Tuesday, August 6, 2013
Why is the creatinine elevated?
This patient felt fine until two hours after lunch. He had spent the morning doing construction as usual. At lunch he ate the ham sandwich he had prepared that morning. At 3 p.m. he started vomiting. The vomiting, accompanied by abdominal cramping, continued for several bouts until nothing more could come up. And then the diarrhea started, multiple bouts with large volume watery output. After a few hours he knew that he needed medical help.
He was a star high school athlete 30 years before, and had kept in good shape. He worked out regularly, and had always avoided cigarettes and alcohol. He had never been hospitalized and took no medications.
When he arrived at the emergency department his BP was 86/52 with a pulse of 90. The ED physicians immediately started IV fluids with normal saline. He had one more bout of vomiting and one more diarrhea episode. His initial BMP comes back at 9 p.m.
142, 111, 21, 107
2.8, 20, 2.3, 7
So we ordered a urinalysis that showed (at 3 a.m.):
sp. gr 1.017
3 hyaline casts
At 4:30 a.m. his repeat BMP returns:
139, 106, 29, 106
4.5, 20, 2.9, 7.9
His creatine kinase levels where 390 at 9 p.m. and 345 at 4:30 a.m.
When I saw him at 9 a.m., he had normal BP lying and standing, with a pulse around 90 at all times. He had had a bladder scan that showed minimal urine, and his output was around 5 cc/hour.
So the question for you is what do you do now? You can order more tests. You can order treatment. You could get a consult. You can criticize the new intern and resident.
We had excluded obstruction, and in my mind the differential diagnosis was predominantly volume contraction versus acute tubular necrosis. This differential is often complex, because volume contraction is a major risk factor for ATN. Had the patient become hypotensive enough to damage his kidneys?
I did criticize the intern and resident for not checking an FeNa at admission. I admit a major bias in favor of this test, but only in oliguric patients. The original description in 1976 written by Dr. Carlos Espinel was published while he was my ward attending! He explained it to us, and I have used it ever since. A 1978 article, Urinary Diagnostic Indices in Acute Renal Failure: A Prospective Study, concludes:
"A prospective analysis of the value of urinary diagnostic indices in ascertaining the cause of acute renal failure was undertaken. Our results show that in the setting of acute oliguria a diagnosis of potentially reversible prerenal azotemia is likely with urine osmolality > 500 mosm/kg H2O, urine sodium concentration < 20 meq/litre, urine/plasma urea nitrogen ratio > 8, and urine/plasma creatinine ratio > 40. Conversely, a urine osmolality < 350 mosm/kg, urine sodium concentration > 40 meq/litre, urine/plasma urea nitrogen ratio < 3, and urine/plasma creatinine ratio < 20 suggest acute tubular necrosis. A significant number of oliguric patients will not have urinary indices that fall within these guidelines. In this setting, urine sodium concentration divided by the urine-to-plasma creatinine ratio (the renal failure index) and the fractional excretion of filtered sodium provide a reliable means of differentiating reversible prerenal azotemia from acute tubular necrosis."
So I asked for a stat urine Na and creatinine. We continued maintenance fluids. Some argued with me that the BUN/creatinine ratio was not high enough. But that ratio is quite unreliable as a diagnostic test. Fortunately, the patient was able to give a sample of very dark urine. 2 hours later the results confirmed a diagnosis: urine Na 31 and urine creatinine 335. We immediately started giving saline at 250 cc/hr. A repeat BMP after 2 liters showed:
138, 109, 27, 78
3.9, 19, 1.9, 7.3
Several lessons and caveats pertain:
1. FeNa pertains only to oliguric patients. Too often I see physicians order FeNa in non-oliguric patients and in those patients it is not validated.
2. A low FeNa (< 1%) occurs either in pre-renal azotemia or acute glomerulonephritis. Our patient had no red cells in his urine, and no reason to suspect acute GN. Pre-renal can occasionally include vascular catastrophes of the renal artery or abdominal aorta.
3. The extremely high urine/plasma creatinine ratio (a bit greater than 100) is very strong evidence of pre-renal azotemia. Note that the FeNa was 0.19% also.
4. We can make assumptions about diagnoses at admission, but should always obtain confirmatory tests. Getting the FeNa at admission would have supported more aggressive volume resuscitation.
5. This particular patient was a bit more confusing than most patients, and I hope the lessons are worthwhile.
db is the nickname for Robert M. Centor, MD, FACP. db stands both for Dr. Bob and da boss. He is an academic general internist at the University of Alabama School of Medicine, and is the Associate Dean for the Huntsville Regional Medical Campus of UASOM. He also serves as a frequent ward attending at the Birmingham VA Hospital. This post originally appeared at his blog, db's Medical Rants.
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