KIDNEY INJURY, ACUTE 50A
A 36-year-old woman with diabetes mellitus sustained a fall onto her arm at a construction site. In the emergency department, she had radiography showing a complex radial fracture and then a preoperative computed tomography (CT) scan with contrast. She subsequently underwent pinning and reconstructive surgery of her arm with perioperative broad-spectrum antibiotics. Her blood pressure remained normal throughout her surgery. On the second hospital day, there was a doubling of her serum creatinine, from 0.8 to 1.9 mg/dL. Her urine output dropped to 20 mL/hr. Serum creatine kinase returned at 600 units/L.
What are the salient features of this patient’s problem? How do you think through her problem?
Salient features: Increase in serum creatinine concentration; oliguria; traumatic injury and moderately elevated creatine kinase; administration of iodinated contrast and antibiotics
How to think through: Serum creatinine is an indirect measure of glomerular filtration rate (GFR). What are the limitations to its use as a measure of GFR? (It accurately reflects GFR only when renal function is at a steady state. This patient’s creatinine rose from 0.8 to 1.9 mg/dL in 24 hours, indicating complete cessation of renal function—a GFR of 0!) How would you rank possible causes of acute kidney injury (AKI) in this case? (Contrast nephropathy > rhabdomyolysis > acute tubular necrosis [ATN].) Iodinated contrast can cause rapid onset of AKI, especially in those with diabetes and chronic kidney disease. Rhabdomyolysis generally causes an elevated serum creatine kinase (into the thousands), more often in substance abuse or prolonged stasis. Could the antibiotics have caused ATN? (Possibly, but its onset is typically slower.) Could they have caused acute interstitial nephritis? (Again, the onset is too fast, and there was no evidence of fever, rash, or white blood cell casts.) What are key elements of the workup for AKI? (Urinalysis microscopic examination for red blood cells, white blood cells, and casts; urine protein, creatinine, and sodium; renal ultrasonography.) How is AKI managed? (Daily weights; input and output; volume status; strict monitoring of electrolytes; adjustment of medication doses; avoidance of nonsteroidal antiinflammatory drugs (NSAIDs), angiotensin-converting enzyme (ACE) inhibitors, angiotensin II receptor blockers, and diuretics; low-potassium diet.)
KIDNEY INJURY, ACUTE 50B
What are the essentials of diagnosis and general considerations regarding acute kidney injury?
Essentials of Diagnosis
Defined as a sudden decrease in kidney function, resulting in an inability to maintain acid–base, fluid, and electrolyte balance and to excrete nitrogenous wastes
Sudden increase in blood urea nitrogen (BUN) or serum creatinine
Oliguria often associated
Symptoms and signs depend on cause
General Considerations
5% of hospital admissions and 30% of intensive care unit admissions have AKI.
25% of hospitalized patients develop AKI.
Serum creatinine concentration can typically increase 1.0 to 1.5 mg/dL daily.
There are three categories of AKI: prerenal, intrinsic renal, and postrenal causes.