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| Year : 2012 | Volume
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| Issue : 2 | Page : 374-376 |
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| Bilateral renal infarction due to thromboembolism |
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Riyazuddin S Ansari, Fatima M Domfu, Mohammad Al-Barrak, Basim Felemban, Wael H Mutair
Intensive Care Unit, King Faisal Hospital, Makkah, Saudi Arabia
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| Date of Web Publication | 28-Feb-2012 |
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How to cite this article:
Ansari RS, Domfu FM, Al-Barrak M, Felemban B, Mutair WH. Bilateral renal infarction due to thromboembolism. Saudi J Kidney Dis Transpl 2012;23:374-6 |
How to cite this URL:
Ansari RS, Domfu FM, Al-Barrak M, Felemban B, Mutair WH. Bilateral renal infarction due to thromboembolism. Saudi J Kidney Dis Transpl [serial online] 2012 [cited 2013 May 22];23:374-6. Available from: http://www.sjkdt.org/text.asp?2012/23/2/374/93186 |
To the Editor,
Renal infarction usually occurs due to throm-boembolism from a clot in the left atrium in patient with atrial fibrillation, [1] or due to left ventricular thrombus arising after myocardial infarction, or due to atheromatous plaque from the aorta. [2] Other etiological factors include paradoxical embolism, Behcet's disease, renal vessel anomaly, and hypercoagulable state. The patient usually has a triad of abdominal pain, fever, and vomiting mimicking renal colic. [3] Due to nonspecific manifestation the diagnosis of renal, infarction is usually delayed. We report a 65-year-old male came to emergency department unconscious and with gasping breath. He was intubated and connected to a mechanical ventilator. In the ICU, his blood pressure was unrecordable. He had cold right upper and lower limbs with no palpable pulse. Laboratory investigations were as follows: platelets 114000/mm [3] , urea 121 mg/dL, crea-tinine 4.0 mg/dL, sodium 147 mEq/L, potassium 5.7 mEq/L, lactate dehydrogenase 1909 IU/L, aspartate aminotransferase 2480 IU/L, alanine aminotransferase 647 IU/L, and coagulation profile was within normal range. Respiratory and abdominal examination was unremarkable, with electrocardiogram showing anterolateral ischemia. The CNS examination showed: GCS of 3/15. Doppler showed absent signal on the right upper and lower limb vessels. An urgent CT scan of the brain was carried out, which showed multiple hypodense areas in the cerebellar [Figure 1] right temporal [Figure 2] and both parietal regions. CT aortic angiogram including abdomen was carried out, which revealed atheromatous disease of the thoracic and abdominal aorta, filling defect in right brachiocephalic artery, right common iliac artery and superior mesenteric artery. Both kidneys showed multiple wedge-shaped, hypodense lesions [Figure 3] distributed all over, denoting infarction. The patient was diagnosed as having bilateral renal infarction due to thromboembolism, but succumbed to death due to multiorgan failure. Unfortunately echocardiography could not be done.
Renal infarction usually presents with abdominal or flank pain, vomiting and fever. If patients have multiple thromboembolism they can present with unconsciousness due to cerebral infraction. Patients develop raised Lac-tate dehydrogenase, [4] which is due to necrosis, proteinuria and hematuria due to glomerular injury. [5] Furthermore, the hematuria need not be gross and can be microscopic. Contrast-enhanced CT is the best modality to diagnose renal infarction. [6] The classic radiological finding is a wedge-shaped perfusion defect without any pressure effect on adjacent paren-chyma. [7] Also, it will show the cortical rim sign which is present due to capsular collaterals. The management of renal infarction includes systemic anticoagulation, surgical embolec-tomy, [8] and sometimes thrombolytic therapy. But patients with thromboembolism at multiple tiple sites may need life-time anticoagulation. Because of nonspecific manifestations, a high degree of clinical suspicion remains the key for early diagnosis of renal infarction. In patients who present with h/o atrial fibrillation or the triad of persistent flank, and abdominal pain, and elevated serum LDH and/or hema-turia, contrast-enhanced CT should be performed as soon as possible to rule out or to prove acute renal infarction. Paradoxical embolism must be ruled out in a patient with renal infarction. | Figure 1: CT scan brain without contrast showing multiple hypodense areas in the cerebellar regions (orange arrow).
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 | Figure 2: CT scan brain without contrast showing right temporal (green arrow) and both parietal regions.
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 | Figure 3: CT abdomen with contrast showing multiple wedge-shaped, hypodense lesions in both kidneys (red arrow) distributed all over, denoting infarction.
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 References | |  |
| 1. | Hazanov N, Somin M, Attali M, et al. Acute renal embolism. Fourty four cases of renal infarction in patients with atrial fibrillation. Medicine (Baltimore) 2004;83(5):292. 
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| 2. | Tunick PA, Nayar AC, Goodkin GM, et al. Effect of treatment on the incidence of stroke and other emboli in 519 patients with severe thoracic aortic plaque. Am J Cardiol 2002;90 (12):1320.
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| 3. | Al-Harbi A, Shahat A, Zakaria M. Renal infarction - presentation and causes: a case report and literature review. Saudi J Kidney Dis Transpl 2001;12:179-82.
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| 4. | Bolderman R, Oyen R, Verrijcken A, Knockaert D, Vanderschueren S. Idiopathic renal infarction. Am J Med 2006;119:356-e9-12.
[PUBMED] [FULLTEXT] |
| 5. | Jacques Wallach. Interpretation of Diagnostic Tests: A Synopsis of Laboratory Tests. 6th ed. Boston: Little, Brown and Company, 1996:59-91.
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| 6. | Chu PL, Wei YF, Huang JW, et al. Clinical characteristics of patients with segmental renal infarction. Nephrology 2006;11:336-40.
[PUBMED] [FULLTEXT] |
| 7. | Amilineni V, Lackner DF, Morse WS, Srinivas N. Contrast- enhanced CT for acute flank pain caused by acute renal artery occlusion. AJR Am J Roentgenol 2000;174:105-6.
[PUBMED] [FULLTEXT] |
| 8. | Chuang CH, Lee CT, Cheng YF, et al. Bilateral renal infarctions and lower limbs artery thrombosis in a patient with nephrotic syndrome. J Nephrol 2004;17(20):311-5.
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Correspondence Address:
Riyazuddin S Ansari
Intensive Care Unit, King Faisal Hospital, Makkah
Saudi Arabia
PMID: 22382244
[Figure 1], [Figure 2], [Figure 3] |
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