Contact Hours: 4
This educational activity is credited for 4 contact hours at completion of the activity.
Course Purpose
The purpose of this course is to provide healthcare providers with an overview of hypertension and end stage renal disease, exploring their definitions, underlying physiology, and the pathophysiology that connects them.
Overview
Often regarded in the medical community as a silent killer, recent data has revealed that uncontrolled hypertension is the primary reason for end-stage renal disease (ESRD), the last phase of chronic kidney disease. Understanding the link between hypertension and ESRD is crucial for healthcare professionals, not only for treatment but also for patient education, monitoring, and management. This course aims to provide an overview of hypertension and ESRD, exploring their definitions, underlying physiology, and the pathophysiology that connects them.
Course Objectives
Upon completion of this course, the learner will be able to:
- Define hypertension as described by The American College of Cardiology and the American Heart Association.
- Review the pathophysiology associated with hypertension, uncontrolled hypertension, and hypertensive crisis and their risk factors.
- Review the pathophysiology associated with end stage renal disease, and how disease progression can be influenced hypertension.
- Review dialysis types and transplant options for patients diagnosed with end stage renal disease.
- Comprehend antihypertensive medications commonly prescribed for patients with kidney failure.
Policy Statement
This activity has been planned and implemented in accordance with the policies of FastCEForLess.com.
Disclosures
Fast CE For Less, Inc and its authors have no disclosures. There is no commercial support.
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| Adrenaline | A hormone released from the adrenal glands and its major action, together with noradrenaline, is to prepare the body for ‘fight or flight’ during times of stress or danger. |
| Aldosterone | A steroid hormone made by the adrenal cortex (the outer layer of the adrenal gland). |
| Altruistic Donor (Non-Directed Donation) | A person who wishes to donate an organ to a person he or she does not know. |
| Aneurysm | An abnormal swelling or bulge in the wall of a blood vessel, such as an artery. |
| Angiotensin | A hormone that helps regulate blood pressure by constricting (narrowing) blood vessels and triggering water and salt (sodium) intake. |
| Angiotensin II Receptor Blockers (ARBs) | Also known as angiotensin II receptor antagonists, arbs are used to treat high blood pressure and heart failure. |
| Angiotensin-Converting Enzyme (ACE) Inhibitors | Medicines that help relax the veins and arteries to lower blood pressure. |
| Angiotensinogen | The only precursor of all angiotensin peptides. |
| Antidiuretic Hormone (ADH) | A hormone that helps blood vessels constrict and helps the kidneys control the amount of water and salt in the body. |
| Artery | A blood vessel in humans and most other animals that takes oxygenated blood away from the heart in the systemic circulation to one or more parts of the body. |
| Arteriolar Sclerosis | Any hardening (and loss of elasticity) of medium or large arteries. |
| Arteriole | A small-diameter blood vessel in the microcirculation that extends and branches out from an artery and leads to capillaries. |
| Arteriovenous Fistula (AVF) | An irregular connection between an artery and vein. |
| Atherosclerosis | Thickening or hardening of the arteries caused by a buildup of plaque in the inner lining of an artery. |
| Automated Peritoneal Dialysis (APD) | A home dialysis option that is done using a machine that fills the peritoneal cavity with fresh dialysis solution, and after a specified time, drains the solution with body waste and then fills the peritoneal cavity with new dialysis solution. |
| Baroreceptors | A type of mechanoreceptors allowing for relaying information derived from blood pressure within the autonomic nervous system. |
| Beta-Blocker | Drugs that can lower stress on the heart and blood vessels by blocking the action of adrenaline. |
| Biosensor | A device that measures biological or chemical reactions by generating signals proportional to the concentration of an analyte in the reaction. |
| Calcium Channel Blocker | A group of medications that limit cells’ use of calcium and treats high blood pressure and certain heart conditions. |
| Catecholamine | A monoamine neurotransmitter, an organic compound that has a catechol and a side-chain amine. |
