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Saudi Journal of Kidney Diseases and Transplantation
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Table of Contents   
CASE REPORT  
Year : 2017  |  Volume : 28  |  Issue : 1  |  Page : 167-169
An unusual cause of hematuria following coronary intervention


1 Department of Nephrology, Indo-US Hospitals, Hyderabad, Andhra Pradesh, India
2 Department of Cardiology, Indo-US Hospitals, Hyderabad, Andhra Pradesh, India
3 Department of Radiology, Indo-US Hospitals, Hyderabad, Andhra Pradesh, India

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Date of Web Publication12-Jan-2017
 

   Abstract 

Acute renal infarction is rare. Its true incidence is not known. The paucity of literature and unawareness among the physicians makes it an underdiagnosed entity. Herein, we report a case of renal infarction following coronary intervention.

How to cite this article:
Yadla M, Koduganti SC, Jariwala P, Madhavaram B. An unusual cause of hematuria following coronary intervention. Saudi J Kidney Dis Transpl 2017;28:167-9

How to cite this URL:
Yadla M, Koduganti SC, Jariwala P, Madhavaram B. An unusual cause of hematuria following coronary intervention. Saudi J Kidney Dis Transpl [serial online] 2017 [cited 2017 Mar 24];28:167-9. Available from: http://www.sjkdt.org/text.asp?2017/28/1/167/198242

   Introduction Top


Renal infarction is rare. It is a close mimicker of acute pyelonephritis (APN) clinically and radiologically. Computed tomography (CT) and magnetic resonance imaging may be useful in differentiating the two conditions. It presents with fever, loin pain, and other inflammatory features. It may occur spontaneously or following vascular interventions.

Herein, we report one such case of renal infarction following coronary intervention.


   Case Report Top


A 45-year-old woman, known diabetic and hypertensive, presented with sudden onset of breathlessness. There was no history of angina, facial puffiness, or oliguria. On examination, she had tachycardia, tachypnea, and the blood pressure was 220/130 mm Hg. All the peripheral pulses were equally felt, and there was no peripheral or renal bruit. Bilateral crepitations were present in the infrascapular area. On laboratory evaluation, complete hemogram was normal, blood urea was 30 mg/dL, and serum creatinine was 1 mg/dL. Urinalysis was normal. Electrocardiography showed tachycardia. She underwent coronary angiogram which showed 70% stenosis of left anterior descending artery and 80% stenosis in left circumflex artery (LCx). Percutaneous transluminal coronary angioplasty (PTCA) was done to LCx. One day after PTCA, she developed oligoanuria, gross hematuria, and breathlessness. Her serum creatinine increased to 2.3 mg/dL and serum potassium was 6 mEq/L. Blood gas analysis showed metabolic acidosis. In view of hyperkalemia, metabolic acidosis, and anuria, she was initiated on hemodialysis. Urinalysis showed 40-50 pus cells, plenty of RBCs. Urine culture showed Escherichia coli 1000 CFU/mL. Prothrombin time, activated prothrombin time, and clotting time were within normal limits. Ultrasound of the abdomen showed normal-sized kidneys with mild dilatation of pelvicalyceal system in the left kidney. Clinical diagnosis of APN was considered. Plain CT scan abdomen showed retained contrast in the right kidney, areas of hypodensities in the left kidney. Perinephric stranding, intra renal, and perirenal collections were absent. The cortical rim sign could not be seen in the the plain CT abdomen ([Figure 1] and [Figure 2]). Serum lactate dehydrogenase (LDH) was 464 IU/mL. A diagnosis of renal infarction was made based on the presence of gross hematuria, absence of features suggestive of APN. Cortical rim sign was not made out as it can be seen on arterial phase of CT angiogram. Our patient did not undergo CT angiogram. She was supported with hemodialysis. Over the next 24-48 h, her urine output improved to 4 L and serum creatinine decreased to 2.7 mg/dL. At the time of discharge, her serum creatinine was 1.4 mg/dL. Nuclear scan done two weeks after the recovery showed reduced tracer uptake in left kidney and preserved perfusion in right kidney.
Figure 1. Plain CT scan abdomen showing hypodensity in upper half of left kidney.

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Figure 2. Plain CT scan abdomen showing diffuse hypodensity in the left kidney. Note the absence of peri-inflammatory changes and the wedge shape. Retained contrast in the right kidney is also seen.

