Acute Kidney Injury 4

Question 1

What are the components involved in intrinsic AKI?

Answer 1

Glomerular, tubulointerstitial, or vascular components.

Question 2

What is the most common cause of intrinsic AKI in the ICU?

Answer 2

Acute Tubular Necrosis (ATN) due to ischemia.

Question 3

What are key features of nephritic syndrome in glomerular disease?

Answer 3

Glomerular hematuria, edema, azotemia, and hypertension.

Question 4

What is the leading cause of glomerular disease worldwide?

Answer 4

IgA nephropathy.

Question 5

What is the most common glomerular disease in children?

Answer 5

Post-streptococcal glomerulonephritis (PSAGN).

Question 6

What is a hallmark feature of rapidly progressive glomerulonephritis (RPGN)?

Answer 6

Rapid loss of renal function and crescents in glomeruli.

Question 7

What causes glomerular injury in nephritic syndrome?

Answer 7

Immune-mediated damage to the basement membrane, mesangium, or capillary walls.

Question 8

What are common symptoms of PSAGN?

Answer 8

Edema and tea-colored urine following a sore throat or skin infection by 1–3 weeks.

Question 9

What urine findings suggest glomerular disease?

Answer 9

Hematuria, RBC casts, dysmorphic RBCs, and proteinuria.

Question 10

What lab values suggest glomerular disease?

Answer 10

Urine osmolality <350 mOsm/kg, urine sodium >20 mEq/L, FENa >2%, and BUN-to-creatinine ratio <10.

Question 11

What are the phases of ATN progression?

Answer 11

Initiation (tubular injury), Maintenance (sustained GFR reduction), and Recovery (tubular regeneration).

Question 12

What causes tubular obstruction in ATN?

Answer 12

Necrotic cell debris leading to GFR decline and filtrate back leak.

Question 13

What are the hallmark findings in the urinalysis of ATN?

Answer 13

Muddy brown granular casts and epithelial cell casts.

Question 14

What differentiates oliguric from nonoliguric ATN?

Answer 14

Oliguric ATN presents with edema and hypertension, while nonoliguric ATN may have normal BP.

Question 15

What are the common nephrotoxins causing intrinsic AKI?

Answer 15

Aminoglycosides, NSAIDs, calcineurin inhibitors, ACE inhibitors, ARBs, acyclovir, and radiocontrast agents.

Question 16

What are the mechanisms of nephrotoxin-induced kidney injury?

Answer 16

Tubular necrosis (e.g., aminoglycosides), reduced renal blood flow (e.g., NSAIDs), and tubular obstruction (e.g., acyclovir).

Question 17

What strategies prevent nephrotoxic AKI?

Answer 17

Avoiding nephrotoxins, dose monitoring, adequate hydration, and urine alkalinization.

Question 18

What causes sepsis-induced AKI?

Answer 18

Immune-mediated injury, cytokine release, T-cell activation, and altered renal hemodynamics.

Question 19

How does sepsis-induced AKI differ from ischemic ATN?

Answer 19

It involves systemic inflammation rather than just reduced renal blood flow.

Question 20

What diagnostic findings are seen in sepsis-induced AKI?

Answer 20

Similar to ATN, including muddy brown casts and FENa >2%.

Question 21

How is PSAGN managed?

Answer 21

Supportive care as it is usually self-limiting.

Question 22

How are other types of glomerulonephritis treated?

Answer 22

Immunosuppressants and plasmapheresis.

Question 23

What imaging findings support intrinsic AKI diagnosis?

Answer 23

Enlarged kidneys with increased echogenicity on renal ultrasound.

Question 24

What is the significance of muddy brown casts in AKI?

Answer 24

They are diagnostic of ATN.

Question 25

What should be avoided in patients at risk of AKI?

Answer 25

Nephrotoxins, especially in volume-depleted patients.