Acute renal infarction as a cause of low-back pain. (Case Report).

Abstract: Detection of acute renal infarction is often delayed or missed because of both the rarity of the disease and its nonspecific clinical presentation. Abrupt onset of low-back pain in a patient at high risk for a thromboembolic event may be the first indication of renal infarction. We report a case of acute renal infarction and review its diagnosis and management.

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Key Points

* Detection of acute renal infarction is often delayed or missed due to both the rarity of the disease and its unspecific clinical presentation.

* Most patients have a history associated with a high risk of thromboembolism.

* Atrial fibrillation, previous embolism, and valvular or ischemic heart disease are major risk factors for acute renal infarction.

* Most patients show elevated serum levels of lactate dehydrogenase and/or hematuria within 24 hours after pain onset.

Low-back pain is a prevalent problem and can account for up to 15% of all new outpatient visits. (1) Low-back pain is usually a benign condition related to posture or physical strain, and it generally resolves spontaneously or is easily treated. Therefore, low-back pain often is not regarded as a symptom of serious disease. We encountered a case of acute renal infarction in a patient who had sudden onset of low-back pain. Patients with acute renal infarction usually present with persistent low-back, abdominal, and flank pain that suggests other, more common diseases such as lumbago, abdominal disease, urolithiasis, or even myocardial infarction. (2) In addition, neither risk factors nor laboratory examinations that have a clinically acceptable specificity for acute renal infarction exist, Early diagnosis is mandatory to establish effective acute and long-term therapy for the preservation of renal function.

Discussion

Patients with acute renal infarction commonly present with persistent abdominal, flank, or low-back pain. Detection is often delayed or missed, because the condition is rare and its clinical presentation is nonspecific. Most patients have a history associated with a high risk of thromboembolism. Atrial fibrillation, previous embolism, and valvular or ischemic heart disease are the major risk factors for acute renal infarction, (3-5) These risk factors generally are recognized early, either at the history taking or on clinical examination. However, acute renal infarction also has been associated with rare conditions, including trauma, hereditary and acquired clotting disorders, cocaine use, vessel anomalies such as fibromuscular dysplasia or hereditary diseases such as Marfan syndrome or EhlersDanlos syndrome, medical interventions such as surgery for valve replacement, kidney transplantation, endovascular catheterization and application of intraluminal stents, and malignant disease. (5,6)

According to the literature, the clinical diagnosis of acute renal infarction is usually based on typical clinical findings that are nonspecific and increased risk for thromboembolism, (2,4,5) a profile that was present in our patient. If at this point a physician does not consider acute renal infarction, the addition of laboratory results such as hematuria and elevated LDH should suggest the possible diagnosis of acute renal infarction.

Urinalysis by dipstick is a simple screening test for many renal diseases. The sensitivity of this test to detect hematuria is high in contrast to a low specificity because of crossreaction in the presence of myoglobinuria. (7) Domanovits et al (5) reported that hematuria was present at admission in 74% of their patients, but in another 11% the test became positive within the next 24 hours. Consequently, serial urinalysis within the first 24 hours of pain onset should be performed to increase its diagnostic value.

Serum LDH as a characteristic marker for cell necrosis is known to be elevated in patients with acute renal infarction. (8) Because serum LDH is highly sensitive but not specific, other causes of LDH elevation, such as acute myocardial infarction, tumor, mesenteric embolism, and hemolysis, must be excluded as soon as possible.

Angiography, renal scintigraphy, intravenous pyelography, ultrasonography, and enhanced CT may be useful in diagnosing acute renal infarction ante mortem. Contrast-enhanced CT is the noninvasive standard of reference for imaging acute renal infarction and is potentially available 24 h/d. (5) A recent renal infarct maintains the normal anatomic border of the organ, is isodense or slightly hypodense, and shows no enhancement after contrast injection. Although ultrasonography still has its role in excluding obstructive uropathy, it lacks sensitivity to detect early renal infarction. Selective renal artery angiography is an invasive diagnostic method that is not without morbidity.

Therapeutic gnidelines for renal artery embolism have not been established. Prompt recognition of acute occlusion of the renal artery is important, because thrombolysis, anticoagulation, or embolectomy may minimize the loss in renal function. Because of the rarity of the disease, it is questionable that the superiority of a particular treatment can be evaluated in prospective randomized clinical trials. Moyer et al (9) compared the results of surgical and medical management for unilateral renal involvement and found conservative therapy to be favorable. Our patient had unilateral involvement and was treated conservatively. In addition, because these patients are also at high risk for repeated thromboembolism to other organs, this might be prevented by long-term anticoagulation. Although Domanovits et al (5) found signs of slightly impaired renal function in only 6 of their 17 patients after 7 days, we stress that early diagnosis of acute renal infarction is mandatory to establish effective acute and long-term therapy for the preservation of renal function.

Conclusion

Although nonspecific, the common symptom of low-back pain may be the first indication of a serious illness such as acute renal infarction. History, symptoms, and laboratory findings may suggest many other diseases. Thus, a high degree of clinical suspicion remains the key for early diagnosis of renal infarction. In patients who present with the triad of high risk for a thromboembolic event, persistent low-back, flank, and abdominal pain, and elevated serum LDH and/or hematuria, contrast-enhanced CT should be performed as soon as possible to rule out or to prove acute renal infarction.

