagia, agenesis and vascular)
Pathophysiologic (degenerative, anomaly, metabolic, neoplasia, infection/inflamm, trauma/toxin, genetic)

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3
Q

CS associated with chr. kidney dz

A

WL, PU/PD, ↓ appetite and old age
(more likely in cats)
↓ nutrition status and poor hair coat

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4
Q

Dx chr. kidney dz

A

↑ azotemia and ↓ USG
Persistent glomerular proteinuria, non-regen anemia, and genetic biomarkers of inherited kidney dz
NEXT STEP: IRIS stage

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5
Q

Anatomical kidneys signs associated with chr. kidney dz

A

Small kidneys, mineralization and cysts/ pseudocysts

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6
Q

What are the stages of chr. kidney dz based on?

A

Elevated serum creatinine
1. Azotemia (if hydrated)- pre (non kidney), renal (kidney failure), post (obstruction)
2. Substage with proteinuria and hypertension

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7
Q

Stage 1 of chr. kidney failure

A

Inadequate urine conc. ability (cats)
Progressive ↑ in creat/ SDMA
Renal abnorms (imaging)
Persistant renal proteinuria
↓ GFR

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8
Q

How to tx stage 1 of chr. kidney failure

A

Tx underlying dz
Renal therapeutic diet (tx proteinuria)
Keep P (phosphate binder)
Fresh H20 available

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9
Q

Stage 2 of chr. kidney failure

A

Mild (years survival)
Animal progresses

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10
Q

How to tx stage 2 of chr. kidney failure

A

Renal therapuetic diet
Tx hypokalemia (cats)
Same as stage 1

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11
Q

Stage 3 of chr. kidney failure

A

Moderate
Complication: hypertension
Anemia and poor appetite

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12
Q

How to tx stage 3 of chr. kidnye failure

A

Keep P
Tx met. acidosis, anemia, V, inappetence and nausea
↑ fluids
Calcitriol tx (dogs)
Same as 2

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13
Q

Stage 4 of chr. kidnye failure

A

Severe (week- month survival)
Creat >5 (bad CS)
Complication: infection

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14
Q

How to tx Stage 4 of chr. kidnye failure

A

Feeding tube for nutrition and hydration
Same as 3

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15
Q

What does progressive chr. kidney dz look like?

A

Glomerulosclerosis
Tubulointestinal injury
Cell death

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16
Q

Mechanisms promoting progression

A

Hypoxemia, hyperphosphatemia, hypertension, renal proteinuria, persistence/ recurrence of initial or new cause, advancing age

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17
Q

EG toxicity (acute kidney dz)

A

Once azotemic 100% die
Ca oxalate crystals in urine (death soon)
Severe met. acid and ↑ anion gap seen before azotemia and crystals

18
Q

Significance of EG

A

Dx b4 azotemia
Normal creat. doesn’t rule out AKI
Urinalysis in initial evaluation if you suspect kidney dz

19
Q

Acute kidney dz

A

Sudden and rapid decline in kidney function <1w

20
Q

Anion gap

A

Helps localize aciodsis
(Na + K) - (Cl +HCO3)
Norml: 15-25

21
Q

How to dx AKI

A

Historical data (EG, lilies, grapes, etc)
Clinical markers (renal pain, oliguric)
Lab data (↑ creat, cystatin B, UA, MDB)

22
Q

What can cause AKI

A

Hemodynamic (hypovelmia, hypotension, shock, anesthesia)
Infectious (lepto)
Nephrotoxicity (EG, grapes, NSAIDs)
Systemic Dz (sepsis)
Urinary obstruction (ureteral)

23
Q

CS associated with AKI

A

Oligonuria, kidney pain and enlargement
Lethargy, anorexia, V/D, PU/PD, WL

24
Q

Phase 1 of AKI: Initiation

A

GFR goes to 0 right away
Creatinine low or normal
Specific therapy can halt damage

25
Q

Phase 2 of AKI: Extension

A

Continues damage
Specific/ supportive therapy can halt damage + permit renal repair

26
Q

Phase 3 of AKI: Maintenance

A

Measures ↓ kidney function
1-3w
Oliguria
Targeted supportive therapy (allows kidney time to repair)

27
Q

Phase 4 of AKI: Recovery

A

Renal repair, not all recover
Weeks to months
Urine output ↑
Consequences: CKD/ death (50%)

28
Q

Most important step for tx AKI

A

Correcting prerenal azotemia
1. Correct perfusion within first hrs to dx
2. Correct dehydration over 12-24 hrs

29
Q

What is the most common error when dx AKI?

A

Failure to perform the urinalysis

30
Q

Other ways to dx AKI

A

Glucosuria without hyperglycemia (tubular damage and proteinuria)
↓USG (with ↑ azotemia)
Urine sediment

31
Q

What seen in a urine sediment of a pet dx with AKI

A

Acute tubular necrosis: granular casts (muddy brown) with epithelial cells and casts
Ca oxalate crystals (EG, hypocalcemia)
Glomerunephritis/ vasculitis: proteinuria, red cells and red cell casts
Interstitial nephritis/ pyelonephritis: Polyuria and WBC casts

32
Q

How to tx AKI

A

Specific therapy: eliminate, remove underlying cause
Supportive (water, electrolyte, calorie, acide/base correction, removal of retained wastes, endocrine)
Symptomatic therapy: nausea and pain

33
Q

How to tx persistent oliguria

A

Patients remaining oliguric after complete rehydration
Therapeutic trial with diuretics (don’t give unless completely hydrated)

34
Q

What drugs to use for AKI

A

Mannitol (osmotic diuretic)
Glucose (OD)
Furosemide (loop diuretic)
Fenoldopam/ dopamine (vasodilation ↑ renal blood flow and naturesis)
Diltiazem (Ca channel blocker causing preglo vasodilation)

35
Q

Pathologic oliguria/anuria

A

Small urinary bladder, hyperkalemia, urinary obstruction and uroabdomen

36
Q

What does pathologic oliguria/anuria lead to?

A

azotemia, fluid overload, met acidosis

37
Q

Pathologic nonoliguria and polyuria

A

Large urinary bladder and hypokalemia

38
Q

What does nonpathologic oliguria/polyuria lead to?

A

Signals onset of recovery of AKI
Dehydration and hypokalemia

39
Q

Leptospirosis

A

Common cause of AKI in dogs
PCR accurate (abx and test timing disrupt)
Confirm with convalescent Ab titer

40
Q

Indications for Renal Replacement Therapy

A

Fluid overload
Unrelenting hyperkalemia acid/ base imbalance
Inadequate urine production
Progressive unrelenting azotemia
Acute poisoning/ drug overdose

!Small Animal Medicine (32 decks)

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