eMedicine Specialties > Nephrology > Hypertension and the Kidney

Hypertension: Follow-up

Author: Sat Sharma, MD, FRCPC, Professor and Head, Division of Pulmonary Medicine, Department of Internal Medicine, University of Manitoba; Site Director, Respiratory Medicine, St. Boniface General Hospital
Coauthor(s): Claude Kortas, MD, Program Director, Associate Professor, Department of Medicine, University of Western Ontario, Canada
Contributor Information and Disclosures

Updated: Aug 6, 2008

Follow-up

Further Inpatient Care

  • Hypertensive crisis: Hypertensive crisis rarely occurs and is characterized by extremely high blood pressure, diastolic pressure usually exceeding 130 mm Hg, and evidence of potentially life-threatening end organ dysfunction. The clinical conditions associated with hypertensive crisis include hypertensive encephalopathy, extreme hypertension with acute pulmonary edema, extreme hypertension with acute aortic dissection, extreme hypertension with intracerebellar hemorrhage, extreme hypertension with an acute myocardial infarction, and malignant hypertension. Hypertensive crisis should be differentiated from very high blood pressure without evidence of acute, severe end organ dysfunction.
  • Malignant hypertension: Malignant hypertension may or may not be associated with clinical conditions present in hypertensive crisis. A patient with malignant hypertension always has retinal papilledema and flame-shaped hemorrhages and exudates. Other clinical features of malignant hypertension may include encephalopathy, confusion, left ventricular failure, intravascular coagulation, and impaired renal function, with hematuria and weight loss. The pathological hallmark of malignant hypertension is fibrinoid necrosis of the arterioles, which occurs systemically, but specifically in the kidneys. These patients develop fatal complications if untreated, and more than 90% will not survive beyond 1-2 years.
  • Treatment of hypertensive crisis consists of the acute reduction of blood pressure using aggressive pharmacological therapy, followed by maintenance therapy with oral medications.
    • Sodium nitroprusside is a commonly used medication. It is a short-acting agent, and the blood pressure response can be titrated from minute to minute. However, patients must have constant monitoring in an intensive care unit. The potential exists for thiocyanate and cyanide toxicity with prolonged use or if the patient has renal or hepatic failure.
    • Diazoxide may also be used in hypertensive crisis. Small boluses of 100 mg are administered every 5 minutes, as indicated. Diazoxide is not preferred with concomitant congestive heart failure or low cardiac output.
    • Labetalol, an alpha- and beta-blocking agent, has proven to be quite beneficial in the treatment of patients with hypertensive emergencies. Labetalol is particularly preferred in patients with acute dissection. Boluses of 10-20 mg may be administered, or the drug may be infused at 1 mg/min until the desired blood pressure is obtained. Once an adequate blood pressure level is obtained, oral hypertensive therapy should be initiated, and patients are gradually weaned from parenteral agents.
    • Clevidipine, a dihydropyridine calcium channel blocker, is administered intravenously for rapid and precise blood pressure reduction. Clevidipine is rapidly metabolized in the blood and tissues and does not accumulate in the body. Initiate IV infusion at 1-2 mg/h; titrate the dose at short intervals (ie, 90 seconds) initially by doubling the dose. As blood pressure approaches its goal, increase the dose by less than double and lengthen the time between dose adjustments to every 5-10 minutes. An approximately 1- to 2-mg/h increase produces an additional 2- to 4-mm Hg decrease in systolic pressure. Typically, the therapeutic response is achieved with 4-6 mg/h, although severe hypertension may require higher doses. Most patients have received maximum doses of 16 mg/h or less; experience is limited with short-term dosing as high as 32 mg/h. Because of lipid load restrictions, do not exceed 1000 mL or an average of 21 mg/h within a 24-hour period; experience is limited with use beyond 72 hours.

Further Outpatient Care

  • Interventions can be used to improve the control of blood pressure in patients with hypertension.
    • Various interventions can be implemented to treat uncontrolled hypertension. These interventions include the following: (1) self-monitoring, (2) educational interventions directed to the patient, (3) educational interventions directed to the health professional, (4) health professional (nurse or pharmacist)–led care, (5) organizational interventions that aim to improve the delivery of care, and (6) appointment reminder systems.
    • The Cochrane Collaboration has shown that these interventions are associated with large net reductions in blood pressure and that health professional (nurse or pharmacist)–led care may be a promising way of delivering care. Their recommendations include that family practices and community-based clinics should have an organized system of regular follow-up and review of their patients with hypertension. Antihypertensive drug therapy should be implemented by means of a vigorous stepped care approach when patients do not reach target blood pressure levels.