Accepted December 17, 2001.

References

(1.) Silman AJ, Jayson MI, Papageorgiou AC, Croft PR. Hospital referrals for low back pain: More coherence needed. J R Soc Med 2000;93:135-137.

(2.) Gasparini M, Hofmann R, Stoller M. Renal artery embolism: Clinical features and therapeutic options. J Urol 1992;147:567-572.

(3.) Argiris A. Splenic and renal infarctions complicating atrial fibrillation. Mt Sinai J Med 1997;64:342-349.

(4.) Goldberg G. Renal infarction. Ann Emerg Med 1985;14:611-614.

(5.) Domanovits H, Paulis M, Nikfardjam M, Meron G, Kurkciyan I, Banker AA, et al. Acute renal infarction: Clinical characteristics of 17 patients. Medicine (Baltimore) 1999;78:386-394.

(6.) Kramer RK, Turner RC. Renal infarction associated with cocaine use and latent protein C deficiency. South Med J 1993;86:1436-1438.

(7.) Braun JS, Straube W. A new rapid test for diagnosing microhematuria, compared with results of microscopic examination [in German]. Dtsch Med Wochenschr 1975;100:87-89.

(8.) Winzelberg GG, Hull JD, Agar JW, Rose BD, Pletka PG. Elevation of serum lactate dehydrogenase levels in renal infarction. JAMA 1979;242:268-269.

(9.) Moyer JD, Rao CN, Widrich WC, Olsson CA. Conservative management of renal artery embolus. J Urol 1973;109:138-143.

RELATED ARTICLE: Case Report

A 52-year-old woman was admitted to the hospital because of dyspnea. The patient had been well until 4 days earlier, when she had begun to have palpitations and progressive exertional dyspnea. Two days before admission, she had paroxysmal nocturnal dyspnea, orthopnea, and finally dyspnea at rest. The patient had a childhood history of rheumatic fever, and valvular heart disease had been diagnosed 6 years before admission. She took no medications.

At admission, the patient's body temperature was 36.4[degrees]C, pulse rate was 140 beats/min, respiratory rate was 22 breaths/min, and blood pressure was 120/60 mm Hg. Physical examination revealed an elevation in jugular venous pressure. Crackles were heard at both lung bases, and a Grade 3 apical systolic murmur was heard. Results of blood chemistry studies were normal, including myocardial enzymes and thyroid function tests. A thoracic x-ray film revealed cardiac enlargement, Kerley B lines, and redistribution to the apices. An electrocardiogram showed atrial fibrillation with a ventricular rate of 140/min. Treatment with acenocoumarol, low molecular weight heparin, digoxin, furosemide, and enalapril produced prompt regression of symptoms and signs of heart failure. Two-dimensional echocardiography showed an enlarged left atrium (5.5 cm), normal left ventricular size with normal ejection fraction, an aortic valve with thickened leaflets and good aperture, and a fibrotic and calcified rheumatic mitral valv e with mitral stenosis (orifice size, 1.39 [cm.sup.2]; maximum instant transmitral valvular gradient, 33 mm Hg). Doppler ultrasonography also showed Grade III/IV to IV mitral regurgitation, Grade II/IV tricuspid regurgitation, and moderately elevated systolic pulmonary pressure (45 mm Hg).

On the second hospital day, the patient had sudden onset of steady low-back pain without radiation accompanied by nausea and vomiting. Respiratory movements and position changes did not alter the pain. She reported no alterations in bowel habit and no urinary symptoms. Physical examination revealed no mass, no liver or spleen enlargement, no peritoneal irritation, and only mild tenderness to deep palpation in the left flank. The test for Lasegue's sign was negative. No pulmonary abnormalities were present, and the patient's heart rate was 85 beats/mm. Blood chemistry values were blood urea nitrogen 33 mg/dl, creatinine 1 mg/dl, creatine kinase 66 U/L, alanine aminotransferase 41 U/L, and lactate dehydrogenase (LDH) 957 U/L. The results of urinalysis were normal except for 6 to 8 red blood cells per lowpower field.

Computed tomography (CT) of the abdomen showed two triangular-shaped peripheral areas of the left renal parenchyma that remained hypodense after the injection of contrast medium and showed no enhancement (Fig. 1). Intravenous unfractionated heparin was started, and acenocoumarol was administered concurrently to obtain an international normalized ratio of 2.5. Analgesic therapy stopped the pain in 36 hours, and the serum creatmine level remained at 1 mgldl. Five weeks later, the patient had mitral valve replacement; after 6 months, she was completely asymptomatic.

From the Short Stay Medical Unit and the Department of Radiology, Complexo Hospitalario Juan Canalejo, A Coruna, Spain.

Reprint requests to Fernando de la Iglesia, MD, PhD, UCEM-[3.sup.a] Planta, Complexo Hospitalario Juan Canalejo, Xubias de Arriba 84, E-15006 A Courna, Spain.

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