Renal disease: acute kidney disease

Question 1

Definition of Acute kidney injury.

Answer 1

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

Question 2

Phases of Acute kidney injury. (4)

Answer 2

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

Question 3

Grades of AKI.

Answer 3

I-V

Question 4

Acute kidney injury Categorization. (3)

Answer 4

Prerenal (hemodynamic): renal hypoperfusion.

Intrinsic renal: ischemia/nephrotoxin damages the renal parenchyma.

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

Question 5

Prerenal kidney injury due to

Answer 5

hemodynamic: renal hypoperfusion → decreased GFR, normal renal parenchyma

● Rapid correction of GFR following restoration of renal perfusion.

Question 6

Intrinsic renal injury due to

Answer 6

ischemia/nephrotoxin damages the renal parenchyma.

Question 7

Postrenal kidney injury due to

Answer 7

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

Question 8

Difference between AKI and acute kidney disease.

Answer 8

AKI ≤7 days
AKD >7 days
CKD ≥3 months

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

Question 9

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

Answer 9

Monitor and treat Acute kidney disease like AKI.

● Grades (I-V) based on creatinine.

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

Question 10

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

Answer 10

multiply mg/dL by 88 to mcmol/L

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

Question 11

AKD grade I is further categorized:

Answer 11

AKD grade I subtypes:
IC
IB
IA

Question 12

Drugs/conditions contributing to AKI (7)

Answer 12

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

Question 13

Intrinsic renal etiology for AKI? (4)

Answer 13

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

Question 14

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

Answer 14

● Infectious diseases: leptospirosis, babesiosis, parvovirosis

● Sepsis and MODS

● Hypo-and hyperadrenocorticism

● Pancreatitis

● Heatstroke

● Cutaneous and renal glomerular vasculopathy

Question 15

Describe Nephrotoxins and kidney injury.

Answer 15

● Endogenous (e.g. myoglobin) or exogenous

● Different mechanisms of injury

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

Question 16

Name some exogenous nephrotoxins.

Answer 16

● Contrast agents

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

● Grape, raisin, currant (dogs)

● Lily (cats)

● Ethylene glycol

● Melamine

● Cholecalciferol (vitamin D) - rodenticide

Question 17

How is vitamin D used as a rodenticide?

Answer 17

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.

Question 18

Give 2 examples of infectious intrinsic cause for kidney injury.

Answer 18

● Leptospirosis
● Pyelonephritis (bacterial)

Question 19

Clinical signs of acute kidney injury. (7)

Answer 19

● Uremia: GI, neurologic, cardiovascular

● Hypothermia
● Hypertension
● Hypervolemia

● Ventricular premature complex arrhythmias

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

● Obtundation, coma, seizures

Question 20

laboratory evaluation of acute kidney injury - CBC (2)

Answer 20

● Leukocytosis
● Hemoconcentration

Question 21

laboratory evaluation of acute kidney injury - biochemistry (4)

Answer 21

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

Question 22

laboratory evaluation of acute kidney injury - urinalysis (4)

Answer 22

Urine volume not helpful.

● Isosthenuria
● Casts

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

Urine culture
● Pyelonephritis

● Leptospira PCR

Question 23

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

Answer 23

● 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.

Question 24

Uroabdomen diagnosis. (3)

Answer 24

● 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)

Question 25

define Xerostomia

Answer 25

dry mouth

Question 26

parameters to monitor after acute kidney injury (6)

Answer 26

● 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

Question 27

Treatment principles for acute kidney disease. (3)

Answer 27

● 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

Question 28

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

Answer 28

● 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.

Question 29

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

Answer 29

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)

Question 30

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

Answer 30

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.

Question 31

How does insulin help correct hyperkalemia?

Answer 31

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

Question 32

How to treat hypokalemia in acute kidney disease.

Answer 32

by supplementing IV fluids with potassium, and ensuring feeding PO

Question 33

How to treat hypocalcemia in acute kidney disease.

Answer 33

slow bolus IV Ca, followed by a CRI

Question 34

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

Answer 34

reduced P diets, enteric phosphate binders

Question 35

Treatment of GI complications in acute kidney disease.

Answer 35

● 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.

Question 36

Treatment of systemic hypertension in acute kidney disease.

Answer 36

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.

Question 37

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

Answer 37

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

Question 38

Signs of Oligo/anuria and way to assess them.

Answer 38

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)

Question 39

Treatment of oligo/anuria

Answer 39

● 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)

Question 40

Extracorporeal renal support therapy

Answer 40

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.

Question 41

Peritoneal dialysis mechanism of action.

Answer 41

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.

Question 42

Prognosis for acute kidney disease.

Answer 42

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