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Renal infarction a cause of acute flank pain

We report a case of a 34-year old woman who presented with acute pain in the left flank and lower abdomen, with a definitive diagnosis idiopathic renal infarction.

 

Authors: R.P. Meijer1, L.M.C.L. Fossion2, K.R. van IJzendoorn2, H.P. Beerlage3

1. Department of Urology, Antoni van Leeuwenhoek Ziekenhuis, Amsterdam, the Netherlands
2. Department of Urology, MMC Veldhoven, Veldhoven, the Netherlands
3. Department of Urology, Jeroen Bosch Ziekenhuis, ‘s-Hertogenbosch, the Netherlands

Corresponding Author: Kevin van IJzendoorn, Department of Urology, MMC Veldhoven, De Run 4600, 5500 MB Veldhoven, The Netherlands.  E-mail: [email protected] or [email protected]

 

Abstract
 

 

Renal infarction can mimic more common entities causing acute flank or abdominal pain, thereby delaying the commencement of proper treatment. Such a delay may lead to irreversible loss of renal function. We report a case of a 34-year old woman who presented with acute pain in the left flank and lower abdomen. Blood biochemistry revealed an elevated white blood cell count (23.6/microL) and high lactate dehydrogenase (1699U/L). Urinalysis showed microscopic hematuria and mild leukocyturia. A contrast-enhanced CT scan revealed multiple segmentary wedge shaped hypo-echoic lesions in the parenchyma of the left kidney, indicating ischemia. The definitive diagnosis was an idiopathic renal infarction. The patient was started on anti-coagulants and recovered gradually. Many urologists and physicians are unfamiliar with the diagnosis of renal infarction. This often leads to a delay in the process of decision-making. One should not be reluctant to perform an early contrast-enhanced CT-scan in such a case.

 

Introduction

 

Renal infarction is a diagnosis which is often missed in clinical practice. It can mimic more common entities causing acute flank pain, thereby delaying the commencement of proper treatment. In the literature only a few articles, mostly case reports, can be found on this subject. Many urologists and physicians are unfamiliar with the diagnosis of renal infarction. This often leads to a delay in the process of decision-making, and may lead to irreversible loss of renal function.

 

Case report

 

We report the case of a 34-year old woman, with no previous medical history, who presented with acute pain in the left flank and lower abdomen. She had no urinary complaints She appeared moderately unwell, but without a fever. Clinical examination indicated pain in the left loin and lower abdomen. Laboratory results revealed an elevated white blood cell count (23.600/microL) and a high lactate dehydrogenase (1699 U/L). Urinalysis showed microscopic hematuria and mild leukocyturia. Abdominal X-ray (KUB) did not show any calculi. Initial ultrasound of the abdomen and the kidneys did not show abnormality. An empirical intravenous antibiotic regimen was started, on the likelihood that the diagnosis was acute pyelonephritis of the left kidney. However, the patient failed to respond to this treatment, was therefore reinvestigated. Ultrasound of the kidneys was repeated the following day and showed an oedematous left kidney with  diminished venous blood flow on Doppler. Contrast-enhanced computer tomography (CT) revealed multiple segmentary wedge shaped hypo-echoic lesions in the parenchyma of the left kidney (Fig 1).

 

Figure 1. Contrast-enhanced CT-scan, with multiple wedge shaped lesions in the parenchyma of the left kidney, indicating ischemia.

 


 

 

Angiography was performed, and showed multiple thrombi in several segmental arteries, primarily interpolar and in the lower pole of the left kidney; however no abnormalities of the vascular endothelium were seen (Fig 2).

 

Figure 2. Renal angiography. A filling defect can be seen due to thrombi in segmental  arteries, primarily interpolar and in the lower pole of the left kidney.

 


 

 

In order to identify any possible underlying pathology, which may have caused the renal ischemia, the patient underwent further investigation. Coagulation disorders were excluded. Electrocardiography (ECG) did not show any dysrhythmia. Echocardiography was performed, and showed  good ventricular function and no signs of valvular pathology. The patient was started on anti-coagulants. In the following days she recovered progressively and the pain resolved gradually. Creatinine clearance stayed within the normal range (100 mL/min). During initial follow-up she did not develop hypertension.

