Renal · Acute Kidney Injury
The facts most likely to be tested
Prerenal AKI is caused by decreased renal perfusion leading to a drop in glomerular filtration rate while the renal parenchyma remains structurally intact.
The fractional excretion of sodium (FeNa) is less than 1% because the kidneys are avidly reabsorbing sodium to restore intravascular volume.
The BUN/Creatinine ratio is typically greater than 20:1 due to increased urea reabsorption in the proximal tubule.
Urine osmolality is elevated, typically >500 mOsm/kg, reflecting the kidney's preserved ability to concentrate urine in response to ADH.
Hyaline casts are the classic finding on urinalysis in prerenal AKI, representing concentrated protein without cellular debris.
Hypovolemia from hemorrhage, dehydration, or third-spacing is the most common clinical etiology of prerenal azotemia.
The definitive treatment for prerenal AKI is isotonic fluid resuscitation to restore effective arterial blood volume and renal perfusion.
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A 68-year-old male is brought to the emergency department with lethargy and decreased urine output for two days. He has a history of congestive heart failure and has been taking high-dose furosemide. Physical exam reveals dry mucous membranes, poor skin turgor, and tachycardia. Laboratory studies show a BUN of 60 mg/dL and a serum creatinine of 1.5 mg/dL (baseline 0.9 mg/dL). Urinalysis shows hyaline casts and no protein or blood.
What is the most likely diagnosis?
Prerenal Acute Kidney Injury
The patient's elevated BUN/Creatinine ratio (>20:1) and the presence of hyaline casts in the setting of volume depletion are classic for prerenal AKI, as described in bets 3 and 5.
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Etiology / Epidemiology
Caused by decreased renal perfusion due to hypovolemia, heart failure, or sepsis. Most common cause of AKI in hospitalized patients.
Clinical Manifestations
Presents with azotemia, oliguria, and signs of volume depletion like turgor loss. Orthostatic hypotension is a classic finding.
Diagnosis
Diagnosed by BUN:Cr ratio > 20:1 and FENa < 1%. Urine sediment is typically bland (hyaline casts).
Treatment
Restore isotonic saline volume. Avoid NSAIDs and nephrotoxins to prevent progression to ATN.
Prognosis
Rapidly reversible if perfusion is restored. If untreated, leads to Acute Tubular Necrosis (ATN).
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Epidemiology & Etiology
Prerenal AKI accounts for 60-70% of community-acquired AKI. Primary drivers include hypovolemia (hemorrhage, GI losses), decreased cardiac output, and systemic vasodilation (sepsis). Patients on ACE inhibitors or NSAIDs are at significantly higher risk due to impaired autoregulation.
Pertinent Anatomy
The kidneys receive 20-25% of cardiac output. The afferent arteriole relies on prostaglandins for vasodilation, while the efferent arteriole relies on Angiotensin II for vasoconstriction to maintain glomerular filtration rate (GFR).
Pathophysiology
Reduced renal blood flow triggers the renin-angiotensin-aldosterone system to preserve volume. The kidney maximally reabsorbs sodium and water to maintain perfusion, resulting in concentrated urine. Prolonged ischemia leads to tubular cell death, transitioning the state into Acute Tubular Necrosis.
Clinical Manifestations
Patients present with oliguria (<400 mL/day) and signs of dehydration such as dry mucous membranes and tachycardia. Altered mental status may occur in severe cases. Physical exam often reveals poor skin turgor and orthostatic hypotension.
Diagnosis
The BUN:Cr ratio > 20:1 is the hallmark laboratory finding. Fractional excretion of sodium (FENa) < 1% confirms intact tubular function. Urinalysis is typically bland, showing only hyaline casts, which helps distinguish it from the muddy brown casts of ATN.
Treatment
The primary goal is isotonic saline resuscitation to restore effective arterial blood volume. Discontinue NSAIDs, ACE inhibitors, and diuretics immediately. If the patient is in cardiogenic shock, inotropic support is required rather than aggressive fluid loading.
Prognosis
Prognosis is excellent if the underlying cause is corrected promptly. Failure to restore perfusion within hours leads to ischemic ATN, which carries a higher mortality rate and requires longer recovery times.
Differential Diagnosis
Acute Tubular Necrosis: FENa > 2% and muddy brown casts
Acute Interstitial Nephritis: WBC casts and eosinophiluria
Glomerulonephritis: RBC casts and dysmorphic RBCs
Postrenal Obstruction: Hydronephrosis on ultrasound
Hepatorenal Syndrome: FENa < 1% in the setting of cirrhosis