Saudi Journal of Kidney Diseases and Transplantation

CASE REPORT
Year
: 2006  |  Volume : 17  |  Issue : 2  |  Page : 208--212

Acute Renal Infarction Secondary to Atrial Fibrillation - Mimicking Renal Stone Picture


Salih Bin Salih1, Huda Al Durihim1, Ahmed Al Jizeeri2, Ghassan Al Maziad3,  
1 Department of Medicine, King Fahad National Guard Hospital, King Abdulaziz Medical City, Riyadh, Saudi Arabia
2 King Abulaziz Cardiac Center, King Fahad National Guard Hospital, King Abdulaziz Medical City, Riyadh, Saudi Arabia
3 Department of Medical Imaging, King Fahad National Guard Hospital, King Abdulaziz Medical City, Riyadh, Saudi Arabia

Correspondence Address:
Salih Bin Salih
Department of Medicine, King Fahad National Guard Hospital, King Abdulaziz Medical City, P.O Box 22490, Riyadh 11426
Saudi Arabia

Abstract

Acute renal infarction presents in a similar clinical picture to that of a renal stone. We report a 55-year-old Saudi female, known to have atrial fibrillation secondary to mitral stenosis due to rheumatic heart disease. She presented with a two day history of right flank pain that was treated initially as a renal stone. Further investigations confirmed her as a case of renal infarction. Renal infarction is under-diagnosed because the similarity of its presentation to renal stone. Renal infarction should be considered in the differential diagnosis of loin pain, particularly in a patient with atrial fibrillation.



How to cite this article:
Salih SB, Al Durihim H, Al Jizeeri A, Al Maziad G. Acute Renal Infarction Secondary to Atrial Fibrillation - Mimicking Renal Stone Picture.Saudi J Kidney Dis Transpl 2006;17:208-212


How to cite this URL:
Salih SB, Al Durihim H, Al Jizeeri A, Al Maziad G. Acute Renal Infarction Secondary to Atrial Fibrillation - Mimicking Renal Stone Picture. Saudi J Kidney Dis Transpl [serial online] 2006 [cited 2021 Mar 5 ];17:208-212
Available from: https://www.sjkdt.org/text.asp?2006/17/2/208/35792


Full Text

 Introduction



Acute embolic renal infarction is an in­frequently encountered condition and is rarely recognized at presentation. It is often confused with other, more common diagnoses because of similarity of presenting symptoms. This leads to delay in initiating treatment and significantly decreases the chances of renal salvage.[1]

We present a patient with embolic renal infarction secondary to atrial fibrillation complicating rheumatic mitral stenosis who presented with typical symptoms of renal stone, and briefly review the literature.

 Case Report



We report a 55-year-old Saudi female, a known case of rheumatic heart disease (mitral stenosis with atrial fibrillation) on Digoxin and Warfarin therapy. She had closed valvo­tomy 10 years ago, and was non-compliant regarding her anticoagulation therapy. She presented to Emergency Department, King Fahad National Guard Hospital, Riyadh with complaint of right flank pain of two days duration. The pain was continuous and not relieved by any specific factor; she also exhibited no hematuria, frequency, fever, dysuria, rigors, nausea or vomiting and had no history of trauma or previous renal stones. Physical examination at admission revealed a conscious middle-aged woman, not in distress, not pale or jaundiced and afebrile. She had a pulse rate of 63/minute - an irregularly irregular, respiratory rate 18/min, and a blood pressure of 110/65 mmHg, without postural drop. Her chest was clear, and a cardiovascular examination showed S1 + S2 - irregular rhythm with left parasternal heave. Abdominal examination showed mild right loin tenderness. ECG showed atrial fibrillation rhythm with right ventricular hypertrophy pattern. Uri-nalysis showed +++ RBC, WBC 2-5/HPF, and ++ protein. BUN, creatinine, electrolytes and liver function tests were all normal. LDH was 705 IU/L, WBC 12.78x 10 9 /L (with normal differential), Hb 11.9 gm/dL, platelets 396 x10 9 /L, PT 14.6 sec, INR 1.1. She was treated with analgesics without much response and non enhanced CT scan of her abdomen was done, which showed a small attenuated area noted at the anterior part of the cortex of the right kidney, wedge-shaped (most probably representing an infarct) [Figure 1], and arterial contrast enhancement confirmed diagnosis by showing characteristics capsular enhance­ment of the right kidney [Figure 2]. Otherwise both kidneys showed good concentration and excretion of contrast media, and no evidence of hydronephrosis, stones peri- or para-renal collection. The patient was treated with analgesics and anti-coagulants (Heparin and Warfarin). Thrombolytic therapy was not considered because of late diagnosis. The patient was discharged home after getting a therapeutic INR and PT.

