About a year before applying for life insurance, a 43-year-old male nonsmoker presented to his doctor with flank pain, nausea and vomiting for 10 days. At the time of the illness, an abdominal Computed Tomography (CT) scan revealed a renal infarct in the upper pole of the right kidney. The applicant had an insurance blood profile with total cholesterol of 180 mg/dl and an HDL cholesterol of 45 mg/dl. His serum creatinine was 1.1 mg/dl and the BUN was 25 mg/dl. The remainder of the insurance bloodwork and urinalysis was normal. At the time of application he was on a statin, Plavix & aspirin. He reportedly had a cardiac work-up at the time of the episode, but there were no details in the record.
What causes a renal infarct and what are the implications for future mortality?
Renal infarction (RI) is caused by the obstruction of blood flow in the renal artery or one of its smaller branches, resulting in ischemia to a segment of kidney tissue. It is a rare disorder, with one autopsy study from the 1940s showing a prevalence of 1.4%. Another study looked at all emergency-room cases over a four-year period and found an RI diagnosis in only .007% of these cases.
The clinical diagnosis of renal infarction is likely often missed due to the nonspecific nature of the symptoms. Flank pain, abdominal pain, nausea and vomiting are the most common presenting symptoms, and these can be mistaken easily for kidney stones or infections. One laboratory test that may aid in differentiating between RI and these other disorders is the serum lactate dehydrogenase. Serum levels routinely are reported as being two to four times the upper limit of normal in the setting of renal infarction and normal in the setting of stones or infection.
Trauma may result in renal infarction at any age, but the etiology of non-traumatic RI varies somewhat by age group. The elderly are more likely to have atherosclerosis of the aorta or renal arteries which may spawn emboli that occlude an arterial branch. Atrial fibrillation is often mentioned as a cause of renal infarction, and a study of almost 30,000 patients with atrial fibrillation noted an RI incidence of 2% over a 13-year follow-up period.
1 - Detailed Etiology of Renal Infarction from a Series of 94 patients
diagnosed between 1989 and 2011|
|Groups||SubGroups||Number affected||Percent (of 94)|
|Atheroma aorta - emboli||4||4.3|
|Renal artery dissection||17||18.1|
|Aortic dissection involving the
|Ehlers-Danlos with thrombotic
|Amyloidosis and nephrotic syndrome||1||1.1|
The study examined 94 diagnosed patients from 1989-2011 and grouped the patients into four categories based on etology.–. (Clin J Am Soc Nephrol 2013;8:392–398)
One more recent study of 94 RI cases (61 men and 33 women) was designed to place subjects into one of four categories based on underlying cause:
- Infarction in the youngest group (average age 44) was due to “renal injury.” This group was 86% male and comprised 31% of the total cases.
- The next youngest group (average age 46, 16% of total) presented RI due to an underlying hypercoagulable disorder. One-third of this group suffered from bilateral renal infarction.
- The third group (average age of 65, 24% of total) exhibited cardiac causes like atrial fibrillation, endocarditis, etc.
- The final group (average age 56, 29% of total) was the second largest group. This group was deemed idiopathic and had no discernable cause for renal infarction. A prior history of arrhythmic heart disease was reported in 11% of this idiopathic group and a history of previous embolic event in 7.4%.
In this study the overall frequency of hypertension at the time of RI diagnosis was 39%. Separately mentioned in medical literature are several case reports of individuals suffering a renal infarction soon after smoking or injecting cocaine.
Diagnosis and Treatment
When there is a suspicion of renal infarction, the most commonly used test for diagnosis is CT scan with contrast enhancement. Ultrasound of the kidney is not very sensitive and may appear normal in acute RI. Angiography is usually reserved for extensive infarction or in the setting of planned endovascular procedures.
There are no standardized treatment guidelines for renal infarction, likely due to the rarity and the varied underlying causes. Clinicians often initialize heparin followed by warfarin. If an embolus or clot is identified quickly, thrombolysis or endovascular intervention may be pursued. Anti-hypertensive treatment may be indicated, and dialysis may be needed if renal damage is severe. Anticoagulants are often continued indefinitely in the setting of atrial fibrillation.
The prognosis after renal infarction depends on the underlying cause/coexisting conditions, the extent of infarction and the resulting renal function. The extent of kidney damage and ultimate outcome may be related to the time it takes to make the diagnosis, as earlier treatment may save more renal tissue. Additional clots from an embolic source may also put other organs at risk. A study of 44 patients with atrial fibrillation and renal infarction (average age 69) found a mortality rate of 11.4% in the first month after diagnosis. At a follow-up of three years: 61% had normal renal function; 13% had mild impairment; 18% had more severe impairment (serum creatinine > 2 mg/dl), and 8% were on dialysis. Additional embolic events occurred in 13% of these patients.
Returning to the Case
The etiology of the renal infarct is not apparent from the information provided. It would be important to obtain the cardiac work-up in hopes that an echocardiogram, an electrocardiogram and ambulatory, 24-hour heart monitoring were done. One would also like to see a work-up to exclude a hypercoagulable disorder.
The rating for any of the underlying conditions that might have been discovered (atrial fibrillation, other arrhythmias, hypercoagulable state, etc.) would be a good starting point with additional moderate rating for the infarction. If no underlying etiology was discovered, it would be prudent in this age group to start with a rating for paroxysmal atrial fibrillation as a likely occult etiology.
Korzets Z et al. “The Clinical Spectrum of Acute Renal Infarction.” IMAJ 2002;4:781-784.
Bourgault M, et al. “Acute Renal Infarction: A Case Series.” Clin J Am Soc Nephrol 2013;8:392–398.
Bemanian S, et al. “Cocaine-induced renal infarction: report of a case and review of the Literature.” BMC Nephrology 2005;6:10.
Bolderman R, et al. “Idiopathic Renal Infarction.” Am J Med 2006;119(4):356.e9-12.
UpToDate online, last accessed 2/10/15.