Deterrence/Prevention

  • A comprehensive strategy for reduction in mortality and morbidity from hypertension must include prevention strategies, earlier detection, and adequate treatment. Ideally, a population strategy should be used in order to lower blood pressure in the community. More intensive efforts are required to lower blood pressure in high-risk population groups, which include individuals with a family history of hypertension, black ancestry, obesity, excessive sodium consumption, physical inactivity, and/or alcohol consumption. Even a small reduction in blood pressure confers significant health benefits. A 2-mm Hg reduction in diastolic pressure is estimated to decrease the risk of stroke by 15% and the risk of coronary heart disease by 6%.
  • Prevention of hypertension may be achieved by the following interventions:
    • Weight control
    • Increased physical activity
    • Moderated sodium and alcohol intake
    • Increased potassium intake
    • A dietary pattern rich in fruits and vegetables and low-fat meat, fish, and dairy products

Complications

  • Central nervous system - Intracerebral hemorrhage, lacunar infarcts, encephalopathy, thrombotic stroke, transient ischemic attack
  • Ophthalmologic - Fundal hemorrhages, exudates, papilledema
  • Cardiac - LVH, congestive heart failure, angina pectoris, myocardial infarction
  • Vascular - Aortic dissection, diffuse arthrosclerosis
  • Renal - Nephrosclerosis, renal artery stenosis

Prognosis

  • Most individuals diagnosed with hypertension will have increasing blood pressure as they age.
  • Untreated hypertension is notorious for increasing the risk of mortality and is often described as a silent killer.
  • Mild-to-moderate hypertension, if left untreated, is associated with a risk of atherosclerotic disease in 30% of people and organ damage in 50% of people after only 8-10 years of onset.

Patient Education

  • Hypertension is a lifelong disorder. For optimal control, a long-term commitment to lifestyle modifications and pharmacological therapy is required. Therefore, repeated in-depth patient education and counseling not only improve compliance with medical therapy but also reduce cardiovascular risk factors.
  • Various strategies to decrease cardiovascular disease risk include the following:
    • Prevention and treatment of obesity
    • Appropriate amounts of aerobic physical activity
    • Diets low in salt, total fat, and cholesterol
    • Adequate dietary intakes of potassium, calcium, and magnesium
    • Limited alcohol consumption
    • Avoidance of cigarette smoking
  • For excellent patient education resources, visit eMedicine's Diabetes Center and Cholesterol Center. Also, see eMedicine's patient education articles High Blood Pressure, High Cholesterol, Chest Pain, Coronary Heart Disease, and Heart Attack.

Miscellaneous

Medicolegal Pitfalls

  • Hypertension is one of the most common modifiable risk factors for atherosclerotic disease.
  • According to the JNC VI enrollment report, only 53% of patients with hypertension are being treated in the United States. Of these, only 27% have adequately controlled blood pressure, and only 45% of treated patients have a blood pressure less than 140/90 mm Hg.
  • Despite an array of pharmaceutical agents to treat hypertension, JNC VI recommends diuretics and beta-blockers as the preferred initial agents because of proven efficacy and lower cost.
  • Patients with hypertension should be identified and staged based on blood pressure determinations and cardiovascular risk and the presence or absence of target organ damage.
  • JNC VI recommends lower target blood pressure goals in 2 select populations: (1) patients with diabetes mellitus (blood pressure <130/85 mm Hg) and (2) patients with renal disease (blood pressure <130/85 mm Hg; if urinary protein is >1 g/d, a blood pressure <125/75 mm Hg).
  • Malignant hypertension is a medical emergency and requires hospitalization and urgent therapy. The blood pressure should be reduced rapidly, but diastolic blood pressure should be maintained at approximately 95 mm Hg.

