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Saudi Journal of Kidney Diseases and Transplantation
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CASE REPORT  
Year : 2018  |  Volume : 29  |  Issue : 5  |  Page : 1223-1226
A rare cause of acute renal failure: Aortic occlusion


1 Department Nephrology, Faculty of Medicine, Cukurova Unıversity, Balcali, Saricam, Adana, Turkey
2 Department of Cardiology, Osmaniye State Hospital, Osmaniye, Turkey

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Date of Submission27-May-2017
Date of Decision04-Dec-2017
Date of Acceptance06-Dec-2017
Date of Web Publication26-Oct-2018
 

   Abstract 

Aortic occlusion usually occurs in the infrarenal abdominal aorta while occlusion of the suprarenal aorta is much less common. The clinical presentation may vary from limb ischemia, neurologic symptoms of the lower extremities, abdominal symptoms, renal failure, and resistant hypertension (HTN). We present a case of suprarenal aortic occlusion presenting with renal failure and resistant HTN but without lower limb ischemia.

How to cite this article:
Kaya B, Yildiz I, Yildiz PO. A rare cause of acute renal failure: Aortic occlusion. Saudi J Kidney Dis Transpl 2018;29:1223-6

How to cite this URL:
Kaya B, Yildiz I, Yildiz PO. A rare cause of acute renal failure: Aortic occlusion. Saudi J Kidney Dis Transpl [serial online] 2018 [cited 2018 Dec 16];29:1223-6. Available from: http://www.sjkdt.org/text.asp?2018/29/5/1223/243944

   Case Report Top


A 59-year-old male presented to the emergency department with five-day history of watery diarrhea two times per day, nausea, vomiting, and loss of appetite. He was referred to the nephrology department of our hospital for evaluation of impaired renal function and arterial hypertension (HTN). He had been treated for HTN by irbesartan + hydrochlorothiazide 300/12.5 mg once daily for five years. On examination, he had a blood pressure of 170/100 mm Hg and 160/100 mm Hg from his right and left arms, respectively, with no postural drop, a pulse rate of 88 beats/min, and a body temperature of 36.7°C. Pulses from his popliteal and dorsalis pedis arteries of the bilateral lower extremities were detected weakly. No further abnormalities were found during the physical examination. The laboratory tests resulted as following: White blood cell 9.9 × 103 u/L, hemoglobin 10.6 g/dL, hematocrit 30.6%, mean corpuscular volume 90 fl, ferritin 186 ng/mL, platelet count 342 × 103 u/L, creatinine 10.9 mg/dL, international normalized ratio 1.1, prothrombin time (PT) 15.4 s, activated partial thromboplastin time (aPTT) 28 s, glucose 99 mg/dL, serum sodium 139 mmol/L, serum potassium 6 mmol/L, serum Ca 8.4 mg/dL, serum phosphorus 6 mg/dL, serum creatine kinase (CK) 13.2 mg/dL, aspartate aminotransferase (AST) 6 u/L, serum albumin 3.4 g/dL and serum thyroid-stimulating hormone 2 MIU/mL [Table 1].
Table 1: Laboratory result of patients.

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Gastrointestinal workup failed to reveal any cause of gastrointestinal symptoms. No leukocytes, erythrocytes, cysts, or trophozoites were observed in microscopy of stool samples. Ongoing treatment of irbesartan + hydrochlorothiazide was interrupted and IV hydration was initiated. Diarrhea resolved spontaneously within a few days without any treatment. The combination treatment of respectively amlodipine 1 × 10 mg + doxazosin 2×8 mg + carvedilol 1 × 12.5 mg was administered for HTN aiming for a blood pressure target lower than 140/90 mm Hg. Abdominal ultrasonography (USG) revealed the normal size of the right kidney (11 cm × 6 cm × 3 cm) and atrophic left kidney. The left renal artery was not encountered by renal Doppler USG while the formation of plaque and scattering artefact were observed in the area of the right renal artery. Abdominal magnetic resonance (MR) angiography was performed to evaluate the aorta and renal arteries. Abdominal MR angiography revealed that the abdominal aorta was totally occluded beginning from the upper portion of renal arteries and blood supply to the lower portion of the aorta is mediated by the collateral arteries [Figure 1]. The patient became anuric. Arterial blood gas revealed a pH of 7.16, pCO2 of 20 mm Hg, and a bicarbonate level of 10 mmol/L. Hemodialysis was initiated in the patient with progressively impaired kidney function and uremic symptoms. Urine myoglobin was negative. The diagnosis of mesenteric ischemia in the patient was eliminated considering the absence of abdominal defense and rebound tenderness and bloody diarrhea. The diagnosis of renal infarction for the patient was eliminated according to normal laboratory values of lactate dehydrogenase (151 mg/dL), AST (6 u/L), CK (13.2 mg/dL). The possibility of acute tubular necrosis due to occlusion in the arterial system was considered arteries around the abdominal artery and atrophic left kidney was in favor of obstruction chronicity. Excessive fluid loss due to diarrhea may have played a role in the acute aortic occlusion superimposed to severe chronic aortic obstruction. Preexisting atherosclerosis combined with a low-flow state, due to severe volume depletion, has been reported to be a relatively frequent cause of acute aortic occlusion.[1] PT, APTT, factor 5 Leiden, anticardiolipin antibodies, protein C, protein S, and anti-thrombin three were found normal. Intensive workup failed to reveal any underlying cancer or systemic disease. Transthoracic echocardiography was also performed, but it was incon-sistent with embolic origin. The patient was referred to the cardiovascular surgery department. In this case presentation, resistant HT and acute renal failure (ARF) were detected in the patient who presented to the emergency department with nonspecific symptoms and acute suprarenal aortic occlusion was found as an underlying factor.
Figure 1: Abdominal magnetic resonance angiography: Left atrophic kidney, total abdominal aortic occlusion, collateral vascular structures around the aorta.

