Complete post-operative resolution of “temporary” end-stage kidney disease secondary to aortic dissection without static renal artery obstruction: a case study

Abstract

Background Acute kidney injury (AKI), which may progress to end-stage kidney disease (ESKD), is a potential complication of aortic dissection. Notably, in all reported ESKD cases secondary to aortic dissection, imaging evidence of static obstruction of the renal arteries always shows either renal artery stenosis or extension of the dissection into the renal arteries. Case presentation We present the case of a 58-year-old man with hypertension who was diagnosed with a Stanford type B aortic dissection and treated with medications alone because there were no obvious findings indicative of dissection involving the renal arteries. He had AKI, which unexpectedly progressed to ESKD, without any radiological evidence of direct involvement of the renal arteries. Thus, we failed to attribute the ESKD to the dissection and hesitated to perform any surgical intervention. Nevertheless, the patient’s hormonal levels, fractional excretion values, ankle brachial indices, and Doppler resistive indices seemed to indirectly suggest kidney malperfusion and implied renal artery hypo-perfusion. However, abdominal computed tomography imaging only revealed progressive thrombotic obstruction of the false lumen and compression of the true lumen in the descending thoracic aorta, despite the absence of anatomical blockage of renal artery perfusion. Later, signs of peripheral malperfusion, such as intermittent claudication, necessitated surgical intervention; a graft replacement of the aorta was performed. Post-operatively, the patient completely recovered after 3 months of haemodialysis, and the markers that had pre-operatively suggested decreased renal bloodstream normalised with recovery of kidney function. Conclusions To the best of our knowledge, this is the first report of severe AKI, secondary to aortic dissection, without direct renal artery obstruction, which progressed to “temporary” ESKD and was resolved following surgery. This case suggests that only coarctation above the renal artery branches following an aortic dissection can progress AKI to ESKD, despite the absence of radiological evidence confirming an obvious anatomical blockage. Further, indirect markers suggestive of decreased renal blood flow, such as ankle brachial indices, renal artery resistive indices, urinary excretion fractions, and hormonal changes, are useful for evaluating concomitant AKI and may indicate the need for surgical intervention after a Stanford type B aortic dissection.

Surgical timing of endoluminal repair of Stanford type B aortic coarctation and relationship to prognosis: a single-center retrospective cohort study

“…Endoleaks and retrograde entrapment are the more common complications after endoluminal repair, which are mainly related to the inability of the overlapping stent to fit the aortic wall adequately. Studies have pointed out that patients with TBAD have some degree of renal injury after surgery due to the use of large amounts of contrast agent during endoluminal repair and the effect of postoperative stent placement on renal artery hemodynamics ( 18 , 19 ). The causes of ischemic diseases (mainly stroke) are mostly inadequate proximal anchoring distance and cerebrovascular hypoperfusion.…”

“…Studies have pointed out that patients with TBAD have some degree of renal injury after surgery due to the use of large amounts of contrast agent during endoluminal repair and the effect of postoperative stent placement on renal artery hemodynamics (18,19). The causes of ischemic diseases (mainly stroke) are mostly inadequate proximal anchoring distance and cerebrovascular hypoperfusion.…”