Resistant hypertension (RH) is defined as above-goal elevated blood pressure (BP) in a patient despite the concurrent use of 3 antihypertensive drug classes, commonly including a long-acting calcium ...channel blocker, a blocker of the renin-angiotensin system (angiotensin-converting enzyme inhibitor or angiotensin receptor blocker), and a diuretic. The antihypertensive drugs should be administered at maximum or maximally tolerated daily doses. RH also includes patients whose BP achieves target values on ≥4 antihypertensive medications. The diagnosis of RH requires assurance of antihypertensive medication adherence and exclusion of the “white-coat effect” (office BP above goal but out-of-office BP at or below target). The importance of RH is underscored by the associated risk of adverse outcomes compared with non-RH. This article is an updated American Heart Association scientific statement on the detection, evaluation, and management of RH. Once antihypertensive medication adherence is confirmed and out-of-office BP recordings exclude a white-coat effect, evaluation includes identification of contributing lifestyle issues, detection of drugs interfering with antihypertensive medication effectiveness, screening for secondary hypertension, and assessment of target organ damage. Management of RH includes maximization of lifestyle interventions, use of long-acting thiazide-like diuretics (chlorthalidone or indapamide), addition of a mineralocorticoid receptor antagonist (spironolactone or eplerenone), and, if BP remains elevated, stepwise addition of antihypertensive drugs with complementary mechanisms of action to lower BP. If BP remains uncontrolled, referral to a hypertension specialist is advised.
Abstract
Renovascular disease (RVD) remains a major cause of secondary and treatment-resistant hypertension. Most cases are related either to fibromuscular or atherosclerotic lesions, but a variety ...of other causes including arterial dissection, stent occlusion, and embolic disease can produce the same syndrome. Recent studies emphasize the kidney’s tolerance to moderate flow reduction during antihypertensive drug therapy and the relative safety of medical therapy to control blood pressure. Several prospective trials in moderate RVD fail to identify major benefits from endovascular revascularization for moderate atherosclerotic disease. However, high-risk and progressive renovascular syndromes are recognized to be relatively refractory to medical therapy only and respond better to combining renal revascularization with ongoing medical therapy. Clinicians caring for complex hypertension should be familiar with pathogenic pathways, imaging techniques, and a rational approach to managing renovascular hypertension in the current era.
Renal artery disease produces a spectrum of progressive clinical manifestations ranging from minor degrees of hypertension to circulatory congestion and kidney failure. Moderate reductions in renal ...blood flow do not induce tissue hypoxia or damage, making medical therapy for renovascular hypertension feasible. Several prospective trials indicate that optimized medical therapy using agents that block the renin-angiotensin system should be the initial management. Evidence of progressive disease and/or treatment failure should allow recognition of high-risk subsets that benefit from renal revascularization. Severe reductions in kidney blood flow ultimately activate inflammatory pathways that do not reverse with restoring blood flow alone.
In response to the 2012 KDIGO (Kidney Disease: Improving Global Outcomes) guideline for blood pressure management in patients with chronic kidney disease not on dialysis, the National Kidney ...Foundation organized a group of US experts in hypertension and transplant nephrology to review the recommendations and comment on their relevancy in the context of current US clinical practice and concerns. The overriding message was the dearth of clinical trial evidence to provide strong evidence-based recommendations. For patients with CKD with normal to mildly increased albuminuria, goal blood pressure has been relaxed to ≤140/90 mm Hg for both diabetic and nondiabetic patients. In contrast, KDIGO continues to recommend goal blood pressure ≤130/80 mm Hg for patients with chronic kidney disease with moderately or severely increased albuminuria and for all renal transplant recipients regardless of the presence of proteinuria, without supporting data. The expert panel thought the KDIGO recommendations were generally reasonable but lacking in sufficient evidence support and that additional studies are greatly needed.