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   Discussion Top


Aortic occlusion usually occurs in the infrarenal abdominal aorta; often at or near the bifurcation, while occlusion of the suprarenal aorta is much less common.[2] The clinical presentation may vary from limb ischemia, neurologic symptoms of the lower extremities, abdominal symptoms and refractory hypertension.[1] This clinical picture is caused by embolic occlusion or, more often, by superimposed thrombosis of an atherosclerotic abdominal aorta. Preexisting atherosclerosis combined with a low-flow state, due to reduced cardiac performance or severe volume depletion, is a relatively frequent cause of acute aortic occlusion.[1] Some cases are due to hypercoagulable states.[3] ARF can be the sole symptom in acute aortic occlusion, when collateral vessels prevent lower extremity ischemia.[4] Our case presented to the emergency department due to the complaints of nonspecific symptoms such as nausea, vomiting, and appetite loss. When details of his medical history were obtained, it was found that the patient has had claudication; however, he did not consult any physician or hospital since he had no discomfort because of this claudication. In our case, an occlusion beginning from the upper portion of the renal arteries in the abdominal aorta was detected.

Extended collateral circulation and atrophic left kidney in our patient suggested a chronic, severe aortoiliac atherosclerotic obstructive disease. The atrophic left kidney was indicative of ischemic nephropathy for a long time. Excessive fluid loss due to diarrhea in the recent three to four days may have probably increased hyperviscosity, induced hypercoagulability and prothrombotic condition and consequently caused progression of the chronic stenosis of the abdominal aorta and acute aortic occlusion. Despite atherosclerotic obstruction severity, the development of extensive collateral vasculature can maintain adequate basal perfusion of the intestines and lower extremities and cause a delay in diagnosis and treatment.[5] The extended collateral vascular network may have protected the patient from ischemic manifestations and was probably responsible for the late recourse of the patient.

Extensive testing looking for immunohematological abnormalities was unremarkable. Considering acute arterial embolic occlusion, two-dimensional transthoracic echocardiography was performed which revealed normal left ventricle function. Electrocardiogram was normal and echocardiography did not find any argument for cardiac embolism. Intensive workup failed to reveal any underlying cancer or systemic disease. Risk factors for development aortic occlusion include black race, smoking cigarette, diabetes mellitus, dyslipidemia, HTN, advanced age, female gender, high level of CRP, hyperhomocysteinemia, hypercoagulopathy, and chronic renal failure.[6] Our case was not a cigarette smoker and had HTN, advanced age and probably chronic renal failure of those risk factors.

The treatment options for aortic occlusion are the treatment of the risk factors, endovascular intervention, and surgical revascularization. Surgery is the treatment of choice for patients with diffuse disease involving the aorta and both iliac arteries.[7] Surgical revascularization was decided on in an attempt to restore renal function and to restore arterial flow to the legs. Recovery of renal function could not be evaluated since the patient died of disseminated intravascular coagulopathy and sepsis postoperatively.


   Conclusion Top


Abdominal aortic occlusion is a peripheral arterial disease that occurs due to most commonly atherosclerosis. Aortic occlusion is usually represented by the symptoms due to ischemia in the lower extremities. In our case, these findings did not develop because of the rising collateral arteries. The diagnosis of suprarenal aortic occlusion is really an interesting condition in a patient who presented to the emergency department due to nonspecific symptoms and was detected to have ARF and resistant HT.

Conflict of interest: None declared.

 
   References Top

1.
Babu SC, Shah PM, Nitahara J. Acute aortic occlusion – Factors that influence outcome. J Vasc Surg 1995;21:567-72.  Back to cited text no. 1
    
2.
Hackam DG, Thain LM, Abassakoor A, McKenzie FN, Spence JD. Trapped renal arteries: Functional renal artery stenosis due to occlusion of the aorta in the arch and below the kidneys. Can J Cardiol 2001;17:587-92.  Back to cited text no. 2
    
3.
Perrino C, Scudiero L, Petretta MP, et al. Total occlusion of the abdominal aorta in a patient with renal failure and refractory hypertension: A case report. Monaldi Arch Chest Dis 2011; 76:43-6.  Back to cited text no. 3
    
4.
Jongkind V, Kievit JK, Wiersema AM. Recovery of renal function after prolonged anuria in acute suprarenal aortic occlusion. Ann Vasc Surg 2016;30:307.e11-4.  Back to cited text no. 4
    
5.
Sukharev II, Guch AA, Novosad EM, Vlaĭkov GG. Collateral compensation of blood flow and hemodynamics of the lower extremities in atherosclerotic occlusion of abdominal aorta. Klin Khir 2001;12:14-6.  Back to cited text no. 5
    
6.
Criqui MH, Vargas V, Denenberg JO, et al. Ethnicity and peripheral arterial disease: The San Diego Population Study. Circulation 2005; 112:2703-7.  Back to cited text no. 6
    
7.
Norgren L, Hiatt WR, Dormandy JA, et al. Inter-society consensus for the management of peripheral arterial disease (TASC II). Eur J Vasc Endovasc Surg 2007;33 Suppl 1:S1-75.  Back to cited text no. 7
    

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Correspondence Address:
Dr. Bulent Kaya
Department of Nephrology, Faculty of Medicine, Cukurova Unıversity, Balcali, Saricam, Adana
Turkey
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DOI: 10.4103/1319-2442.243944

PMID: 30381525

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