Renal Infarction secondary to renal artery thrombosis

Renal infarction can be due to many causes such as trauma, embolism, arterial thrombosis, vasculitis and sudden complete renal vein thrombosis. Acute embolic renal infarcts are often misdiagnosed as a renal calculus leading to delay in treatment which increases the morbidity [1]. Blunt abdominal trauma with traumatic avulsion often results in unilateral global renal infarction. Emboli and vasculitis often cause bilateral multiple focal renal infarctions [2]. Most common cause for thromboembolism is from cardiovascular diseases such as rheumatic heart disease , cardiac arrhythmias, myocardial infarction, mural thrombi and sub acute bacterial endocarditis (septic emboli). Arterial thrombosis leading to renal infarction can be due to arteriosclerosis, aneurysm or dissection of aorta, thrombangitis obliterance, syphilitic cardiovascular disease and sickle cell disease [1,2]. Earliest report of renal embolic renal disease is reported in 1856. The commonest presenting features are flank pain, tenderness, nausea, vomiting, hematuria and hypertension. Serum LDH level had shown to be a sensitive marker for infarction and measuring the urinary LDH levels can be a useful in differentiating the cause for. Contrast enhance CT scan is considered a safe non invasive easily available and highly accurate method for detecting renal embolic disease leading to renal infarction. Renal angiography is not usually required unless an operative approach is considered[3]. Intravenous urography feature are a large kidney with smooth contour and expanded renal cortical thickness. A diminished nephrogram with cortical rim enhancement and the collecting system which attenuated and is often opacified by retrograde pyelography [1]. On grey scale sonography acute complete renal arterial occlusion may demonstrate a morphologically normal kidney and segmental or focal infarction appear as a wedge shape mass which simulate acute pyelonephritis [4]. Kodama K et al has shown that there is thickening and increase echogenisity of the perirenal fascia in global renal infarction. This change seen in perirenal fascia is correlated with the thickening of perirenal fascia demonstrated on CT scan [5]. CT findings depend on the age and the extent of the disease. If the main renal artery is occluded global renal infarction results and on contrast enhanced CT scans the effected kidney shows lack of enhancement and the high density cortical rim which represents perfusion supplied by collaterals to the outer rim of cortex. Renal collateral circulation is supplied by renal capsular vessels, peripelvic vessels and periureteral vessels. If a branch renal artery is occluded resulting a focal infarction, the CT scan demonstrate a wedge shape low attenuating renal parenchymal lesion where there is a sharp margination between the infracted and the normal parenchyma. Base of the wedge is contiguous with renal capsule and the apex is directed towards the renal hilus. Acute focal and global renal infarctions can be associated with perinephric fluid collections, hemorrhage and thickening of the renal fascia. Chronic infarcts manifest as renal cortical scars or a small shrunken kidney. The main CT differential diagnosis for acute renal infarction is acute pyelonephritis. Contrast enhanced CT scan in acute pyelonephritis also demonstrate wedge shape hypodense lesions and has similar clinical presentation, although a cortical rim sign strongly suggest the diagnosis of acute renal infarction. Small renal infarcts may simulate lymphomatous lesions or metastasis [1]. MRI scans on T1W and T2W sequences shows lower signal intensity compared to the non infarcted area and obliterated corticomedullary demarcation on T1W sequences. Signal intensities can be higher in cases associated with hemorrhage. On post contrast T1W studies demonstrate wedge shaped infarcted region similar to CT. Other features observed on MRI study are subcapsular hematoma or fluid collection, mass effect or focal areas of renal enlargement and thickened renal fascia [6]. 99 M Tc DMSA scan demonstrate photon deficient area in relation to infarcted region.