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Small animal internal medicine > Renal disease: acute kidney disease > Flashcards

Renal disease: acute kidney disease Flashcards

1
Q

Definition of Acute kidney injury.

A

Clinical syndrome characterized by rapid decline in GFR and renal function of varying severity, initiated by a multitude of causes.

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2
Q

Phases of Acute kidney injury. (4)

A
  1. Induction
  2. Extension
  3. Maintenance
  4. Recovery
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3
Q

Grades of AKI.

A

I-V

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4
Q

Acute kidney injury Categorization. (3)

A

Prerenal (hemodynamic): renal hypoperfusion.

Intrinsic renal: ischemia/nephrotoxin damages the renal parenchyma.

Postrenal (obstructive): acute obstruction of the urinary tract.

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5
Q

Prerenal kidney injury due to

A

hemodynamic: renal hypoperfusion → decreased GFR, normal renal parenchyma

● Rapid correction of GFR following restoration of renal perfusion.

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6
Q

Intrinsic renal injury due to

A

ischemia/nephrotoxin damages the renal parenchyma.

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7
Q

Postrenal kidney injury due to

A

acute obstruction of the urinary tract.

Uroabdomen
● Trauma
● Bladder may be palpable
● May not be grossly hematuric

Ureteral/urethral obstruction
● Uroliths/debris
● Urethral/bilateral ureteral obstruction

● Unilateral ureteral - no biochemical abnormalities if the other kidney is normal

● Unilateral ureteral with CKD - acute on chronic
● Renal pelvis dilation, blunting of diverticuli, proximal ureteral dilation

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8
Q

Difference between AKI and acute kidney disease.

A

AKI ≤7 days
AKD >7 days
CKD ≥3 months

Acute kidney disease is a Post-AKI state/early CKD.

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9
Q

How should acute kidney disease be treated?
Graded?
Monitored?

A

Monitor and treat Acute kidney disease like AKI.

● Grades (I-V) based on creatinine.

● Recovery monitored with GFR biomarkers (creatinine, SDMA, BUN).

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10
Q

Unit conversion for creatinine: mg/dL to mcmol/L

A

multiply mg/dL by 88 to mcmol/L

e.g. creatinine 5 mg/dL = creatinine 440 mcmol/L

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11
Q

AKD grade I is further categorized:

A

AKD grade I subtypes:
IC
IB
IA

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12
Q

Drugs/conditions contributing to AKI (7)

A

● NSAIDs, ACEIs,
diuretics, cyclosporine,
radiocontrast agents,
hypercalcemia,
bacterial endotoxins.

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13
Q

Intrinsic renal etiology for AKI? (4)

A

Diseases of large renal vessels
● Renal artery thrombosis, vasculitis, renal vein compression

Diseases of the renal microvasculature and glomeruli
● Glomerulonephritis, vasculitis, hypertension…

Ischemic/nephrotoxic acute tubular necrosis
● Renal hypoperfusion, endogenous/exogenous toxins

Other processes involving the tubulointerstitium
● Neoplastic infiltration, oxidative injury, infectious disease

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14
Q

Intrinsic systemic disease with potential to cause prerenal AKI? (6)

A

● Infectious diseases: leptospirosis, babesiosis, parvovirosis

● Sepsis and MODS

● Hypo-and hyperadrenocorticism

● Pancreatitis

● Heatstroke

● Cutaneous and renal glomerular vasculopathy

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15
Q

Describe Nephrotoxins and kidney injury.

A

● Endogenous (e.g. myoglobin) or exogenous

● Different mechanisms of injury

● Intrarenal vasoconstriction, tubular cell toxic injury, intratubular obstruction.

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16
Q

Name some exogenous nephrotoxins.

A

● Contrast agents

● Drugs: aminoglycosides, amphotericin B, cyclosporine, tacrolimus, albumin…

● Grape, raisin, currant (dogs)

● Lily (cats)

● Ethylene glycol

● Melamine

● Cholecalciferol (vitamin D) - rodenticide

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17
Q

How is vitamin D used as a rodenticide?

