Prerenal AKI Flashcards
What is the pathophysiology of prerenal acute kidney injury (AKI)?
Prerenal AKI occurs due to decreased renal perfusion, leading to reduced glomerular filtration rate (GFR). The kidneys respond by activating the renin-angiotensin-aldosterone system (RAAS) to retain sodium and water, increasing vascular resistance to maintain perfusion.
What are the common causes of prerenal AKI?
1) True volume depletion (hemorrhage, dehydration, diarrhea, vomiting).
2) Decreased effective arterial blood volume (EABV) (heart failure, cirrhosis, nephrotic syndrome).
3) Impaired renal autoregulation (NSAIDs, ACE inhibitors, ARBs).
4) Sepsis-related hypotension (systemic vasodilation, poor renal perfusion).
5) Renal artery stenosis
What are the clinical findings in prerenal AKI?
1) Signs of hypovolemia: Tachycardia, hypotension, dry mucous membranes.
2) Signs of volume overload (in heart failure or cirrhosis-related AKI): Jugular venous distension (JVD), edema, ascites.
3) Oliguria (low urine output) due to sodium and water retention leading to high urine osmolarity (> 500 mOsm/kg) and low urinary sodium (< 20 mEq/L)
4) Hypertension
What laboratory findings are characteristic of prerenal AKI?
1) Elevated blood urea nitrogen (BUN)/creatinine ratio (>20:1) due to increased urea reabsorption.
2) Fractional excretion of sodium (FeNa) <1% due to sodium retention.
3) Fractional excretion of urea (FeUrea) <35% (useful in patients on diuretics).
4) Urine osmolality >500 mOsm/kg (concentrated urine due to intact tubular function).
5) Bland urinalysis (no casts, protein, or RBCs).
How does prerenal AKI differ from intrinsic renal failure (acute tubular necrosis, ATN)?
- Prerenal AKI: FeNa <1%, BUN/Cr ratio >20:1, concentrated urine, bland urinalysis.
- ATN: FeNa >2%, BUN/Cr ratio ~10-15:1, muddy brown casts, isosthenuria (fixed urine osmolality).
What is the best initial test for suspected prerenal AKI?
Serum BUN/Creatinine ratio, which is greater than 20, and urine sodium concentration (FeNa <1%) to assess kidney perfusion. Uremia can cause coagulopathies, anorexia, vomiting, pericarditis, and encephalopathy.
What is the prognosis of prerenal AKI?
Prerenal AKI is reversible if the underlying cause (volume depletion, cardiac failure, sepsis) is corrected early.
What happens if prerenal AKI is not corrected?
It can progress to acute tubular necrosis (ATN), leading to intrinsic renal damage.
What is the primary treatment for prerenal AKI?
1) Volume repletion with IV fluids (normal saline for dehydration, albumin for cirrhosis-related AKI).
2) Diuretics for fluid overload (only in volume-overloaded states, e.g., heart failure).
3) Treat underlying cause (stop nephrotoxic agents like NSAIDs, ACE inhibitors, optimize cardiac output in CHF).
When should diuretics be used in prerenal AKI?
Only in volume-overloaded patients (e.g., heart failure, cirrhosis) to reduce venous congestion.
Why should NSAIDs and ACE inhibitors be avoided in prerenal AKI?
- NSAIDs constrict the afferent arteriole, reducing glomerular perfusion.
- ACE inhibitors/ARBs dilate the efferent arteriole, reducing glomerular filtration pressure.
What is the most common cause of prerenal AKI in hospitalized patients?
Sepsis-induced hypotension (leading to systemic vasodilation and reduced renal perfusion).
What is the defining characteristic of prerenal AKI compared to intrinsic AKI?
Prerenal AKI is reversible with volume resuscitation, while intrinsic AKI (ATN) involves tubular injury and takes longer to recover.