Special Concerns

  • Renovascular hypertension is likely the curable form of secondary hypertension. The causes of renovascular hypertension include atherosclerosis, fibromuscular dysplasia, coarctation of the aorta, embolic renal artery occlusion, aneurysm of the renal artery, and diffuse arteritis. Additionally, causes of diffuse bilateral renal ischemia, such as accelerated hypertension, vasculitis, hepatitis B, and intravenous drug abuse, may also lead to hypertension. Although the true incidence of renovascular hypertension is not known, an incidence of 1% is estimated in patients with hypertension.3 In hypertensive individuals who had one or more clinical features known to be associated with renovascular hypertension, 24% had renal artery stenosis and 14% had renovascular hypertension.4 This study also demonstrated that renovascular hypertension is more common in the white population (18%) than in the black population (9%).
    • A workup for renovascular hypertension should be recommended for patients who meet the following criteria:
      • Recent onset of moderate-to-severe hypertension
      • Sudden unexplained exacerbation of preexisting hypertension
      • Hypertension associated with an abdominal bruit
      • Onset of hypertension in a young patient (<30 y)
      • Severe hypertension resistant to pharmacologic management
      • Deterioration of renal function following treatment for hypertension
    • The workup for renovascular hypertension is recommended only in patients in whom further interventional therapy, such as angioplasty or surgery, is feasible and will be pursued.
    • Digital subtraction angiography (DSA) is performed following intravenous contrast injection to detect the abdominal aorta and its branches. The radioisotope renogram may be performed as a screening test, but renal arteriography is required for definitive diagnosis. Duplex ultrasonography of the renal arteries has a sensitivity of greater than 90% for both the presence and degree of renal disease.5 Renography using iodohippurate sodium I 131 or technetium TC 99m diethylenetriamine pentaacetic acid after administration of the oral ACE inhibitor captopril can identify right ventricular hypertrophy with about 80% sensitivity and specificity.
    • Appropriate management of patients with bilateral or unilateral renal artery stenosis and significant renal dysfunction is controversial. Correction of stenosis may not result in improvement of renal function or reduction in blood pressure because renal dysfunction and hypertension may be caused by renal parenchymal disease. Recent studies have shown only a modest improvement in blood pressure control in medication reduction and in significant improvement in renal function following percutaneous transluminal renal angioplasty.
  • Pheochromocytoma is an infrequent cause of hypertension, but cure often is possible with surgical therapy. The incidence is not known, but up to 0.1% of individuals with hypertension may have these lesions. Pheochromocytomas are chromaffin cell tumors, which arise mainly in the adrenal medulla, symptomatic ganglia, and paraganglia along the symptomatic chain. Up to 80-90% of pheochromocytomas are found in one or both adrenal glands. Most patients with pheochromocytoma have headache, sweating, or palpitations. Hypertension may be sustained or paroxysmal. Patients may manifest nervousness, nausea, vomiting, weight loss, and funduscopic changes of hypertension. Headaches are paroxysmal, throbbing, and bilateral. Sweating is quite profuse and generalized. Palpitations are due to the concomitant tachycardia.
    • The workup of pheochromocytoma includes measurement of urinary catecholamines and their metabolites. Urinary excretion of metanephrine, normetanephrine, free catecholamines, and vanillylmandelic acid can be performed. Measurement of catecholamines increases the sensitivity from 70-90%, compared to measuring metanephrine alone. When an abnormal value is detected by metanephrine or vanillylmandelic acid assay, measurement of free catecholamines should be performed to confirm the diagnosis.
    • Once the diagnosis of pheochromocytoma is confirmed by chemical analysis, the precise location and extent of the tumor is assessed with an imaging study. An abdominal CT scan often allows localization of the tumor, but the absence of a lesion on CT scan requires adrenal venous sampling or exploratory laparotomy. Initial stabilization is with medical therapy. Surgical resection is required because up to 10% of tumors may be malignant. In difficult cases, plasma, catecholamine assays, and a clonidine suppression test may be used. In normal and essential hypertension, clonidine suppresses plasma norepinephrine levels. An inability to suppress catecholamines may indicate pheochromocytoma; however, the sensitivity and specificity of this test is not known.
  • Mineralocorticoid-induced hypertension: Mineralocorticoid excess secondary to primary aldosteronism is infrequently observed and is characterized by excessive production of aldosterone. Renal sodium retention, kaliuresis, hypokalemia, and hypochloremic metabolic alkalosis are the common manifestations. These patients develop increased intravascular volume, resulting in hypertension. The blood pressure increase may vary from mild hypertension to marked elevation in primary aldosteronism. Patients may have underlying adenoma or hyperplasia of the adrenal gland and rarely have an extra-adrenal source for aldosterone.
  • Oral contraceptive–associated hypertension: The most common form of secondary hypertension is an endocrine cause: oral contraceptive use. Activation of the renin-angiotensin-aldosterone system is the likely mechanism because hepatic synthesis of angiotensinogen is induced by the estrogen component of oral contraceptives. Approximately 5% of women prescribed oral contraceptives may develop hypertension, which abates within 6 months of discontinuation. The risk factors for oral contraceptive–associated hypertension include mild renal disease, familial history of essential hypertension, age greater than 35 years, and obesity.
  • For the patient who has hypertension and is hypokalemic, a 24-hour urine specimen should be collected for sodium and potassium measurement. If the urine sodium level is more than 100 mmol/L and urine potassium is less than 30 mmol/L, aldosteronism is unlikely. If urinary potassium exceeds 30 mmol/L, the patient should have PRA measured. If the PRA is high, the likely causes are estrogen therapy, renovascular hypertension, malignant hypertension, or salt-wasting renal disease. In the presence of low PRA, the serum aldosterone level can be measured. A low aldosterone level indicates licorice ingestion or other mineralocorticoid ingestions. A high aldosterone level indicates primary aldosteronism. A CT scan may identify the presence of an adenoma. In the absence of CT scan findings, differentiating hyperplastic aldosteronism from adenoma is often difficult.
  • Recent advances in understanding of the regulation of blood pressure and pathophysiologic events that result in hypertension have led to the development of new classes of drugs. These agents are in various stages of development and include the following:
    • Vasopressin antagonists
    • Compounds to enhance the effects of endogenous vasodilators (eg, natriuretic peptides)
    • Endothelin antagonists
    • Renin inhibitors
    • Antagonists of the angiotensin receptors: Several of these have already been marketed.
    • T-calcium ion channel–selective antagonists
 