A

Cholecalciferol is a form of vitamin D3 that is commonly used as a rodenticide to control rat and mouse populations. While vitamin D3 is essential for calcium regulation in the body, in high doses, it can become toxic.

Hypercalcemia causes acute renal failure as calcium crystals deposit in the kidneys and lead to death, typically within several days.

While cholecalciferol is primarily used for rodents, accidental ingestion by pets (like dogs and cats) or humans can lead to similar toxic effects, requiring immediate medical intervention to manage calcium levels and prevent permanent damage.

18
Q

Give 2 examples of infectious intrinsic cause for kidney injury.

A

● Leptospirosis
● Pyelonephritis (bacterial)

19
Q

Clinical signs of acute kidney injury. (7)

A

● Uremia: GI, neurologic, cardiovascular

● Hypothermia
● Hypertension
● Hypervolemia

● Ventricular premature complex arrhythmias

● Nausea, vomiting, diarrhea, anorexia, GI and oral ulceration

● Obtundation, coma, seizures

20
Q

laboratory evaluation of acute kidney injury - CBC (2)

A

● Leukocytosis
● Hemoconcentration

21
Q

laboratory evaluation of acute kidney injury - biochemistry (4)

A

Azotemia (increase in creatinine, BUN)
● Time lag!
● Prerenal: mild to moderate, BUN>creatinine
● Postrenal: marked, but no azotemia with unilateral obstruction

● Electrolytes:
hyperP,
hyperK,
hypoNa

22
Q

laboratory evaluation of acute kidney injury - urinalysis (4)

A

Urine volume not helpful.

● Isosthenuria
● Casts

● Prerenal: UOP decreased, USG >1.030,
hyaline casts

Urine culture
● Pyelonephritis

● Leptospira PCR

23
Q

describe diagnostic imaging for evaluation of acute kidney injury (5)

A

● Radiographs: kidney size, radiopaque calculi

● U/S: cortical thickness, cortical-medullary densities, renal pelvis dilation, calculi

● but in Prerenal: kidneys will have normal size, shape, and architecture.

● Perirenal effusion - nonspecific sign.

● Peritoneal/retroperitoneal effusion indicates uroabdomen.

24
Q

Uroabdomen diagnosis. (3)

A

● effusion Creatinine and K compared to serum

Cytology of effusion fluid.
● Urine is a chemical irritant that may cause non-septic neutrophilic inflammation
- Cell count >5000/mcL
- Total solids >3.0 g/dL (>30 g/L)

25
Q

define Xerostomia

A

dry mouth

26
Q

parameters to monitor after acute kidney injury (6)

A

● Hydration
- Xerostomia
- Overhydration: serous ocular/nasal discharges, SC edema, cavitary effusions, pulmonary edema, hypertension (hypervolemia)

● Body weight
● Physical examination

● Hematocrit, total protein, electrolytes, creatinine, BUN, acid-base status q24h

● Blood pressure q12h
● UOP

27
Q

Treatment principles for acute kidney disease. (3)

A

● Limit further renal damage, enhance cellular recovery.

● Most successful during induction and extension phases of disease.

● Treatment of specific diseases that are behind the kidney disease.
e.g. Obstruction, infectious diseases, toxins

28
Q

Describe Fluid therapy treatment of acute kidney disease. (5)

A

● Correct dehydration, hypovolemia, acid-base and electrolyte disturbances,
maintain cardiac output, renal perfusion, systemic oxygen delivery, promote
diuresis.

● Fluid type: initially isotonic crystalloid, maintenance with lower Na.

● Correction of hypovolemia rapidly, dehydration over 6-24 h, then maintenance.

● Rate: metabolic water demands, insensible losses, sensible losses (increased
with PU), correct volume deficits.

● Complications: hypervolemia, hypertension, edema.

29
Q

How to treat hyperkalemia in acute kidney disease. (4)

A

relieve urethral obstruction if present,

C+ gluconate administration to protect the heart,

IV regular insulin + dextrose (encourages cellular K+ uptake),

extracorporeal renal support therapy (dialysis)

30
Q

How does C+ gluconate administration protect the heart in cases of hyperkalemia?