 

Discussion

 

Renal infarction may cause a variety of symptoms: acute abdominal or flank pain (65%)[1], nausea and vomiting (20%), fever, hypertension and hematuria[1,2], but it may also be asymptomatic. Patients with a history of thrombo-embolic disease (e.g. atrial fibrillation, coagulation disorders) are more at risk for renal ischemia[2-4]. Biochemistry may reveal an elevated white blood cell count (>11.000/microL) and mostly a raised serum lactate dehydrogenase (LDH) level (>450 U/L) (95%)[1,2,4,5]. Urinalysis may show hematuria (55-70%), leukocyturia (50%) or proteinuria (70%)[1,2]. The diagnosis may be confirmed by the following imaging techniques: abdominal ultrasound with Doppler,  contrast-enhanced CT, angiography and DTPA renography. The CT scan has proven to be a valuable diagnostic tool in renal infarction because of its high sensitivity and its non-invasive characteristics[1,2,6]. Depending on the duration of ischemia,  renal angiography should be performed. This invasive procedure, with the possibility to apply thrombolytic agents (e.g. streptokinase) locally, will not help to preserve renal function if it is started after the period of ischemia tolerance of the kidney has elapsed[7]. The tolerance of the kidney for warm ischemia ranges from 30 to 60 minutes[8,9]. In case of a longer delay or a total occlusion of the renal artery, analgesia should be followed by conservative treatment, consisting of anti-coagulation (e.g. heparin)[1,2]. To find possible causes of  renal infarction, ECG and echocardiography should be performed in all patients. Furthermore coagulation disorders should be ruled out. Several causes of renal infarction are listed in Table 1.

 

Table 1. Causes of Renal Infarction 

 

 

After considering the possible causes, it was concluded that in this patient, the definitive diagnosis was an idiopathic renal infarction. Possible complications following renal infarction include: transient hypertension, which may resolve spontaneously, or permanent hypertension, which may require treatment. Hypertension ensues from renal hypoperfusion and the following activation of the renin-angiotensin system. Permanent hypertension may be treated with an angiotensin converting enzyme (ACE)-inhibitor[10]. In case of therapy-resistant hypertension, surgical treatment of the occlusion or even nephrectomy may be necessary. Many urologists and physicians are unfamiliar with the diagnosis of renal infarction. This often leads to a delay in the process of decision-making. Therefore we stress the need to consider the possibility of a renal infarction in all patients who present with acute flank or abdominal pain, high serum lactate dehydrogenase and an elevated white blood cell count. One should not be reluctant to perform an early contrast-enhanced CT-scan in such a case.

 

References
 

 

1. Hazanov N, Somin M, Attali M, et al. Acute renal embolism: forty-four cases of renal infarction in patients with atrial fibrillation. Medicine 2004; 83(5): 292-99.
2. Domanovits H, Paulis M, Nikardjam M, et al. Acute renal infarction: clinical characteristics of 17 patients. Medicine 1999; 78(6): 386-94.
3. Braun DR, Sawczuk IS, Axelrod SA. Idiopathic renal infarction. Urology 1995; 45(1): 142-45.
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5. Winzelberg GG, Hull JD, Agar JW, Rose BD, Pletka PG. Elevation of serum lactate dehydrogenase levels in renal infarction. JAMA 1979; 242(3): 268-69.
6. Glazer GM, Francis IR, Brady TM, Teng SS. Computed tomography of renal infarction: Clinical and experimental observations. AJR Am J Roentgenol 1983; 140(4): 721-27.
7. Blum U, Billmann P, Krause T, et al. Effect of local lowdose thrombolysis on clinical outcome in acute embolic renal artery occlusion. Radiology 1993; 189: 549-54.
8. Kane CJ, Mitchell JA, Meng MV, Anast J, Carroll PR, Stoller ML. Laparoscopic partial nephrectomy with temporary arterial occlusion: description of technique and renal functional outcomes. Urology 2004; 63(2): 241-6.
9. Shekarriz B, Shah G, Upadhyay J. Impact of temporary hilar clamping during laparoscopic partial nephrectomy on postoperative renal function: a prospective study. J Urol 2004; 172(1):54-7.
10. Tullis MJ, Caps MT, Zierler RE, et al. Blood pressure, antihypertensive medication, and atherosclerotic renal artery stenosis. Am J Kidney Dis 1999; 33(4): 675-81.

 
Date added to bjui.org: 13/02/2012 


DOI: 10.1002/BJUIw-2011-120-web

 

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