More on Hypertension

Overview: Hypertension
Differential Diagnoses & Workup: Hypertension
Treatment & Medication: Hypertension
Follow-up: Hypertension
References
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Further Reading

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Contributor Information and Disclosures

Author

Sat Sharma, MD, FRCPC, Professor and Head, Division of Pulmonary Medicine, Department of Internal Medicine, University of Manitoba; Site Director, Respiratory Medicine, St. Boniface General Hospital
Sat Sharma, MD, FRCPC is a member of the following medical societies: American Academy of Sleep Medicine, American College of Chest Physicians, American College of Physicians-American Society of Internal Medicine, American Thoracic Society, Canadian Medical Association, Royal College of Physicians and Surgeons of Canada, Royal Society of Medicine, Society of Critical Care Medicine, and World Medical Association
Disclosure: Nothing to disclose.

Coauthor(s)

Claude Kortas, MD, Program Director, Associate Professor, Department of Medicine, University of Western Ontario, Canada
Claude Kortas, MD is a member of the following medical societies: American Society of Nephrology, College of Physicians and Surgeons of Ontario, Ontario Medical Association, and Royal College of Physicians and Surgeons of Canada
Disclosure: Nothing to disclose.

Medical Editor

L Michael Prisant, MD, FACC, Director of Hypertension and Clinical Pharmacology Unit, Professor of Medicine, Department of Medicine, Medical College of Georgia
L Michael Prisant, MD, FACC is a member of the following medical societies: American College of Cardiology, American College of Chest Physicians, American College of Clinical Pharmacology, American College of Forensic Examiners, American College of Physicians, American Heart Association, and American Medical Association
Disclosure: Abbott Grant/research funds Investigator; Boehringer-Ingelheim Grant/research funds Other; Eli Lilly None Investigator; Novartis None Investigator; Abbott, Boehringer-Ingelheim, Forest, Gilead, Merck, Merck/Schering-Plough, Novartis, Oscient, Sciele, SunTech Medical Consulting fee Consulting; Abbott, Boehringer-Ingelheim, Merck, Merck/Schering-Plough, Novartis, Oscient Honoraria Speaking and teaching

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

George R Aronoff, MD, Director, Professor, Departments of Internal Medicine and Pharmacology, Section of Nephrology, Kidney Disease Program, University of Louisville School of Medicine
George R Aronoff, MD is a member of the following medical societies: American Federation for Medical Research, American Society of Nephrology, Kentucky Medical Association, and National Kidney Foundation
Disclosure: Nothing to disclose.

CME Editor

Rebecca J Schmidt, DO, FACP, FASN, Professor of Medicine, Section Chief, Department of Medicine, Section of Nephrology, West Virginia University School of Medicine
Rebecca J Schmidt, DO, FACP, FASN is a member of the following medical societies: American College of Osteopathic Internists, American College of Physicians, American Medical Association, American Society of Nephrology, International Society of Nephrology, National Kidney Foundation, Renal Physicians Association, and West Virginia State Medical Association
Disclosure: Abbott Grant/research funds Speaking and teaching; Genzyme Honoraria Consulting; Roche Honoraria Consulting

Chief Editor

Vecihi Batuman, MD, FACP, FASN, Professor of Medicine, Section of Nephrology-Hypertension, Tulane University School of Medicine; Chief, Medicine Service, Southeast Louisiana Veterans Health Care System
Vecihi Batuman, MD, FACP, FASN is a member of the following medical societies: American College of Physicians, American Society of Hypertension, American Society of Nephrology, and International Society of Nephrology
Disclosure: Nothing to disclose.

 
 
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