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Saudi Journal of Kidney Diseases and Transplantation
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CASE REPORT Table of Contents   
Year : 2001  |  Volume : 12  |  Issue : 2  |  Page : 179-182
Renal Infarction - Presentation and Causes: A Case Report and Literature Review

1 Department of Nephrology, North West Armed Forces Hospital, Tabuk, Saudi Arabia
2 Department of Radiology & Imaging, North West Armed Forces Hospital, Tabuk, Saudi Arabia
3 Department of Urology, North West Armed Forces Hospital, Tabuk, Saudi Arabia

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Renal infarction usually occurs in patients with severe atherosclerosis or heart disease. We report a 68-year-old lady who presented with total occlusion of the left renal artery of acute onset. Detailed work up did not reveal any specific cause and the infarction was considered to be idiopathic. The patient presented two-and-half years later with atrial fibrillation, which was managed with anti-arrhythmic drugs. Retrospectively, we believe that the cause of renal infarction was embolization secondary to paroxysmal atrial fibrillation. She is doing well on anti-coagulants and anti-arrhythmic drugs and was maintaining sinus rhythm when last seen.

Keywords: Flank pain, Renal infarction, Arrhythmia, Embolism.

How to cite this article:
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

How to cite this URL:
Al-Harbi A, Shahat A, Zakaria M. Renal Infarction - Presentation and Causes: A Case Report and Literature Review. Saudi J Kidney Dis Transpl [serial online] 2001 [cited 2022 Jan 20];12:179-82. Available from: https://www.sjkdt.org/text.asp?2001/12/2/179/33809

   Introduction Top

Renal infarction usually occurs in patients with severe atherosclerosis or heart disease or rarely, in association with autoimmune diseases. [1],[2] Hypercoagulable status can contribute to vascular occlusions. The presentation of renal infarction is usually confused with nephrolithiasis and the diagnosis is often delayed or missed. [1] We herewith report a case of renal infarction wherein the diagnosis was made on the basis of clinical and radiological findings.

   Case History Top

A 68-year-old woman presented to the emergency room in October, 1997 with severe abdominal pain radiating to the back, mainly at the left flank area. She had two episodes of vomiting. There was no history of dysuria, fever or renal stones. She was not a known diabetic or hypertensive, and she was not on any medications.

In the past, she had been seen in the primary medical care department in the year 1995, for fever and was found to have microscopic hematuria with a few pus cells. She was investigated then for pyelonephritis and treated with antibiotics. Intravenous urography (IVU), ultrasound examination of the kidneys and cystoscopy, were all normal. Urine for  Mycobacterium tuberculosis Scientific Name Search i>was negative. Urine cytology failed to show any malignant cells and she refused renal biopsy. Despite being treated with anti­biotics, the patient continued to have pain which was dull aching in nature.

The present clinical examination revealed an elderly lady, not in severe distress with tender left flank area. She also had left upper motor neurone facial palsy of five days duration, from which she was recovering. She had regular sinus rhythm and normal cardiac examination. Urine analysis showed 4+ protein. Ultrasound showed normal sized kidneys, and IVU revealed a non-functioning left kidney. A retrograde pyelogram showed no evidence of obstruction. The serum creatinine at admission was 160 µmol/L, while her baseline creatinine was 80 µmol/L. The blood urea was 9 mmol/L and electrolytes were normal. Hemogram was normal except for evidence of iron deficiency anemia, and the erythrocyte sedimentation rate was 42. The sickle cell test was negative, the transaminases were raised, and the lactate dehydrogenase was 1320 IU. Doppler ultrasound revealed no flow in the left renal artery and the DTPA scan confirmed absence of perfusion of left kidney. Renal angiogram revealed total occlusion of left renal artery and there were two thrombi in the aorta below the origin of renal arteries [Figure - 1]. Other lab tests done including serum c-reactive protein, VDRL, hepatitis B and C were all negative. Serum protein electrophoresis was normal. Echocardiogram was normal and Holter monitor failed to show any arrhythmia. Protein C and protein S deficiencies were excluded. We screened her for auto-antibodies such as ANA and anti-DNA, which were negative. Her anti­thrombin III activity was normal. PT and PTT were normal and anti-cardiolipin IgM, IgG and IgA were negative. Hemocystin level was within normal limits. MRI of the brain was normal. She was managed by heparin infusion and later warfarin and aspirin. She recovered completely from facial pulsy and the renal function normalized. The patient was discharged home and two months later, abdominal MRI showed that the left kidney had shrunk and the right kidney appeared hypertrophied [Figure - 2].

She was kept on warfarin, which she took for 18 months and stopped by herself. She continued on aspirin alone. Follow-up was uneventful for two-and-half years, when she was brought by her family to the emergency room with atrial fibrillation, severe hypo­tension and drowsiness. She was managed and resuscitated, but she developed acute renal failure as a sequel to severe, prolonged hypotension. She was supported by dialysis until her single kidney recovered completely. On the second presentation, she was put on anti-arrhythmic drugs. At discharge, her renal function was back to normal and she was kept on amidoron and warfarin. Retrospectively, we think the cause of left renal infarction was embolus because of paroxysmal atrial fibrillation.

