Understanding Postrenal Failure: A Common Cause of Acute Kidney Injury

 June 3

by Jonathan Downham

Postrenal failure, also known as postrenal acute kidney injury (AKI), is a condition that occurs when urine flow is obstructed after it leaves the kidneys. Unlike prerenal or intrarenal causes of AKI, which affect blood flow or the kidney tissue itself, postrenal failure is due to physical blockages in the urinary tract, preventing normal urine excretion.

What Is Postrenal Failure?

Acute kidney injury refers to a sudden decline in kidney function, usually occurring over hours to days. AKI was formerly known as acute renal failure, but the updated term encompasses a broader range of kidney dysfunction.

In postrenal failure, the problem lies beyond the kidneys — typically in the ureters, bladder, or urethra — where obstructions prevent urine from passing freely. This blockage causes pressure to build up within the renal system, ultimately reducing glomerular filtration rate (GFR) and impairing the kidneys' ability to remove waste products like urea and creatinine from the blood.

Causes of Postrenal Failure

Postrenal AKI may be triggered by both internal and external blockages, including:

  • Benign Prostatic Hyperplasia (BPH): A common cause in older men, where prostate enlargement compresses the urethra.

  • Kidney Stones: These may become lodged in the ureter or urethra, creating a physical blockage.

  • Tumors: Intra-abdominal or pelvic malignancies can compress the urinary tract externally.

  • Urethral Strictures or Neurogenic Bladder: These impair normal urine outflow.

While unilateral ureteral obstruction (affecting only one kidney) may not cause noticeable dysfunction if the other kidney is healthy, bilateral obstruction or urethral blockage can severely impair kidney function.

How Postrenal Failure Affects the Kidneys

Under normal conditions, blood is filtered through the kidneys at a consistent pressure gradient. However, urinary outflow obstruction leads to a pressure buildup, disrupting this filtration process.

Initially, the tubules respond by increasing reabsorption of sodium, water, and urea, which causes:

  • Elevated Urea :Creatinine Ratio (>15:1)

  • Urine sodium <20 mEq/L

  • Fractional Excretion of Sodium (FENa) <1%

  • High urine osmolality (>500 mOsm/kg)

As the obstruction persists and tubular cells are damaged, their ability to reabsorb diminishes. This results in:

  • Urea :Creatinine Ratio <15:1

  • Urine sodium >40 mEq/L

  • FENa >2% in severe cases

  • Urine osmolality <350 mOsm/kg

The consequence is azotemia—the accumulation of nitrogen-containing waste products—and oliguria, defined as low urine output.

Diagnosis and Management

Diagnosis typically involves:

  • Ultrasound or CT imaging to detect hydronephrosis or obstruction.

  • Urinalysis and serum studies to evaluate BUN, creatinine, and electrolytes.

Management of postrenal failure requires rapid identification and relief of the obstruction. This may involve:

  • Catheterization in cases of BPH or urethral stricture.

  • Surgical or urologic intervention for stones or tumors.

  • Supportive therapy to manage electrolyte imbalances and fluid overload.

Conclusion

Postrenal failure is a potentially reversible cause of acute kidney injury if recognized and treated early. Understanding the pathophysiology, causes, and diagnostic markers of postrenal AKI is crucial for timely intervention and the prevention of permanent kidney damage.

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