From the Guidelines
Pre-renal acute kidney injury (AKI) is characterized by elevated BUN-to-creatinine ratio (>20:1), low urine sodium (<20 mEq/L), high urine osmolality (>500 mOsm/kg), and fractional excretion of sodium (FENa) <1%, whereas acute interstitial nephritis (AIN) presents with fever, rash, and eosinophilia, pyuria, hematuria, white blood cell casts, and eosinophiluria, with FENa typically >1%. The diagnosis of pre-renal AKI and AIN can be made based on clinical and laboratory findings, including urine microscopy, serum creatinine, and blood urea nitrogen levels 1.
Clinical Findings
- Pre-renal AKI:
- Elevated BUN-to-creatinine ratio (>20:1)
- Low urine sodium (<20 mEq/L)
- High urine osmolality (>500 mOsm/kg)
- FENa <1%
- Urine microscopy shows few cells and hyaline casts
- Acute interstitial nephritis (AIN):
- Fever, rash, and eosinophilia (though this triad occurs in only about 10% of cases)
- Pyuria, hematuria, white blood cell casts, and eosinophiluria
- FENa typically >1%
- Proteinuria is mild to moderate
Laboratory Findings
The laboratory findings for pre-renal AKI and AIN can be distinguished by the presence of certain markers, such as the BUN-to-creatinine ratio, urine sodium, and FENa 1.
Treatment
Treatment of pre-renal AKI focuses on restoring renal perfusion through volume repletion or improving cardiac output, while AIN management requires removing the offending agent and sometimes using corticosteroids. The use of corticosteroids, such as prednisone 0.5-1 mg/kg/day for 1-2 weeks, then tapered over 4-6 weeks, may be necessary in severe or persistent cases of AIN 1.
Causes
Pre-renal AKI is often caused by conditions that lead to decreased renal perfusion, such as volume depletion, heart failure, or liver disease, while AIN is commonly caused by medications (especially antibiotics like beta-lactams, sulfonamides, and NSAIDs), infections, or autoimmune disorders 1.
Evaluation
The evaluation of patients with AKI or AIN should include a thorough history, physical examination, laboratory analysis of blood and urine, and imaging studies, such as ultrasound or CT scans, to determine the underlying cause and guide treatment 1.
From the Research
Classic Findings in Pre-Renal AKI
- Pre-renal acute kidney injury (AKI) is attributed to decreased renal perfusion associated with low intravascular volume or decreased arterial pressure, which can determine a reduced glomerular filtration rate (GFR) 2.
- Approximately 70% of community-acquired cases of AKI are attributed to pre-renal causes, and in most of these cases, the underlying kidney function may be normal 2.
- Autoregulatory mechanisms can partially compensate renal perfusion reduction in order to maintain GFR, but in patients with pre-existing chronic kidney disease, these mechanisms are impaired, and the susceptibility to develop acute-on-chronic renal failure is higher 2.
Classic Findings in Acute Interstitial Nephritis
- There is limited information available on classic findings in acute interstitial nephritis from the provided studies.
- However, it is known that acute interstitial nephritis is a form of intrinsic AKI, and its diagnosis can be supported by the use of urinary injury biomarkers reflective of tubular damage, including NGAL and KIM-1 3.
Diagnostic Criteria
- The blood urea nitrogen (BUN)/creatinine ratio (BCR) is sometimes used to distinguish pre-renal azotemia (PRA) and acute tubular necrosis (ATN), but its usefulness is debated 4, 5.
- A BCR >20 is traditionally used to diagnose PRA, but studies have shown that this threshold may not be reliable 4, 5.
- A composite biochemical criterion based on the congruency of at least two of the three biochemical ratios, including the fractional excretion of sodium, the urinary-to-plasma creatinine ratio, and the renal failure index, may be more useful in distinguishing pre-renal and intrinsic AKI 3.