Reversal of Refractory Hypertension due to the Goldblatt Kidney Phenomena from a Descending Aortic Dissection Using a Stent and

Case Study and Review

Submitted on Fri, 09/05/2008 - 16:36
Authors

<sup>1</sup>Mohan Nandalur, MD <sup>2</sup>Bruce Abramowitz, MD, <sup>2</sup>Surendra Avula, MD, <sup>2</sup>Nausheen Akhter, MD

Introduction Medical therapy for acute type B aortic dissections primarily involves reduction of aortic shear force by decreasing blood pressure. Rarely, if a dissection plane extends directly into a renal artery, the hypertension may be difficult to control and prevent optimal management of the dissection. We describe a case report of a patient who responded to percutaneous intervention of a dissection flap in a renal artery. Additionally, an off-label, FDA-approved filter device was utilized to prevent further progression of renal insufficiency. Case Presentation An 80-year-old man had no symptoms until the afternoon prior to admission when, shortly after finishing a meal, he experienced sudden onset of severe epigastric pain that subsequently radiated to his mid-back. He had associated nausea and mild diaphoresis, but denied chest pain, shortness of breath, weakness, vomiting, or diarrhea. The patient first took antacids without relief, then went to an urgent care center that referred him to the emergency department. The patient’s medical history includes long-standing hypertension, atrial fibrillation, benign prostate hypertrophy, gastro-esophageal reflux, and osteoporosis. His surgical history consisted of a thoracostomy in childhood for an empyema, and a cholecystectomy. Medications administered upon admission were warfarin 5 mg PO QD, digoxin 0.125 mg PO QD, alendronate 70 mg PO QD and furosemide 20 mg PO QD. He denied any tobacco use. On physical examination, he was afebrile, with a blood pressure of 230/123 mmHg (symmetric in both brachial and thigh measurements), had a heart rate of 95 beats per minute, and respirations of 20 times per minute, with an oxygen saturation of 98% on room air. Cardiac exam revealed an irregular rate and rhythm, with normal S1 and S2 and no murmurs, gallops, or rubs. His lungs were clear to auscultation bilaterally, and his abdomen was soft and tender to palpation in the epigastric region without rebound or guarding. No abdominal bruits were auscultated and bowel sounds were present. He had 1+ femoral and pedal pulses bilaterally. Significant laboratory data upon admission revealed a blood urea nitrogen of 16 mg/dL, a serum creatinine of 1.5 mg/dL, a serum potassium of 3.5 mmol/L, and an international normalized ratio of 1.5. The electrocardiogram showed atrial fibrillation with nonspecific t-wave changes. Transthoracic echocardiogram found left ventricular hypertrophy, preserved left ventricular systolic function with a mildly elevated pulmonary artery systolic pressure and mild aortic insufficiency. A computed tomography scan of the abdomen demonstrates Type B aortic dissection originating after the left subclavian artery, with distal extension into the left renal artery (Figure 1). There is decreased perfusion of the left kidney, with multiple peripheral wedge-shaped low densities consistent with embolic infarcts. After evaluation by vascular surgery, it was felt there would be marginal benefit to the invasive approach, and the patient was admitted to the surgical intensive care unit for optimal medical management. In order to acutely manage the blood pressure, intravenous esmolol and nitroprusside infusions were initiated. Despite continued dose escalation over the next 24 hours of the intravenous medications, the blood pressure continued to be difficult to manage, with mean arterial pressures still greater than 100. Cardiology consultation was obtained, and over the next 24 hours, he was simultaneously started on multiple oral medications, (including amlodipine 10 mg PO QD, lisinopril 20 mg PO QD, spironolactone 50 mg PO QD, and hydralazine 50 mg IV QID), with the hope of avoiding invasive correction. However, over this 24-hour interval, urine output diminished to less than 30 cc/hour, serum Cr had increased to 2.5 mg/dl, and supplemental lasix was utilized with little efficacy. At this juncture, there was a discussion regarding open surgical repair versus fenestration of the dissection flap. While fenestration is known to be beneficial when the mechanism of flow compromise is due to compression of one lumen by higher pressure in the second lumen, it was unclear if the procedure would benefit this patient. In this case, as there was no plan to place a stent graft in the aorta, it was felt that renal hypoperfusion was directly related to the direct extension of the distal end of the dissection plane into the renal artery. Therefore, it was determined that a renal angiogram with possible renal artery stent placement may assist in reducing the refractory hypertension. Abdominal aortic angiogram revealed a descending aortic dissection, with extension into the ostium of the left renal artery (Figure 2). Selective renal angiography was performed with a 7 Fr short IM guide catheter, and revealed a dissection plane extending into the superior portion of the renal artery. Due to a possible need for reversal of anticoagulation, unfractionated heparin was administered as a single bolus, and the endovascular intervention was initiated once it was