| Abstract|| |
Renal artery embolism (RAE) is an uncommon entity that is most often secondary to a cardiac source. Most reported cases have been in patients with underlying atrial fibrillation (AF), and occurrence of RAE, especially in patients with valvular heart disease, and sinus rhythm is very rare. We describe an unusual case of a young female who presented with sudden onset right flank pain, vomiting, anorexia, and hematuria, and was found to have thrombotic occlusion of the distal right renal artery. Although she denied any previous cardiac history, detailed cardiovascular examination revealed the presence of severe rheumatic mitral stenosis without any evidence of AF or left atrial clot. She was initially managed conservatively using low molecular weight heparin followed by oral anticoagulation with resolution of symptoms. A successful balloon mitral valvotomy was performed six weeks later. The patient is asymptomatic at her last follow-up of six months with preserved renal function. In symptomatic patients, clinicians need to consider the possibility of RAE even in patients of valvular heart disease with underlying sinus rhythm. Appropriate management of the underlying cardiac condition is imperative since embolism may be recurrent leading to compromise of renal function, if left untreated.
|How to cite this article:|
Kumar A, Kapoor A, Kumar S. An unusual case of hematuria in a young female: renal artery embolism, mitral stenosis, and sinus rhythm. Saudi J Kidney Dis Transpl 2016;27:398-401
|How to cite this URL:|
Kumar A, Kapoor A, Kumar S. An unusual case of hematuria in a young female: renal artery embolism, mitral stenosis, and sinus rhythm. Saudi J Kidney Dis Transpl [serial online] 2016 [cited 2021 Apr 20];27:398-401. Available from: https://www.sjkdt.org/text.asp?2016/27/2/398/178580
| Introduction|| |
Renal artery embolism (RAE) is usually associated with acute occlusion of blood flow to the renal parenchyma secondary to an embolus from a distant source. Common cardiac sources of embolism include valvular and ischemic heart disease, infective endocarditis, cardiac tumors, and intra-cardiac shunts. ,, Renal infarction and RAE may also be secondary to embolization of atheromatous debris from the aorta, sickle cell disease, spontaneous or traumatic arterial dissection, fibromuscular dysplasia, and connective tissue disorders. ,
Atrial fibrillation (AF) is a common predisposing factor, especially in cases of RAE secondary to valvular heart disease, ,, and RAE in these cases in the presence of sinus rhythm is very rare. We report the unusual case of a young female with severe rheumatic mitral stenosis (MS) without any associated known risk factors for RAE who presented with sudden onset flank pain, vomiting, and hematuria due to a thrombus in the distal portion of the right renal artery and a renal infarct involving the lower half of the right kidney.
| Case Report|| |
A 31-year-old female was admitted with sudden onset severe right flank pain, vomiting, anorexia, and hematuria. She reported a similar episode of flank pain and vomiting one month prior, which had subsided spontaneously. There was no history of fever, trauma, or dysuria. At presentation, she was afebrile in normal sinus rhythm (heart rate 75/min), blood pressure of 135/85 mm Hg, respiratory rate 15/min with tenderness, and guarding noted in the right flank. Cardiovascular system examination revealed an apical diastolic thrill, loud first heart sound, and a long mid-diastolic murmur at the cardiac apex, suggestive of severe MS.
Initial investigations revealed an elevated white blood cell count (18,200/mm 3 and sedimentation rate (60 at 1 h); normal serum creatinine (1.1 mg/dL) and blood urea nitrogen (12 mg/dL), while the lactate dehydrogenase level was elevated (1120 IU/L, normal range 115-221 U/L). On urine examination, macroscopic and microscopic hematuria was noted. Testing for anti-cardiolipin antibody and protein C/S levels were within normal limits.
The 12 lead electrocardiogram demonstrated sinus rhythm, right axis deviation, left atrial enlargement, and right ventricular hypertrophy. A trans-thoracic echocardiography was performed which revealed severe rheumatic MS, mild mitral regurgitation, and mild tricuspid regurgitation. No clot was visualized in the left atrial cavity or in the left atrial appendage, either on trans-thoracic or trans-esophageal echocardiography [Figure 1] and [Figure 2].
|Figure 1: Trans-thoracic echocardiography in the para-sternal short axis view demonstrating severe rheumatic mitral stenosis.|
Click here to view
|Figure 2: Trans-esophageal echocardiography demonstrating absence of any clot in left atrium or atrial appendage.|
Click here to view
An abdominal ultrasound examination showed heterogeneous right renal parenchymal echotexture and evidence of right renal infarction. A computerized tomographic scan hypodense nonenhancing right renal parenchyma and an intraluminal thrombus in the distal portion of the right renal artery with partial re-canalization [Figure 3] and [Figure 4]. A Tc99m-EC diuretic renogram revealed a photopenic nonfunctioning lower half of the right kidney whereas the remaining right renal parenchyma showed adequate perfusion and parenchymal tracer uptake. The left kidney was completely normal.
|Figure 3: Computerized tomographic scan demonstrating renal infarction (see arrow).|
Click here to view
|Figure 4: Computerized tomographic scan demonstrating thrombotic occlusion of distal right renal artery (see arrows).|
Click here to view
She was managed conservatively with low molecular weight heparin followed by oral anticoagulation with acenocoumarol. The patient's symptoms resolved within the next three to four days and in view of the underlying MS, a balloon mitral valvotomy (BMV) was planned. She underwent successful BMV six weeks later and is presently asymptomatic six months later.
| Discussion|| |
Acute RAE is associated with sudden reduction in arterial blood flow to a segment of the renal parenchyma and usually results from thrombo-embolism from the left atrium or left atrial appendage in patients with atrial fibrillation. The reported incidence is about 0.007% among hospitalized patients, while the postmortem incidence of RAE is 1.4%.  It is therefore apparent that RAE often remains unsuspected and requires a high index of suspicion to establish a clinical diagnosis. Most reported cases have been in patients with underlying AF, and occurrence of RAE, especially in patients with valvular heart disease with sinus rhythm is very unusual.
