Page 5 - Carotid and peripheral vascular interventions textbook
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                 The location is often bilateral and frequently ostial or     developing progressive azotemia secondary to ischemia
                 proximal with perirenal aortic wall involvement. Aneurysmal     (a rise in serum creatinine of >30%), or unexplained
                 lesions have rarely been reported. Immunosuppressive   hypokalemia (secondary aldosteronism), or azotemia that is
                 therapy is important to slow the inf ammatory process   drug-induced (administration of ACEI or ARBs), should be
                 and prevent restenosis after revascularization.  examined for RAS (22). The presence of an abdominal or
                     Extrinsic compression of the renal artery caused by     f ank bruit or atherosclerotic disease appearing elsewhere
                 a f bromuscular band beginning from the diaphragm is a    in the body can increase the likelihood of RAS. Kidney
                 rare condition. This disorder causes systemic hypertension    size is also important. Prolonged decrease of blood f ow
                 associated with kinking of the renal artery and stenosis.   with tissue hypoxia causes irreversible kidney damage and
                 Surgical decompression is mandatory in all cases (21).   f brosis, so-called “ischemic nephropathy”. An atrophic
                 Other causes of renal artery stenosis such as dissection or   kidney (length <7cm) or a size discrepancy between
                 embolus can also be treated with endovascular techniques.   the two kidneys of larger than 1.5 cm are important
                                                                 clues of a possible severe stenosis of the renal artery
                                                                 supplying the small kidney. Finally, recurrent episodes
                   Table 10-1. Etiologies of renal artery stenosis.  of CHF, or impaired left ventricular systolic function,
                                                                 or unexplained f ash pulmonary edema without signif cant
                                                                 myocardial ischemia may result from stenosis of the
                   Fibromuscular dysplasia (FMD)
                                                                 renal artery of a solitary kidney, or severe bilateral RAS
                   Extrinsic f brous band
                                                                 (Pickering syndrome). These conditions should be
                   Renal artery dissection
                                                                 considered a hypertensive emergency that will benef t
                   Aortic dissection
                   Arterial embolus                              from an urgent endovascular revascularization. Table 10-2
                   Aortic endograft occluding the renal artery   summarizes the clinical indicators for the diagnosis of
                   Miscellaneous:                                RAS (23).
                     Autoimmune diseases
                     (e.g., Takayasu’s arteritis, polyarteritis nodosa)
                     Hypercoagulable state with renal infarction    Table 10-2. Clinical clues to the diagnosis of
                     (e.g., Lupus anticoagulant)                    renal artery stenosis.
                     Malignancy encircling the renal artery
                     (e.g., Renal cell carcinoma, pheochromocytoma)  •  Onset of hypertension before the age of 30 years
                                                                    •  Onset of severe hypertension after the age of 55 years, when   253
                                                                     associated with CKD or heart failure
                                                                    •  Hypertension and abdominal bruit
                 CLINICAL PRESENTATIONS                             •  Rapid and persistent worsening of previously controlled
                     RAS is assoiciated with a variety of clinical manifes-  •  Resistant hypertension (i.e., other secondary causes unlikely
                 tations as shown in Fig. 10-4. Symptoms can range from   and target blood pressure not achieved despite four drug
                                                                     classes including a diuretic and a mineralocorticoid-receptor
                 mild-to-severe uncontrolled hypertension to worsening
                                                                     antagonist in appropriate doses)
                 renal function and accelerated cardiovascular (CV) events,
                                                                    •  Hypertensive crisis (i.e., acute renal failure, acute heart failure,
                 such as unstable angina and congestive heart failure (CHF).
                                                                     hypertensive encephalopathy, or grade 3-4 retinopathy)
                 Many patients with RAS persist clinically asymptomatic   •  New azotemia or worsening of renal function after treatment
                 because of the large kidney functional reserve and present   with RAAS blockers
                 as an incidental f nding during imaging of other vessels.   •  Unexplained atrophic kidney or discrepancy in kidney size
                 Hypertension with sudden onset in persons <30 years of   (>1.5cm) or unexplained renal failure
                 age usually is a manifestation of FMD. If the diagnosis   •  Flash pulmonary edema
                 of hypertension is initially made in a patient >55 years
                                                                    CKD, chronic kidney disease; RAAS, renin-angiotensin-
                 of age who present with malignant, accelerated or    aldosterone system
                 resistant hypertension, ARAS should be considered. Patients
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