Acute Kidney Injury 4 Flashcards
What are the components involved in intrinsic AKI?
Glomerular, tubulointerstitial, or vascular components.
What is the most common cause of intrinsic AKI in the ICU?
Acute Tubular Necrosis (ATN) due to ischemia.
What are key features of nephritic syndrome in glomerular disease?
Glomerular hematuria, edema, azotemia, and hypertension.
What is the leading cause of glomerular disease worldwide?
IgA nephropathy.
What is the most common glomerular disease in children?
Post-streptococcal glomerulonephritis (PSAGN).
What is a hallmark feature of rapidly progressive glomerulonephritis (RPGN)?
Rapid loss of renal function and crescents in glomeruli.
What causes glomerular injury in nephritic syndrome?
Immune-mediated damage to the basement membrane, mesangium, or capillary walls.
What are common symptoms of PSAGN?
Edema and tea-colored urine following a sore throat or skin infection by 1–3 weeks.
What urine findings suggest glomerular disease?
Hematuria, RBC casts, dysmorphic RBCs, and proteinuria.
What lab values suggest glomerular disease?
Urine osmolality <350 mOsm/kg, urine sodium >20 mEq/L, FENa >2%, and BUN-to-creatinine ratio <10.
What are the phases of ATN progression?
Initiation (tubular injury), Maintenance (sustained GFR reduction), and Recovery (tubular regeneration).
What causes tubular obstruction in ATN?
Necrotic cell debris leading to GFR decline and filtrate back leak.
What are the hallmark findings in the urinalysis of ATN?
Muddy brown granular casts and epithelial cell casts.
What differentiates oliguric from nonoliguric ATN?
Oliguric ATN presents with edema and hypertension, while nonoliguric ATN may have normal BP.
What are the common nephrotoxins causing intrinsic AKI?
Aminoglycosides, NSAIDs, calcineurin inhibitors, ACE inhibitors, ARBs, acyclovir, and radiocontrast agents.
What are the mechanisms of nephrotoxin-induced kidney injury?
Tubular necrosis (e.g., aminoglycosides), reduced renal blood flow (e.g., NSAIDs), and tubular obstruction (e.g., acyclovir).
What strategies prevent nephrotoxic AKI?
Avoiding nephrotoxins, dose monitoring, adequate hydration, and urine alkalinization.
What causes sepsis-induced AKI?
Immune-mediated injury, cytokine release, T-cell activation, and altered renal hemodynamics.
How does sepsis-induced AKI differ from ischemic ATN?
It involves systemic inflammation rather than just reduced renal blood flow.
What diagnostic findings are seen in sepsis-induced AKI?
Similar to ATN, including muddy brown casts and FENa >2%.
How is PSAGN managed?
Supportive care as it is usually self-limiting.
How are other types of glomerulonephritis treated?
Immunosuppressants and plasmapheresis.
What imaging findings support intrinsic AKI diagnosis?
Enlarged kidneys with increased echogenicity on renal ultrasound.
What is the significance of muddy brown casts in AKI?
They are diagnostic of ATN.
What should be avoided in patients at risk of AKI?
Nephrotoxins, especially in volume-depleted patients.