| Central Venous Catheter (CVC) | A thin, flexible tube (catheter) that is placed into the large vein above the heart, usually through a vein in the neck. |
| Choroidopathy | A disease that causes fluid to build up under the retina. |
| Chronic Kidney Disease | Means a gradual loss of kidney function over time. |
| Congestive Heart Failure | A long-term condition that happens when the heart cannot pump blood well enough to give the body a normal supply. |
| Conn’s Syndrome | A condition that causes resistant high blood pressure. |
| Coronary Artery Disease (CAD) | A narrowing or blockage of the coronary arteries, which supply oxygen-rich blood to the heart. |
| Cortisol | A steroid hormone, in the glucocorticoid class of hormones and a stress hormone |
| Cushing’s Syndrome | A disorder that occurs when your body makes too much of the hormone cortisol over a long period of time. |
| Deceased Donor | The process of giving organs, corneas or tissues at the time of the donor’s death for the purpose of transplantation. |
| Dialysate | The part of a mixture which passes through the membrane in dialysis. |
| Dialysis-Related Amyloidosis | A disabling disease characterized by accumulation and tissue deposition of amyloid fibrils consisting of beta2-microglobulin (beta2-m) in the bone, periarticular structures, and viscera of patients with end-stage kidney disease. |
| Diastolic Pressure | The pressure in the arteries when the heart rests between beats. |
| Endothelin | A peptide (small protein) that helps regulate blood pressure by constricting (tightening) blood vessels. |
| Endothelium | A single layer of squamous endothelial cells that line the interior surface of blood vessels and lymphatic vessels. |
| Erythropoietin | A glycoprotein hormone, naturally produced by the peritubular cells of the kidney, that stimulates red blood cell production. |
| Fibrosis | Thickening or scarring of the tissue. |
| Gangrene | Death of body tissue due to a lack of blood flow or a serious bacterial infection. |
| Glomerular Filtration Rate (GFR) | A test used to check how well the kidneys are working. |
| Glomerular Hypertension | Increased mechanical stress affecting glomerular cells, including podocytes, mesangial, and endothelial cells. |
| Glomerulonephritis | Inflammation and damage to the filtering part of the kidneys (glomerulus). |
| Heart Failure | A lifelong condition in which the heart muscle can’t pump enough blood to meet the body’s needs for blood and oxygen. |
| Human Leukocyte Antigen (HLA) | Glycoproteins that reside on the surface of almost every cell in the body. |
| Hyalinosis | A condition characterized by hyalin degeneration. |
| Hyperkalemia | High potassium levels in the blood. |
| Hyperphosphatemia | An abnormally high serum phosphate level. |
| Hypertension (HTN) | A condition in which the blood vessels have persistently raised pressure. |
| Hypertensive Encephalopathy | A syndrome that is characterized by severe elevation of blood pressure, headache, visual disturbances, altered mental status, and convulsions. |
| Hypertensive Retinopathy | Retinal vascular damage caused by hypertension. |
| Hyperthyroidism | A condition in which the thyroid gland makes too much thyroid hormone. |
| Hypothyroidism | A condition where the thyroid gland doesn’t release enough thyroid hormone into the bloodstream. |
| Left Ventricular Hypertrophy (LVH) | A thickening of the wall of the heart’s main pumping chamber. |
| Living Donor | A person who is alive when they donate an organ, usually a kidney or a part of their liver. |
| Metabolic Acidosis | Characterized by an increase in the hydrogen ion concentration in the systemic circulation that results in an abnormally low serum bicarbonate level. |
| Metabolic Syndrome | A cluster of conditions that occur together, increasing the risk of heart disease, stroke and type 2 diabetes. |
| Myocardial Infarction | Caused by decreased or complete cessation of blood flow to a portion of the myocardium. |
| Nephron | The minute or microscopic structural and functional unit of the kidney. |
| Nitric Oxide | A gas formed by combining nitrogen and oxygen. |
| Non-Directed Donor | The donor does not name the specific person to get the transplant. |
| Non-Steroidal Anti-Inflammatory Drug (NSAID) | Medicines that are widely used to relieve pain, reduce inflammation, and bring down a high temperature. |
| Oxidative Stress | An imbalance of free radicals and antioxidants in your body that leads to cell damage. |
