Renal cortical necrosis (RCN) is a rare cause of acute renal failure and is due to significantly prolonged diminished renal arterial perfusion secondary to vasospasm, microvascular injury or intravascular thrombosis. The process usually affects the small intra-cortical vessels, interlobular and afferent arterioles. Typically the arcuate arteries are spared, although they may also be affected (1).
The pathogenesis of RCN is not fully understood, although the final common pathway is microvascular hypoperfusion secondary to endothelial injury. This can occur in pregnancy (for example in placental abruption, placenta praevia or eclampsia), haemodynamic shock (due to sepsis, trauma, hypovolaemia) disseminated intravascular coagulation, acute transplant rejection and haemolytic uraemic syndrome (2-9) and various other pathologies which may contribute to these states.
Clinical presentation is usually with acute renal failure in native kidneys or transplant dysfunction as demonstrated by flank pain, haematuria, rising creatinine, oliguria and hypervolaemia. If left untreated or treatment is delayed, acute renal failure secondary to RCN has a high mortality rate.
RCN is difficult to appreciate on conventional and Doppler ultrasound as these modes can only detect signals from vessels down to approximately 1mm in diameter. CEUS has a higher sensitivity and enables assessment of the renal microcirculation, detecting signals from vessels of the order of 100µm in diameter. (10)
Typically, on B mode the whole kidney may be swollen with reduced or absent flow peripherally. Resistive indices may be elevated.
Contrast-enhanced CT and MR may show a thin rim of enhancing subcapsular tissue (‘rim sign’) due to subcapsular collateral supply. Low signal of the inner renal cortex and columns of Bertin may be seen on T1 and T2 sequences. Dystrophic calcification will eventually occur but is a late sign (11). However, both iodinated and gadolinium contrast agents may be potentially deleterious in renal failure and should ideally be avoided. Biopsy is the gold standard for diagnosis of RCN.
In our patient, a biopsy of the transplant kidney demonstrated cortical infarction secondary to thrombotic microangiopathy and small vessel thrombosis. The cause of the thrombotic microangiopathy was believed to be due to a combination of predisposing factors including SLE, previously demonstrated thromboembolic tendancy in addition to possible acute rejection. He received treatment with plasma exchange and intravenous immunoglobulin therapy with subsequent improvement in renal function.
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