confirmed that the ACT was therapeutic. Due to the size of the distal artery, conventional filter wires and balloon distal protection devices would be unable to create an adequate seal. Therefore, a 7.5 mm RX AccuNet Embolic Protection System (Guidant, Menlo Park, California) filter designed for carotid arteries was utilized off-label and deployed distally. Due to the larger filter size distally and primary objective of compressing and sealing the false lumen proximally, the decision was made to utilize a shorter stent. Therefore, primary stenting was done with a 7.0 x 15.0 mm Hercu/Link Transhepatic Biliary Stent (Guidant). Follow-up angiography revealed no residual stenosis, a sealed dissection plane, and TIMI III distal flow. Once retrieved, the filter device contained a 2.0 x 4.5 mm clot (Figure 3). As there had already been multiple embolic infarcts of the renal parenchyma, it was believed that the thrombus had been compressed out of the false lumen of the renal artery dissection. However, as we were unable to determine if there was a direct communication between the two dissection planes in the renal artery, additional possibilities for the origin of thrombus may include development of a clot on the wire portion of the filter device, or from a pre-existing thrombus dislodged from within the true lumen. Due to rapidly improving hypertension, both the esmolol and nitroprusside could be weaned off over the next 24 hours. The patient was eventually discharged on 81 mg of aspirin and 75 mg of clopidigrel for anti-platelet therapy. One month later, the patient was seen in clinic on the following blood pressure regimen: Metoprolol XL 200 mg PO QD, spironolactone 25 mg PO QD, and diltiazem 120 mg PO QD. He was asymptomatic; blood pressure was 130/80 and his serum creatinine had improved to 1.2 mg/dL. Discussion Acute aortic dissections are differentiated based on whether the intimal flap originates in the ascending aorta (DeBakey types 1 and 2, Stanford type A), or in the descending aorta (DeBakey type 3, Stanford type B) because of a significant difference in treatment modalities. The former, which often presents with chest, shoulder, or thoracic back pain, acute aortic valvular insufficiency, or cranial and limb arterial flow disruption, is considered a surgical emergency, with a mortality of 1–2% per hour during the first 48 hours. Treatment will typically involve the resection of the ascending aorta, and subsequent placement of a prosthetic graft with the associated appropriate modification of the aortic valve. However, based on International Registry of Acute Aortic Dissection data, descending dissections, which present as low back pain, or acute limb, renal or mesenteric ischemia, are found to have a short-term mortality of 10% if managed medically, versus 30% with surgical repair. Some common indications for surgery are an inability to control hypertension, acute ischemia of abdominal arterial branch vessels, aneurysm or rupture of the aorta, and persistent pain.1 This case is an example of an acute type B acute aortic dissection with involvement of the left renal artery causing end-organ ischemia and refractory hypertension. Renal ischemia is a major complication of descending aortic dissections, occurring between 8–60% of cases.2 Typically, perfusion compromise is secondary to variations in luminal pressure on either side of the dissection plane, causing compression of the low-pressure side, and reduced flow to any abdominal arterial branches originating from this side. Here, however, there was a less common presentation of the distal aortic dissection flap extending directly into the renal artery and creating two lumens in a branch aortic vessel. In this particular case, the renal ischemia resulted in acute systemic hypertension, demonstrating the Goldblatt kidney phenomenon. In 1934, Dr. Harry Goldblatt conducted a series of clamp experiments on dog models. He demonstrated that unilateral constriction of a renal artery resulted in temporary elevation of blood pressure, which returned to normal once the clamp was removed. Therefore, a kidney whose arterial blood supply has been reduced by arteriosclerosis, or in this unusual case, a dissection flap, and results in hypertension, is termed a “Goldblatt kidney”.3,4 The acute aortic dissection made resolution of the resistant hypertension imperative for this patient. There are only a handful of case reports about descending aortic dissections involving the renal arteries.5–7 Weiss et al described a case of a patient with end-stage renal disease who had endovascular repair of the left renal artery and cessation of hemodialysis six weeks after stent placement.5 Our case illustrates improvement of refractory hypertension and renal function with percutaneous endovascular therapy, employing a stent and larger diameter off-label filter device. We also wish to highlight the role of distal protection devices in improving patient safety. The clot retrieved in the filter basket after the procedure was likely related to the embolic infarcts of the renal parenchyma. While distal protection devices have been shown to improve patient outcomes and capture a significant amount of embolic atherosclerotic debris during renal artery stenting, they have not been utilized for percutaneous treatment of dissection complications, and may prevent further iatrogenic injury.