| Paired Exchange Transplant | Also known as paired donation, is an option that matches incompatible donor-recipient pairs with other pairs, and they “exchange” donors. |
| Peripheral Vascular Disease (PVD) | A slow and progressive circulation disorder caused by narrowing, blockage or spasms in a blood vessel. |
| Peripheral Vascular Resistance | The resistance in the circulatory system that is used to create blood pressure, the flow of blood and is also a component of cardiac function. |
| Peritoneal Dialysis | A treatment for kidney failure that uses the lining of the abdomen, or belly, to filter blood inside the body. |
| Peritonitis | A redness and swelling (inflammation) of the lining of the belly or abdomen. |
| Pheochromocytoma | A rare tumor that grows in an adrenal gland. |
| Polycystic Kidney Disease | An inherited disorder in which clusters of cysts develop primarily within the kidneys, causing them to enlarge and lose function over time. |
| Preemptive Transplantation | When transplantation is performed before initiation of maintenance dialysis. |
| Pruritis | A medical term that means itching. |
| Renal Artery Stenosis | The narrowing of one or more arteries that carry blood to the kidneys (renal arteries). |
| Renin | An enzyme made by special cells in the kidneys. |
| Renin-Angiotensin-Aldosterone System (RAAS) | A critical regulator of blood volume, electrolyte balance, and systemic vascular resistance. |
| Resistant Hypertension | Blood pressure that remains above 140/90 mmHg despite optimal use of three antihypertensive medications. |
| Retina | A layer of photoreceptors cells and glial cells within the eye that captures incoming photons and transmits them along neuronal pathways as both electrical and chemical signals for the brain to perceive a visual picture. |
| Retinal Detachment | An emergency in which a thin layer of tissue (the retina) at the back of the eye pulls away from the layer of blood vessels that provides it with oxygen and nutrients. |
| Secondary Hyperparathyroidism | Occurs when the parathyroid glands become enlarged and release too much parathyroid hormone (PTH), causing a high blood level of PTH. |
| Sympathetic Nervous System | The network of nerves behind the “fight-or-flight” response. |
| Systolic Pressure | The pressure that blood pushes against the artery walls when the heart beats. |
| Transient Ischemic Attack | A short period of symptoms like those of a stroke. |
| Uncontrolled Hypertension | A condition where blood pressure remains persistently elevated above 140/90 mmHg despite the use of antihypertensive medications, diet changes, and lifestyle modifications. |
| Uremic Frost | A manifestation of severe azotemia where tiny, yellow-white urea crystals deposit on the skin, resulting in a frosted appearance as sweat evaporates. |
| Vascular Dementia | A decline in thinking skills caused by conditions that block or reduce blood flow to various regions of the brain. |
| Vascular Hypertrophy | An early finding in essential hypertension and is related to arterial pressure waveform contour. |
| Vascular Smooth Muscle | A type of smooth muscle that contracts and regulates blood vessel tone, blood pressure and blood flow. |
| Vasoconstrictor | The narrowing (constriction) of blood vessels by small muscles in their walls. |
| Vasodilator | Medicines that open, also called dilate, blood vessels. |
| Β2-Microglobulin Protein | A protein in blood that is filtered by the kidneys. |
Hypertension is a rampant health condition that affects millions of people worldwide. According to the World Health Organization, approximately 1.39 billion of the world’s adult population, aged 30-79 years, have hypertension. In the US, approximately 116 million individuals have hypertension.25 Often regarded in the medical community as a silent killer, recent data shows uncontrolled hypertension is the primary reason for end-stage renal disease (ESRD), the last phase of chronic kidney disease. The National Kidney Foundation estimates that nearly 750,000 Americans are living with ESRD.1 Hypertension occurs in 35% of patients with stage 1 CKD, 48% of stage 2, 59% of stage 3, and 84% of patients with stage 4-5 CKD.29 The incidence continues to rise, posing a substantial burden on healthcare systems. Understanding the link between hypertension and ESRD is crucial for healthcare professionals, not only for treatment but also for patient education, monitoring, and management. This course aims to provide an overview of hypertension and ESRD, exploring their definitions, underlying physiology, and the pathophysiology that connects them.