Renovascular disease remains among the most prevalent and important causes of secondary hypertension and renal dysfunction. Many lesions reduce perfusion pressure including fibromuscular diseases and ...renal infarction, but most are caused by atherosclerotic disease. Epidemiologic studies establish a strong association between atherosclerotic renal-artery stenosis (ARAS) and cardiovascular risk. Hypertension develops in patients with renovascular disease from a complex set of pressor signals, including activation of the renin–angiotensin system (RAS), recruitment of oxidative stress pathways, and sympathoadrenergic activation. Although the kidney maintains function over a broad range of autoregulation, sustained reduction in renal perfusion leads to disturbed microvascular function, vascular rarefaction, and ultimately development of interstitial fibrosis. Advances in antihypertensive drug therapy and intensive risk factor management including smoking cessation and statin therapy can provide excellent blood pressure control for many individuals. Despite extensive observational experience with renal revascularization in patients with renovascular hypertension, recent prospective randomized trials fail to establish compelling benefits either with endovascular stents or with surgery when added to effective medical therapy. These trials are limited and exclude many patients most likely to benefit from revascularization. Meaningful recovery of kidney function after revascularization is limited once fibrosis is established. Recent experimental studies indicate that mechanisms allowing repair and regeneration of parenchymal kidney tissue may lead to improved outcomes in the future. Until additional staging tools become available, clinicians will be forced to individualize therapy carefully to optimize the potential benefits regarding both blood pressure and renal function for such patients.
Management of renovascular hypertension Textor, Stephen C
Current opinion in cardiology,
2020-November, 2020-11-00, 20201101, Volume:
35, Issue:
6
Journal Article
Peer reviewed
PURPOSE OF REVIEWRenovascular occlusive disease remains a common cause of resistant and rapidly progressive hypertension. The present review summarizes current practice regarding management of ...renovascular hypertension (RVH).
RECENT FINDINGSCurrent data using blood oxygen level dependent MR emphasize the tolerance of the kidney to moderate reductions in blood flow and the efficacy of antihypertensive drug therapy for many individuals. Prospective trials have failed to identify benefits of revascularization for moderate disease, either regarding blood pressure or renal function. Antihypertensive drug therapy including renin-angiotensin system blockade is central to management of RVH. Recent and ongoing observational studies report important improvements after revascularization regarding blood pressure, management of refractory or ‘flash’ pulmonary edema, and survival in specific ‘high risk’ clinical populations not included in randomized trials. Research directions underscore the role of adjunctive measures, including mitochondrial protection, therapeutic angiogenesis, and cell-based regenerative repair to protect kidney function in RVH.
SUMMARYClinicians should recognize the potential for disease progression to threaten renal function with severe and prolonged renal ischemia. Improved patient selection for true resistant hypertension with RVH and ‘high-risk’ clinical manifestations is critical to identify those likely to benefit from renal revascularization.
Abstract
Hypertension may be the initial clinical presentation for at least 15 endocrine disorders. An accurate diagnosis of endocrine hypertension provides clinicians with the opportunity to render ...a surgical cure or to achieve an optimal clinical response with specific pharmacologic therapy. It is challenging for the clinician to know when and how to perform case-detection testing for all the endocrine disorders in which hypertension may be the presenting symptom. Herein, we review the different forms of endocrine hypertension, with a focus on prevalence, clinical presentation, guidance on when to perform case detection testing, and currently available case-detection tests.
Background Hypertension may be associated with renal cellular injury. Cells in distress release extracellular vesicles (EVs), and their numbers in urine may reflect renal injury. Cellular senescence, ...an irreversible growth arrest in response to a noxious milieu, is characterized by release of proinflammatory cytokines. We hypothesized that EVs released by senescent nephron cells can be identified in urine of patients with hypertension. Methods and Results We recruited patients with essential hypertension (EH) or renovascular hypertension and healthy volunteers (n=14 each). Renal oxygenation was assessed using magnetic resonance imaging and blood samples collected from both renal veins for cytokine-level measurements. EVs isolated from urine samples were characterized by imaging flow cytometry based on specific markers, including p16 (senescence marker), calyxin (podocytes), urate transporter 1 (proximal tubules), uromodulin (ascending limb of Henle's loop), and prominin-2 (distal tubules). Overall percentage of urinary p16+ EVs was elevated in EH and renovascular hypertension patients compared with healthy volunteers and correlated inversely with renal function and directly with renal vein cytokine levels. Urinary levels of p16
/urate transporter 1
were elevated in all hypertensive subjects compared with healthy volunteers, whereas p16
/prominin-2
levels were elevated only in EH versus healthy volunteers and p16
/uromodulin
in renovascular hypertension versus EH. Conclusions Levels of p16
EVs are elevated in urine of hypertensive patients and may reflect increased proximal tubular cellular senescence. In EH, EVs originate also from distal tubules and in renovascular hypertension from Henle's loop. Hence, urinary EVs levels may be useful to identify intrarenal sites of cellular senescence.
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