Successfully Treated "Accelerated" Renovascular Hypertension with Intravascular Stenting.

Doi, Kent; Moriya, Hideshige; Kobayashi, Shuzo

doi:10.1291/hypres.25.945

Cited by 1 publication

(1 citation statement)

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“…Conversely, it could be said that renal artery stenting was crucial for avoiding dialysis and saving her life during this acute phase. Several reports have also been published showing the effectiveness of renal artery stenting in the acute critical phase, especially in patients with bilateral renal stenosis (8)(9)(10)(11). In cases of unilateral renal artery stenosis (RAS), the contralateral kidney is able to compensate for increases in blood pressure by suppressing renin secretion and aug-menting sodium excretion (12).…”

Section: Discussionmentioning

confidence: 99%

Renal Artery Stenting Crucial to the Recovery from Acute Worsening of Chronic Renal Failure

Nagashima

Yamashita

2014

Intern. Med.

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Recent randomized studies have failed to note any benefits to adding renal artery stenting to optimal medical therapy in patients with atherosclerotic renal artery stenosis (ARAS). We herein present the case of a 75-year-old woman with acute worsening of chronic renal failure in whom renal stenting was essential to saving the patient's life and avoiding dialysis. Although the long-term usefulness of renal artery stenting for ARAS remains controversial, this procedure should be kept in mind as a viable option for treating acute critical cases such as this. Case ReportA 75-year-old woman residing in a chronic care facility was transferred to our hospital due to cardiogenic shock. She was inactive in her daily life and had a history of hypertension, chronic renal failure, subarachnoid hemorrhage and myelodysplastic syndrome. Pre-admission, she took six antihypertensive medications daily (amlodipine: 10 mg, valsartan: 160 mg, diltiazem: 200 mg, carvedilol: 20 mg, spironolactone: 25 mg, hydrochlorothiazide: 25 mg). On admission, her hemodynamics were quite unstable, and her blood pressure was 80/40 mmHg with a pulse rate of 25 bpm. A physical examination revealed coarse crackle in all lung fields and cyanosis of her entire body, while a chest X-ray showed cardiomegaly and pulmonary congestion (Fig. 1A). An electrocardiogram (ECG) indicated sinus arrest with a junctional rhythm of 25/min and augmented T-waves (Fig. 1B). Under the administration of 10 L/min of oxygen, her arterial carbon dioxide (PCO2) and oxygen (PO2) concentrations were 75.5 mmHg and 58.8 mmHg, respectively. The laboratory data obtained on admission are shown in Table. The serum levels of blood urea nitrogen and creatinine were 80.4 mg/dL and 3.0 mg/dL, respectively, with an elevated potassium level of 8.8 mEq/L, which was responsible for the patient's bradycardia. A temporary pacemaker (TPM) was immediately introduced, and glucose-insulin (GI) treatment was started. Non-invasive positive pressure ventilation (NPPV) was also administered to improve oxygenation, with the bi-level positive airway pressure (BiPAP) mode applied using settings of 14 mmHg for the inspiratory positive airway pressure (IPAP) and 6 mmHg for the expiratory positive airway pressure (EPAP) at a concentration of inspired oxygen (FiO2) of 100%. Following these procedures, the patient's blood pressure gradually increased, and her respiratory status improved to a PCO2 of 53 mmHg and a PO2 of 122 mmHg without endotracheal intubation. Echocardiography showed a normal left ventricular systolic function (ejection fraction: 63%). As a result of the improvements in the patient's hemodynamics, her urine output increased temporarily; however, although carperitide was administered in addition to an intravenous injection of furosemide, both the patient's urination and renal function worsened, with an increase in the creatinine level to 3.8 mg/dL. Renal duplex ultrasound showed severe stenosis in the right renal artery [peak systolic velocity (PSV): 439 cm/s, renal/aorta ratio (RAR): ...

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