Hypertension (HTN), or high blood pressure as it is more commonly known, is a chronic medical condition characterized by elevated pressure exerted by the blood against the walls of arteries. It is typically measured by two values:26.
- Systolic pressure – The force when the heart contracts and pumps blood.
- Diastolic pressure – The pressure in the arteries when the heart is at rest between beats.
The American College of Cardiology and the American Heart Association define hypertension as stage 1 and stage 2. Stage 1 hypertension has either systolic pressure measuring at 130 – 139 mmHg, diastolic pressure measuring at 80 -89 mmHg, or both measures being consistently in this range. Stage 2 hypertension presents with either a systolic pressure of 140 mmHg or more, a diastolic pressure of 90 mmHg or more, or both.
Hypertension is caused by the complex interaction of several physiological systems, including the cardiovascular, endocrine, and renal systems.12 In the cardiovascular system, an increase in peripheral vascular resistance is the key mechanism behind hypertension. This is primarily due to structural or functional changes in the small arteries and arterioles. Structural changes limit the volume of blood that can flow through at a time and involve the thickening of the vessel walls and/or narrowing of the central cavity, such as the vessel lumen. 7 These structural changes may be caused by:
- Vascular hypertrophy, which is caused by smooth muscle cells within the blood vessel walls becoming enlarged to handle the increased stress, and to maintain vascular tone.
- Vascular hyperplasia, which involves the heightened proliferation of smooth muscle cells, contributing to the thickening of the vessel walls.
- Increased collagen deposition.
- Increased deposition of extracellular matrix components such as collagen.
This leads to fibrosis, which further thickens and stiffens the arteries, reducing their elasticity and increasing peripheral vascular resistance.
Functional changes in the smaller arteries and arterioles play a crucial role in the development and maintenance of hypertension. These changes involve alterations in the normal function and responsiveness of the vascular smooth muscle cells and the endothelium, which lines the interior surface of blood vessels to vasoconstrictors (substances that cause the narrowing of blood vessels) and vasodilators (substances that cause the widening of blood vessels). These functional changes typically include.21
- Endothelial dysfunction.
- Increased sympathetic nervous system activity.
- Altered calcium handling in vascular smooth muscle cells.
Endothelial dysfunction is a key factor in hypertension, and one major component of this dysfunction is the diminished production of nitric oxide (NO) by the endothelium.21 A potent vasodilator, nitric oxide relaxes blood vessels and reduces vascular resistance. In patients with hypertension, the production of nitric oxide is often diminished, which impairs the ability of blood vessels to dilate and increases peripheral resistance. Concurrently, the endothelium may increase its production of endothelin, a powerful vasoconstrictor. Elevated levels of endothelin in hypertensive patients lead to further narrowing of blood vessels, resulting in elevated blood pressure. Oxidative stress may also play a part in increasing reactive oxygen species in the vasculature. These molecules degrade nitric oxide and further impair endothelial function, promoting vasoconstriction and inflammation.
Increased sympathetic nervous system activity also leads to the functional changes that cause hypertension.21 The sympathetic nervous system regulates blood vessel constriction, and heightened activity can lead to prolonged vasoconstriction. This can cause elevated heart rate and increased cardiac output which can contribute to high blood pressure. In a hypertensive state, the baroreceptors, biosensors that detect changes in blood pressure and help regulate it, are prone to “reset” to a higher threshold. This resetting means the baroreceptors may tolerate higher blood pressure levels without triggering compensatory mechanisms to lower the blood pressure. Changes in calcium levels also plays a part in hypertension, because the contraction of vascular smooth muscle depends largely on intracellular calcium levels. In hypertensive patients, more calcium may enter smooth muscle cells, or sensitivity to calcium may be heightened, resulting in sustained vasoconstriction. The balance between vasodilatory and vasoconstrictive influences is shifted towards increased constriction, raising peripheral resistance and contributing to elevated blood pressure.
