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); 3β4% 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 kidneyβs 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.