   Discussion Top

The renal circulation is considered the final resting place for up to 2.3% of systemic arterial embolizations, and due to the great variability of its presentation, it is often difficult to make the diagnosis of acute renal infarction quickly. [1] In autopsy studies, an incidence of renal infarction of up to 1.4% has been reported. [2] Usually, renal infarction is a sequel to cardiac thrombo­embolism either due to arrhythmias or valvular heart disease. Renal infarction has also been reported as idiopathic [1],[2],[3] and in association with marijuana smoking. [4] Other causes include atheromatous embolization and rarely, some autoimmune related diseases. [5],[6] Complete renal infarction could happen in cases of complete arterial occlusion as in our case. Segmental infarction is seen in cases of dissection of the renal artery, especially in hypertensive patients. [2],[5]

Most patients with renal infarction present with nonspecific symptoms which usually include flank pain, vomiting, nausea and fever. [1] These complaints generally mimic the picture of nephrolithiasis. It is usual to have raised transaminases, lactic dehydro­genase and leukocyte count. It is not usual to have frank hematuria, although micro­scopic hematuria is frequent. [2],[7],[8] Diagnosis of renal infarction requires a high index of suspicion and the diagnosis should be pursued by radiological studies. The gold standard diagnostic test is angiography, and the diagnosis should be suspected when there is a normal sized, non-functioning kidney with a normal retrograde pyelogram.

Treatment depends on the cause of the infarction. In more that 90% of the cases, the embolus comes from the heart, [2] where specific treatment will abort further embolizations. Other causes like lupus erythematosus or anti-phospholipid disease need steroids and anticoagulant therapy. [5],[6] In idiopathic cases, surgical embolectomy in experienced hands may be a good option. [2] Intra-arterial thrombolytic therapy has been tried successfully in one case. [2]

Our patient failed to demonstrate a cause at initial presentation except the thrombi seen in the aorta, but it did not seem to be of atheromatous origin because the abdominal aorta lumen was smooth. The thrombi seen in the aorta were probably part of the phenomenon that led to renal infarction and possibly the source was the heart. The presence of facial palsy was thought to be coincidental since it resolved completely in a short period of time.

Because we failed to demonstrate a definitive cause at first presentation, we treated her with anticoagulant and aspirin only, and our plan was to continue anti­coagulant indefinitely because a major organ was affected. However, the patient refused to continue taking the anticoagulant after 18 months. We advised her to continue taking at least aspirin indefinitely. At second admission, she suffered acute renal failure of the solitary functioning kidney probably secondary to prolonged hypotension, from which she recovered completely. The most3. likely explanation for hypotension was arrhythmia. She was discharged in sinus rhythm and kept on warfarin and amidorone.

Our case further suggests that the commonest cause of embolization is arrhythmia and even some of the so called idiopathic cases could be explained on the basis of paroxysmal arrhythmias which could not be confirmed. We conclude that renal infarction is a serious problem and diagnosis requires a high index of suspicion, and the definitive method of diagnosis is renal angiography. Even if arrhythmia cannot be documented, these patients should be on anti-coagulants life long.

   References Top

1.Goldberg G. Renal infarction. Ann Emerg Med 1985;14(6):611-4.  Back to cited text no. 1    
2.Braun DR, Sawczuk IS, Axelrod SA. Idio-pathic renal infarction. Urology 1995;5:142-5.  Back to cited text no. 2    
3.Alamir A, Middendorf DF, Baker P, Nahman NS Jr, Fontaine AB, Hebert LA. Renal artery dissection causing renal infarction in otherwise healthy men. Am J Kidney Dis 1997;30(6):851-5.  Back to cited text no. 3    
4.Lambrecht GL, Malbrain ML, Coremans P, Verbist L, Verhaegen H. Acute renal infarction and heavy marijuana smoking. Nephron 1995;70:494-6.  Back to cited text no. 4  [PUBMED]  
5.Hernandez D, Dominguez ML, Diaz F, et al. Renal infarction in a severely hypertensive patient with lupus erythematosus and anti-phospholipid antibodies. Nephron 1996;72: 298-301.  Back to cited text no. 5    
6.Sonpal GM, Sharma A, Miller A. Primary anti-phospholipid antibody syndrome, renal infarction and hypertension. J Rheumatol 1993;20:1221-­3.  Back to cited text no. 6  [PUBMED]  
7.Ikeda Y, Sakemi T, Kato A, Kudo S. Renal infarction in a patient without underlying diseases. Nephron 1996;74:447­-8.  Back to cited text no. 7  [PUBMED]  
8.Brown DF, Nadel ES. Acute flank pain. J Emerg Med 1997;15(6):875-8.  Back to cited text no. 8    

Correspondence Address:
Ali Al-Harbi
Head, Nephrology Division, Security Forces Hospital Program, P.O. Box 3643, Riyadh 11481
Saudi Arabia
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PMID: 18209371

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