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   Discussion Top


The clinical incidence of renal infarction was reported to be 0.004-0.007%.[1] It is an infrequent diagnosis with the reported incidence of 1.4% in an autopsy series. It can be due to arterial occlusion, or venous thrombosis causes of renal infarction include vascular disorders, coagulopathies, renal artery occlusion, trauma, renal atheroembolism, and following vascular interventions which can occur due to dissection of the renal artery or cholesterol atheroembolism or renal artery thrombosis.

Features of renal infarction include abdominal pain, oliguria, renal insufficiency, microscopic hematuria, elevated LDH, alanine transferase, aspartate transferase, and leukocytosis. The most common symptom is pain. Anuria is seen in cases of bilateral arterial occlusion and in occlusion of solitary functioning kidney. Severe renal vasospasm may be the reason for oliguria in unilateral occlusion. Renal infarction can cause acute kidney injury (AKI) in up to 40% of cases.

Radiologically, ultrasound and plain CT scan abdomen may not be useful, but on contrastenhanced CT scan, arterial phase may show occlusion of main renal artery in case of global infarction or segmental artery occlusion in cases of lobar infarction. Generally, the iatrogenic infarcts following endovascular procedures are painless and are discovered incidentally on CT scan abdomen.

Korzets et al in a study of 11 cases. In this study, fever, dysuria, elevated LDH, leukocytosis, and factors predisposing to the development of thromboembolic event were noted. Diagnosis was made one to six days after the insult.[2] Domanovits noted that triad of presenting features: unilateral abdominal pain, elevated LDH, and pain (with or without hematuria within 24 h after the onset of and pain).[3]

In our patient, differential diagnosis of atheroembolic renal disease (AERD) and APN was considered in view of the presence of gross hematuria, AKI, and pyuria though gross hematuria is unlikely in APN and pyuria is not seen in AERD. The absence of peripheral signs of atheroembolism and eosinophilia and eosinophiluria made the diagnosis of AERD unlikely. Ultrasound and CT scan would be normal in AERD, but in APN areas of hypointensity/hypodensity are seen on ultrasound and CT, respectively. In our patient, ultrasound did not show areas of hypointensities, but CT scan abdomen showed hypodensity in upper half of left kidney. Although APN mimics renal infarction on CT scan, absence of perinephric inflammatory signs, perinephric collections, absence of typical wedge-shaped hypodensities with apex toward the calyx favored the diagnosis of renal infarction. The infarcts in the left kidney corresponding to the areas of anterior segmental artery, posterior segmental artery suggesting the possibility of arterial occlusion following the vascular intervention. The presence of infarcts in the right kidney could not be appreciated; there were features suggestive of contrast-induced nephropathy. The definitive diagnosis of renal infarction is made on renal angiogram. AKI in our patient may be due to contrast-induced nephropathy and renal infarction.

The role of renal revascularization in renal infarction is not clear. Blum et al reported the critical ischemia time to be <3 h[4] though the renal recovery was reported in intervention even after four days of the insult. Revascularization may be indicated in those with bilateral occlusions or occlusion in a single a functioning kidney.

Systemic anticoagulation with heparin could not be given in our patient due to the presence of gross hematuria. Localized renal reperfusion therapy could not be done as the diagnosis of renal infarction was made 24 h after the onset of symptoms.

Conflict of interest: None declared.

 
   References Top

1.
Huang CC, Lo HC, Huang HH, Kao WF, Yen DH, Wang LM, et al. ED presentations of acute renal infarction. Am J Emerg Med 2007;25:164-9.  Back to cited text no. 1
    
2.
Korzets Z, Plotkin E, Bernheim J, Zissin R. The clinical spectrum of acute renal infarction. Isr Med Assoc J 2002;4:781-4.  Back to cited text no. 2
    
3.
Domanovits H, Paulis M, Nikfardjam M, Meron G, Kürkciyan I, Bankier AA, et al. Acute renal infarction. Clinical characteristics of 17 patients. Medicine (Baltimore) 1999;78: 386-94.  Back to cited text no. 3
    
4.
Blum U, Billmann P, Krause T, Gabelmann A, Keller E, Moser E, et al. Effect of local lowdose thrombolysis on clinical outcome in acute embolic renal artery occlusion. Radiology 1993;189:549-54.  Back to cited text no. 4
    

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Correspondence Address:
Manjusha Yadla
Department of Nephrology, Indo-US Hospitals, Hyderabad, Andhra Pradesh
India
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DOI: 10.4103/1319-2442.198242

PMID: 28098120

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    Abstract
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   Case Report
    References
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