Our patient presented with a sudden onset of flank pain, which is one of the most common symptomatic manifestations of RAE. Although our patient had hematuria, this may often be absent in patients with RAE.  It is postulated that absence of hematuria may be associated with worse renal function, since it may reflect hypoperfusion of the infracted area with reduction of glomerular filtration. Our patient did not develop any significant impairment of renal function. This is also not unusual since gross renal dysfunction may only be noted when renal arteries are affected bilaterally, previous chronic renal insufficiency is present, or there is involvement of a solitary functioning kidney.
Although our patient was in sinus rhythm and no clot was evident in the left atrium on echocardiography, it is most likely that the source of RAE was cardiac. Intermittent paroxysmal episodes of AF or spontaneous formation of small micro-thrombi in the dilated left atrium with systemic embolization could have led to the episode of RAE in this patient.
Prompt recognition of RAE is important, since timely institution of therapeutic measures can minimize the long-term loss of renal function. The usual management strategy of patients with RAE includes anticoagulation with intravenous heparin and oral warfarin. ,, Although perfusion may also be established using local intra-arterial thrombolytic therapy  or surgical embolectomy,  it is not unusual to encounter spontaneous recovery in occasional cases. We elected to use low molecular weight heparin and not thrombolytic therapy, since the occlusion was only in the distal right renal artery, the renal infraction was limited to the lower portion of the right kidney and the patient had preserved renal function.
Renal outcomes associated with RAE are usually favorable and most of the patients return to their baseline renal function. It is important to realize that death in these patients is often related to recurrent embolic phenomenon or to the underlying cardiac condition. Hence, proper management of the associated cardiac co-morbidity is imperative. Since our patient had severe MS, she underwent a successful BMV six weeks following the episode of RAE.
Renal artery thrombo-embolism is a potentially life-threatening condition that can often go undetected, especially in patients without obvious risk factors such as AF. In symptomatic patients, clinicians need to consider the possibility of RAE even in patients of valvular heart disease with underlying sinus rhythm. It is important to treat the underlying cardiac abnormality since long-term morbidity is often related to recurrent embolic phenomenon secondary to the cardiac condition and is presently asymptomatic.
| References|| |
Korzets Z, Plotkin E, Bernheim J, Zissin R. The clinical spectrum of acute renal infarction. Isr Med Assoc J 2002;4:781-4.
Berliner L, Redmond P, DeBlasi J. Renal infarction in bacterial endocarditis diagnosed by computed tomography. Urol Radiol 1982;4: 231-3.
Carey HB, Boltax R, Dickey KW, Finkelstein FO. Bilateral renal infarction secondary to paradoxical embolism. Am J Kidney Dis 1999; 34:752-5.
Poux JM, Boudet R, Lacroix P, et al. Renal infarction and thrombosis of the infrarenal aorta in a 35-year-old man with primary antiphospholipid syndrome. Am J Kidney Dis 1996;27:721-5.
Shankarappa RK, Dwarakaprasad R, Papaiah S, Karur S, Math RS, Nanjappa MC. Bilateral renal artery stenting in a case of mitral stenosis with atrial fibrillation. J Indian Coll Cardiol 2012;2:129.e31.
Yavuzgil O, Gürgün C, Zoghi M, Tekin F. Bilateral renal arterial embolisation in a patient with mitral stenosis and atrial fibrillation: An uncommon reason of flank pain. Anadolu Kardiyol Derg 2003;3:73-5.
Zamirian M, Handjani AM, Ghahramani N. Mitral stenosis complicated by renal artery embolism. MJIR 1989;3:91-6.
Hazanov N, Somin M, Attali M, et al. Acute renal embolism. Forty-four cases of renal infarction in patients with atrial fibrillation. Medicine (Baltimore) 2004;83:292-9.
Moyer JD, Rao CN, Widrich WC, Olsson CA. Conservative management of renal artery embolus. J Urol 1973;109:138-43.
Fort J, Segarra A, Matas M, Segarra A, Camps J. Renal artery embolism: Prospective study of 41 patients based on a diagnostic and therapeutic algorithm. Open Urology & Nephrology Journal, 2008;1:9-15.
Blum U, Billmann P, Krause T, et al. Effect of local low-dose thrombolysis on clinical outcome in acute embolic renal artery occlusion. Radiology 1993;189:549-54.
Bouttier S, Valverde JP, Lacombe M, Nussaume O, Andreassian B. Renal artery emboli: The role of surgical treatment. Ann Vasc Surg 1988;2:161-8.
Department of Cardiology, Sanjay Gandhi Post Graduate Institute of Medical Sciences, Lucknow - 226 014, Uttar Pradesh
[Figure 1], [Figure 2], [Figure 3], [Figure 4]