Low blood flow into the kidney

Pathophysiology

NSAID/ARBS exacerbate but do not cause AKI

1 cause of AKI

• Prolonged acute pre-renal disease can progress into ATN - Acute tubular necrosis (cannot be fixed by giving fluid)

  Labs	Pre-renal AKI	‣ (ATN - Acute tubular necrosis)
  ‣	Normal	‣ / ‣
  ‣	Normal	Hemegranular cast (or other casts)
  ‣	> 20:1	< 10:1
  (less urea re-absorbed)
  ‣	<1%	>1%
  (less Na re-absorbed)
  ‣	< 20 mmol/L	> 20 mmol/L
  (less Na re-absorbed)
  ‣	>500 mmol/L	<350 mmol/L
  (less water re-absorbed)
  Response to ‣	improve GFR → give fluid	don’t improve GFR → give time

Acute Etiology

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Euvolemic/hypervolemic

Decreased effective circulating volume, ECF often expended, fluid pooling in venous circulation, but with low BP

• Extravascular overload
  • !CHF (H+W)
  • HRS - Hepatorenal syndrome
• Distributive shock (!Sepsis, !Anaphylaxis)
• Medication
  • NSAID (Construction of Afferent Arteriole (AA))
  • RAAi (Dilation of Efferent Arteriole)

Hypovolemia

• Dehydration (severe), Emesis(vomiting), Diarrhea
• Major Hemorrhage
• !Rhabdomyolysis
• !TLS - Tumor lysis syndrome (↑PO4, LDH, K, uric acid, ↓Ca) </aside>

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Pre-renal Medications

Constrict AA

• CT Contrast Toxicity ⇒ Iodine contrast dye → Controversial
• SGLT2i (”gliflozin”) (e.g., Empagliflozin)
• NSAID

Dilate EA

• ACEi(-pril)
• ARB (-sartan) </aside>

Chronic

*due to CVD - Atherosclerosis

Presentation

• Hx of
  • Diarrhea
  • Diuretics (ACEi, ARB)
  • Oral intake
  • New medication
• Physical Exam

Lab Finding

• Serum
• Urine