 Discussion



Acute renal infarction is rarely detected in clinical practice. This is reflected in the literature in which multiple scattered case reports are described but a prospective single or multi-center study of the condition is lacking. [2]

The earliest report of renal embolic disease appeared in 1856 by L. Traube from Germany and multiple case reports have been published since that time. In a series reported by Hoxie and Coggin, 205 cases of renal infarction were identified in 14,411 autopsies done at a major metropolitan hospital, an incidence of 1.4%; however the lesion was diagnosed clinically in only two cases [3] . Lessman et al. 3 reported 17 cases, Korzets et al.[2] reported 11 cases, and Hazanov et al. [5] reported 44 cases. Renal infarction secondary to thromboembolism is usually a sequela of cardiac disease, the heart is the source of systemic arterial emboli in up to 94% of cases; the three major causes are: atrial fibrillation, myocardial infarction and rheumatic mitral stenosis [6]. Renal infarction is often confused with other conditions due to similar presenting symptoms. This leads to delay in initiating treatment and significantly decreases the chances of renal salvage.[1]

Patients with acute renal infarction commonly present with persistent abdominal, flank or low back pain. The pain is usually acute in onset, sharp and severe in nature and without radiation. Detection is often delayed or missed because the condition is rare and its clinical presentation is non-specific. [7] Non-specific symptoms such as nausea, vomiting and fever are often present. Gross hematuria, oliguria and anuria are uncommon.[3]

Physical findings in renal infarction may lead directly or indirectly to the diagnosis. Costovertebral angle or flank tenderness, when present, points to a kidney lesion. Cardiac examination can expose the underlying con­dition responsible for the embolus, such as cardiomegaly, an irregular pulse or a murmur. Also, signs of prior or concurrent embolisation to other sites such as hemiplegia, coma and lower extremity cyanosis may provide clues to the existence of renal infarction.[6]

The most sensitive (but not specific) labora­tory test for renal infarction is lactate dehydrogenase (LDH) level. Elevation of more than 2,000 IU/ml can occur within 24 hours of renal infarction and can persist for up to 14 days. LDH 1 and 2 are the isoenzymes that are usually elevated. [8] Urinary LDH can be helpful in differentiating the causes of serum LDH elevation.[1] Other laboratory abnormalities include leukocytosis, elevated serum CK and haematuria; since these are all common and nonspecific, they are therefore not helpful.[9]

Radiologic findings in renal infarction depend on both the extent and age of the infarction. These findings parallel the known pathologic changes that occur after renal arterial occlusion. By one hour after occlusion of an arcuate or interlobular artery, a triangular hyperemic area is seen, with its apex pointing toward the medulla and its base paralleling the subcapsular region. Beginning seven days after arterial occlusion, the infarct begins to shrink. Definite cortical depression below the surface is pronounced by 28 days. As the infarct becomes smaller, the central dead area collapses, while organi­zation and regeneration occur at the peri­phery of the infarct. Calcification of dead tubules may develop by 3 days after infarction, persisting during the next week and is most pronounced in the tubules lying close to the surface of the kidney. [10] Contrast-enhanced CT is the non-invasive standard for imaging acute renal infarction. The classic finding is of a wedge-shaped zone of peripheral diminished density without enhancement. [4] The findings on CT have been summarized in a series of 37 cases described by Suzer et al. The most common finding was a hypoattenuated area with an associated mass effect, which was present in 32% of cases, followed by the cortical rim sign in 19%. [11] The cortical rim nephrogram sign represents opacification of a rim of functioning nephrons, supplied by capsular collaterals, surrounding an otherwise non-functioning kidney.[12]

The therapeutic guidelines of renal artery embolism are not established. Generally treat­ment options include: systemic anticoagulation, intra-arterial thrombolytic therapy and surgical embolectomy. [13] Treatment with anticoagulation should lead to reduced morbidity.[14] Revas­cularization via surgical embolectomy or percutaneous transcatheter thrombolytic therapy during the first 24 hours can result in the complete reversal of renal failure and should be attempted, even when no significant collateral circulation is demonstrated. This is particularly true in proximal rather than distal renal artery thrombosis.[15]

 Conclusion



We conclude that acute renal infarction secondary to atrial fibrillation is a rare clinical condition, and that its clinical picture is similar to that of renal stone; this resemblance may therefore delay its proper diagnosis and treatment. A high index of clinical suspicion is important to increase the chance of renal salvage.

 Acknowledgement



We gratefully acknowledge Dr. Osaima Khair and our Administrative Assistants, Sofie Claridad and Melinda Meyer, for their valuable secretarial assistance.

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