A

in hyperkalemia, excess potassium disrupts this electrical activity, which can lead to life-threatening arrhythmias.

Calcium gluconate stabilizes the heart’s electrical system by counteracting the effects of high potassium on the heart muscle.

Specifically, calcium restores the normal electrical gradient across the cardiac cells’ membranes, which Increases the threshold for depolarization.

31
Q

How does insulin help correct hyperkalemia?

A

encourages cellular K+ uptake

This process occurs via stimulation of Na⁺/K⁺-ATPase pumps, which actively transport potassium into cells in exchange for sodium.

32
Q

How to treat hypokalemia in acute kidney disease.

A

by supplementing IV fluids with potassium, and ensuring feeding PO

33
Q

How to treat hypocalcemia in acute kidney disease.

A

slow bolus IV Ca, followed by a CRI

34
Q

How to treat hyperphosphatemia in acute kidney disease. (2)

A

reduced P diets,
enteric phosphate binders

35
Q

Treatment of GI complications in acute kidney disease.

A

● Treat Vomiting, nausea, anorexia, ileus with antiemetics, prokinetics, appetite
stimulants.
- Maropitant, ondansetron, metoclopramide, mirtazapine

Treat Oral and GI ulcerations (lingual ulcers, abdominal pain, and melena) with gastric
acid suppressants.
- Proton pump inhibitor, famotidine

Nutrition via Feeding tube if needed.

36
Q

Treatment of systemic hypertension in acute kidney disease.

A

Amlodipine, and can be given rectally if needed.

Avoid ACEi and ARB (Angiotensin receptor blockers). They can reduce glomerular filtration, may exacerbate hyperkalemia, can worsen the kidney’s ability to manage fluid and electrolyte balance.

But Once the acute phase resolves and kidney function stabilizes, ACEi or ARBs may be reconsidered for long-term management if appropriate.

37
Q

Normal urine output?
What counts as polyuria?
And oliguria?
Anuria?

A

normal UOP 1-2 ml/kg/h,
>2 ml/kg/h PU,
<1-2 ml/kg/h oliguria,
0-0.5 ml/kg/h anuria

38
Q

Signs of Oligo/anuria and way to assess them.

A

SC edema, increased RR and effort, abdominal distention/pain, bladder size

Volume and hydration status;
PCV/TS, chemistry with electrolytes, acid-base analysis

U/S (bladder size)

Thoracic radiographs, U/S (pulmonary edema, pleural effusion)

39
Q

Treatment of oligo/anuria

A

● Hypovolemia: isotonic replacement solution rapidly IV

● Dehydration: calculated and replaced over 6-8 h

● Converting oligo/anuria to PU: mannitol, furosemide, fenoldopam (promotes sodium excretion via dopamine receptors)

● Hypervolemia in an oligoanuric patient - extracorporeal renal replacement
therapy (dialysis)

40
Q

Extracorporeal renal support therapy

A

Peritoneal dialysis (Instead of using a machine and blood filters (like hemodialysis), peritoneal dialysis uses the patient’s peritoneum (the lining of the abdominal cavity) as a natural filter to clean the blood.)

Hemodialysis and continuous renal
replacement therapies.

41
Q

Peritoneal dialysis mechanism of action.

A

A special fluid called dialysate (a sterile solution containing water, glucose, and electrolytes) is introduced into the patient’s abdominal cavity through a catheter that is surgically placed in the abdomen.

waste products (like urea and creatinine), excess electrolytes, and extra fluid to pass from the blood vessels into the dialysate solution in the abdomen.

After a certain period (usually 4-6 hours), the used dialysate, now containing the waste products, is drained out of the abdomen through the catheter and discarded.

42
Q

Prognosis for acute kidney disease.

A

Depends on the Underlying cause
● Infectious - better prognosis

Mortality rate 45-64%

Oligo/anuria make for a worse prognosis.

Full recovery 19-25%

CKD common sequalae

Small animal internal medicine (18 decks)

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