Ordinarily, the clinician will consider consultation for renal or adrenal vein sampling during the diagnostic investigation of hypertensive patients in whom there is a high index of suspicion for selected types of secondary hypertension. Renal vein renin assays are sometimes required to establish the diagnosis of or in preparation for the treatment of the following renovascular or renal causes of secondary hypertension: the various forms of renal artery stenosis, renal dysplasia, large renal cyst or renal carcinoma, renal compression by extensive perirenal fibrosis, unilateral hydronephrosis, and neoplasia of juxtaglomerular apparatus (JGA) cells. Less commonly, renal vein sampling would be requested to decide whether to remove a poorly functioning or nonfunctioning kidney in a patient with severe, refractory hypertension. Adrenal vein sampling may be required to establish the diagnosis of or make surgical decisions regarding primary hyperaldosteronism and pheochromocytoma.

  Renal Vein Sampling in Secondary Hypertension

Renovascular Hypertension

The reported diseases causing hypertension as a result of involvement of the renal arteries are shown in Table 49–1. The most common of these are atherosclerosis (60 to 70% of cases) and fibromuscular dysplasia (FMD) and its histopathologic variants. Renal artery stenosis (RAS) from atherosclerosis is more likely to occur in men, especially over the age of 50 years, and FMD is more likely to occur in women, especially under the age of 40 years, and in children and young adults. As with all aspects of clinical medicine, however, there are exceptions to the rule. Although it has generally been accepted that correctable renovascular hypertension occurs infrequently in black patients, in selected patients with clinical features suggestive of RAS (see later), the incidence may approach that seen in white subjects.^1,2 The remainder of causes of RAS are uncommon or rare, and their consideration is reserved for highly selected patient presentations or for patients whose renal arteriograms suggest these alternative diagnoses.

It is estimated that from 2 to 5% of all hypertensive persons have hemodynamically significant RAS. Thus, diagnostic evaluation of patients for RAS is limited to those for whom the physician develops a high index of suspicion for this possibility.³ Circumstances that may prompt further evaluation for RAS are listed in Table 49–2.

Although essential hypertension remains the most common cause of elevated blood pressure (BP) in children and adolescents, hypertensive children prior to puberty, and adolescents who are not obese, who do not smoke, who do not eat a lot of “fast” or particularly salty foods, and who do not have evidence of underlying renal disease warrant at least a screening evaluation. Children and adolescents with severe hypertension (diastolic BP ≥ 110 mm Hg) should have a definitive diagnostic evaluation (i.e., renal arteriography). In patients presenting with malignant hypertension, in whom alternative diagnoses (e.g., polyarteritis nodosa) are absent, the probability of underlying RAS is sufficiently greater than that in patients with less severe hypertension to ustify evaluation by renal arteriography directly. A documented abrupt onset and rapid worsening of moderate to severe hypertension, especially in a woman in her twenties or thirties, and the documented new development of moderate to severe hypertension after the age of 50 are circumstances that raise the index of suspicion for RAS. Patients with hemodynamically significant RAS often require three or more antihypertensive drugs in large doses to achieve acceptable (not necessarily optimal) control. Alternatively, they may be reasonably responsive to treatment initially, but during months to years of follow-up require ever increasing doses and numbers of antihypertensive drugs. Thus, patients on numerous medications, especially those experiencing substantial medication-induced side effects or suboptimal BP control, are candidates for further investigation. The hypertensive patient with hypokalemia also raises suspicion because of the secondary hyperaldosteronism associated with excess renin secretion.

Another drug-related event that can be an important indicator of possible underlying RAS is an abrupt rise in the blood urea nitrogen (BUN) and serum creatinine when a patient is started on treatment with any of the angiotensin-converting enzyme (AGE) inhibitors.^4,5 The intrarenal renin-angiotensin system plays a critical role in the autoregulatory mechanisms that preserve glomerular filtration rate (GFR) as renal arterial flow or perfusion pressure decrease. Intrarenally generated angiotensin II (All) causes more constriction of the efferent arterioles exiting the glomeruli than of the afferent arterioles entering them. This blunts the decrease in intraglomerular capillary pressure, thereby “blunting” the fall in GFR. Inhibition of All generation by an ACE inhibitor impairs the effectiveness of this protective autoregulatory mechanism and may result in a clinically significant decrease in renal function. This kind of adverse consequence of ACE inhibitor treatment is far more likely to occur in a patient with bilateral RAS or with RAS affecting a single functioning kidney.

The above-described circumstances represent the traditional conditions leading to an evaluation for RAS. There are other, often more subtle circumstances that may alert the seasoned or astute clinician to the possibility of underlying RAS. These include the various manifestations of ischemic renal disease resulting from high-grade obstruction of the major renal arteries, usually from atherosclerosis.⁶ Affected patients are usually, but not always, aged over 60 years, or they have diseases (diabetes mellitus) or other risk factors (heavy smoking, hypercholesterolemia) associated with premature or accelerated atherosclerotic cardiovascular disease. RAS should be strongly considered in elderly patients with progressive azotemia of obscure etiology.^7,8 In addition, RAS often results in end-stage kidney disease,^9,10 and it accounted for about 15% of patients older than 50 years in one survey of a renal dialysis population.¹¹

Patients who develop ischemic acute renal failure (ARF) associated with ACE inhibitors or nonsteroidal antiinflammatory drugs (NSAIDs), or after transient hypotensive episodes, the severity of which would not have been anticipated to cause ARF, also would be highly suspect. The same would be true for volume-overloaded patients who develop acute renal insufficiency when treated with a reasonable diuretic regimen. Hypertensive patients who manifest a substantial deterioration in renal function whenever their BP is lowered into the desired normal range, and those who manifest a subacute progressive decline in renal function at a rate appreciably greater than expected for the natural history of their underlying kidney disease, are Other examples of potential candidates for further diagnostic evaluation.

Another somewhat insidious presentation of renovascular hypertension is the patient with recurrent episodes of sudden (or so-called flash) pulmonary edema associated with severe acute hypertension but without convincing evidence for myocardial ischemia predominantly from obstructive coronary artery disease. Such patients often are not recognized because patients with myocardial ischemia from coronary artery disease may develop high blood pressure secondarily as a result of increased sympathetic nervous system responses and catecholamine release when they experience acute pulmonary edema from ischemia-induced left ventricular failure.

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