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AKI Types and Diagnostics

Aug 12, 2025

Overview

This lecture reviews the causes, classifications, and diagnostic lab values for acute kidney injury (AKI), focusing on pre-renal, intrinsic, and post-renal types.

Organs Involved in Acute Kidney Injury

  • Acute kidney injury (AKI) involves the heart, kidneys, and bladder.
  • The heart pumps blood to the kidneys, which produce urine excreted by the bladder.

Categories of Acute Kidney Injury

  • Pre-renal AKI: Caused by factors before the kidney, mainly involving reduced blood flow (e.g., heart failure).
  • Intrinsic AKI: Results from direct damage within the kidney itself.
  • Post-renal AKI: Due to obstruction after the kidney, typically in the bladder or urinary tract.

Pre-renal Causes

  • Often caused by decreased blood flow from the heart (e.g., massive myocardial infarction).
  • Hypovolemia results from diuresis, diarrhea, or dehydration (the "three Ds").
  • Any cause of reduced effective circulating volume leads to pre-renal azotemia.

Intrinsic Causes

  • Includes glomerulonephritis (inflammation of kidney filters).
  • Renal tubular acidosis (RTA) can be ischemic (from low blood flow) or toxic (from nephrotoxic drugs like cisplatin, vancomycin, or aminoglycosides).
  • Interstitial nephritis is an allergic-type reaction inside the kidney, seen with NSAIDs or penicillin, presenting with fever, rash, and eosinophilia.

Post-renal Causes

  • Caused by urinary obstruction (e.g., stones, tumors).
  • Benign prostatic hyperplasia (BPH) in older males causes outflow blockage leading to post-renal AKI.

Lab Diagnostics for AKI Types

  • BUN/Creatinine Ratio: >20:1 in pre-renal; <10:1 in intrinsic; post-renal starts as pre-renal, then shifts to intrinsic values if untreated.
  • Fractional Excretion of Sodium (FENa): 1% in pre-renal (kidney reabsorbs sodium); 3–4% in intrinsic (damaged kidney can't reabsorb sodium); not clinically significant in post-renal.

Key Terms & Definitions

  • Pre-renal AKI β€” Acute kidney injury due to decreased blood flow to the kidneys.
  • Intrinsic AKI β€” Kidney injury from direct damage within the kidneys.
  • Post-renal AKI β€” Kidney injury from obstruction after the kidneys.
  • Azotemia β€” Elevated blood urea nitrogen (BUN) and creatinine.
  • Glomerulonephritis β€” Inflammation of the kidney’s filtering units.
  • Renal Tubular Acidosis (RTA) β€” Disorder of kidney tubules affecting acid-base balance.
  • Interstitial Nephritis β€” Allergic inflammation of kidney tissue.
  • BUN/Creatinine Ratio β€” Lab value comparing blood urea nitrogen to creatinine to distinguish AKI types.
  • FENa β€” Fractional excretion of sodium, estimates kidney's ability to reabsorb sodium.

Action Items / Next Steps

  • Memorize BUN/Creatinine ratio and FENa values for differentiating AKI types.
  • Review causes and presentations of pre-renal, intrinsic, and post-renal AKI.
  • Prepare to answer questions based on clinical scenarios for each AKI type.