Reversal of end-stage renal disease after aortic dissection using renal artery stent: a case report

BACKGROUND: Medical management is the conventional treatment for Stanford Type B aortic dissections as surgery is associated with significant morbidity and mortality. The advent of endovascular interventional techniques has revived interest in treating end-organ complications of Type B aortic dissection. We describe a patient who benefited from endovascular repair of renal artery stenosis caused by a dissection flap, which resulted in reversal of his end-stage renal disease (ESRD). CASE PRESENTATION: A 69 y/o male with a Type B aortic dissection diagnosed two months earlier was found to have a serum creatinine of 15.2 mg/dL (1343.7 μmol/L) on routine visit to his primary care physician. An MRA demonstrated a rightward spiraling aortic dissection flap involving the origins of the celiac artery, superior mesenteric artery, and both renal arteries. The right renal artery arose from the false lumen with lack of blood flow to the right kidney. The left renal artery arose from the true lumen, but an intimal dissection flap appeared to be causing an intermittent stenosis of the left renal artery with compromised blood flow to the left kidney. Endovascular reconstruction with of the left renal artery with stent placement was performed. Hemodialysis was successfully discontinued six weeks after stent placement. CONCLUSION: Percutaneous intervention provides a promising alternative for patients with Type B aortic dissections when medical treatment will not improve the likelihood of meaningful recovery and surgery entails too great a risk. Nephrologists should therefore be aggressive in the workup of ischemic renal failure associated with aortic dissection as percutaneous intervention may reverse the effects of renal failure in this population

Renin, endothelial no synthase and endothelin gene expression in the 2Kidney-1clip goldblatt model of long-term renovascular hypertension

<p>Abstract</p> <p>Objective</p> <p>Numerous reports have shown the influence of renin, nitric oxide (NO) and the endothelin (ET) systems for regulation of blood pressure and renal function. Furthermore, interactions between these peptides have been reported. Aim of our study was to investigate the relative contribution of these compounds in long-term renovascular hypertension/renal ischemia.</p> <p>Methods</p> <p>Hypertension/left-sided renal ischemia was induced using the 2K1C-Goldblatt rat model. Renal renin, ET-1, ET-3 and endothelial NO synthase (eNOS) gene expression was measured by means of RNAse protection assay at different timepoints up to 10 weeks after induction of renal artery stenosis.</p> <p>Results</p> <p>Plasma renin activity and renal renin gene expression in the left kidney were increased in the clipped animals while eNOS expression was unchanged. Furthermore, an increase in ET-1 expression and a decrease of ET-3 expression was detected in early stenosis.</p> <p>Conclusions</p> <p>While renin is obviously involved in regulation of blood pressure and renal function in unilateral renal artery stenosis, ET-1, ET-3 and endothelium derived NO do not appear to play an important role in renal adaptation processes in long-term renal artery stenosis, although ET-1 and ET-3 might be involved in short-term adaptation processes.</p

3D Point Cloud Compression

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