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Difficulty: MediumNephrology

A nephrologist is evaluating laboratory data and urinalysis findings from several patients. Match each clinical laboratory presentation with its most likely underlying etiology.

  • Urine specific gravity 1.030, Fractional Excretion of Sodium (FENa) < 1%, and Urine osmolality > 500 mOsm/kg.Prerenal azotemia
  • Urine specific gravity 1.010, FENa > 2%, Urine osmolality < 350 mOsm/kg, and muddy brown granular casts on microscopy.Acute tubular necrosis
  • Non-anion gap metabolic acidosis, positive urine anion gap, urine pH 6.0, and a history of recurrent calcium phosphate kidney stones.Type 1 (distal) renal tubular acidosis
  • Non-anion gap metabolic acidosis, negative urine anion gap, and significant hyperkalemia in a patient with long-standing diabetes mellitus.Type 4 (hyperkalemic) renal tubular acidosis
  • Urinalysis demonstrating dysmorphic red blood cells, red blood cell casts, and mild to moderate proteinuria.Acute glomerulonephritis

Answer

The presentations map to Prerenal azotemia (concentrated urine, low FENa), Acute tubular necrosis (muddy brown casts, high FENa), Type 1 RTA (high urine pH, kidney stones), Type 4 RTA (hyperkalemia, diabetes), and Acute glomerulonephritis (RBC casts), respectively.
Each laboratory and clinical profile correctly corresponds to a specific nephrologic disorder based on pathophysiologic mechanisms of sodium handling, concentrating ability, acid-base balance, and glomerular integrity.

Step-by-Step Solution

1
Analyze the urinalysis and electrolyte parameters for the first two items to differentiate forms of acute kidney injury.
Low FENa and high osmolality indicate intact tubular function responding to hypoperfusion (prerenal). High FENa, low osmolality, and muddy brown casts indicate intrinsic tubular damage (acute tubular necrosis).
Differentiating prerenal from intrinsic renal failure relies on markers of tubular concentrating ability and sodium handling.
2
Evaluate the acid-base and electrolyte profiles for the next two items to distinguish forms of renal tubular acidosis (RTA).
A positive urine anion gap with high urine pH and stones points to Type 1 RTA. Hyperkalemia in a diabetic patient points to Type 4 RTA.
RTAs share non-anion gap metabolic acidosis but are differentiated by serum potassium, urine pH, and specific clinical associations.
3
Assess the urinary sediment in the final item.
RBC casts and dysmorphic RBCs indicate glomerular origin of hematuria.
RBC casts are pathognomonic for glomerulonephritis.

Key Concept

Interpretation of urinalysis, electrolyte panels, and acid-base status to diagnose renal etiologies.
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Topics

Nephrology

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