Considering the many renal processes, research has shown that the dysregulation of the renin-angiotensin-aldosterone system (RAAS) is crucial in hypertension. The renin-angiotensin-aldosterone system is a vital hormone system that regulates fluid balance and blood pressure in the body.14 In normal function, the kidneys release an enzyme called renin in response to several stimuli, including low blood pressure, low sodium concentration in the distal tubules of the kidney, and sympathetic nervous system activity.8 Renin has two chief functions. First, it acts on angiotensinogen, a protein produced by the liver, transforming it into angiotensin I, then angiotensin II, an effective vasoconstrictor that also stimulates the release of antidiuretic hormone (ADH). Antidiuretic hormone helps increase blood volume by reducing the amount of water excreted by the kidney. Second, renin stimulates the release of aldosterone from the adrenal glands, promoting sodium and water retention by the kidneys. Combined, these pathways work together to increase blood volume and pressure. However, when the RAAS experiences enhanced activity, as seen in hypertension, levels of angiotensin II increase abnormally, contributing to additional vascular constriction. In addition, heightened levels of aldosterone escalate sodium and water reabsorption in the kidneys, expanding blood volume and raising blood pressure. Excess aldosterone can also cause vascular remodeling and fibrosis, which further contributes to hypertension.
Uncontrolled hypertension is a condition where blood pressure remains persistently elevated above 140/90 mmHg despite the use of antihypertensive medications, diet changes, and lifestyle modifications.10 There are several factors that can contribute to uncontrolled hypertension, including unhealthy lifestyle habits, inadequate treatment, poor adherence to prescribed antihypertensive medications, and resistant hypertension, which results in elevated blood pressure despite treatment with multiple antihypertensive medications. This resistance may be caused by underlying medical conditions that elevate high blood pressure, such as kidney disease, adrenal gland disorders, or thyroid disorders.6 Conditions such as polycystic kidney disease, chronic kidney disease, renal artery stenosis, and glomerulonephritis can lead to secondary hypertension by affecting the kidneys’ ability to regulate blood pressure and fluid balance. Disorders of the adrenal glands, such as Conn’s syndrome, Cushing’s syndrome, pheochromocytoma, and adrenal hyperplasia, affect the production of hormones that regulate blood pressure, such as aldosterone, cortisol, and adrenaline, and may lead to hypertension. Thyroid disorders, including hyperthyroidism and hypothyroidism, can also influence blood pressure regulation. In hyperthyroidism, an overactive thyroid produces excessive thyroid hormone, which increases heart rates, and consequently, blood pressure. Hypothyroidism caused by an underactive thyroid can lead to fluid retention and increased peripheral resistance.
Risks Associated with Uncontrolled Hypertension
Uncontrolled hypertension, or persistently high blood pressure that is not effectively managed poses significant risks to numerous body systems, including the cardiovascular, neurological, ocular, metabolic, endocrine, and renal systems.23
Cardiovascular risks include left ventricular hypertrophy (LVH), coronary artery disease (CAD), peripheral vascular disease (PVD), heart failure, and aneurysm.13 Left ventricular hypertrophy occurs as a result of persistent high blood pressure that forces the heart to work harder to pump blood. Over time, the increased workload causes the left ventricle, the heart’s main pumping chamber, to thicken and stiffen, making it unable to pump blood efficiently. In CAD, hypertension accelerates the process of atherosclerosis, where arteries become clogged with fatty deposits (plaques). Narrowed coronary arteries cut back the blood flow to the heart, raising the risk of angina, myocardial infarction, and sudden cardiac death. If this narrowing and hardening of vessels extends to the peripheral arteries, it can reduce blood flow to limbs (especially the legs). This is known as peripheral vascular disease, and it causes pain and numbness. In severe cases, PVD can lead to tissue death (gangrene) that must be amputated.
Uncontrolled chronic hypertension eventually leads to heart failure, where the heart cannot pump blood efficiently. The increased resistance in the blood vessels requires the heart to exert more effort, eventually weakening and dilating the heart muscle, leading to heart failure.31 Aneurysms are swellings in the blood vessel wall that can rupture and cause life-threatening internal bleeding. They often arise as a result of blood vessel walls weakened by constant high blood pressure. Common sites include the aorta (aortic aneurysm) and the brain (cerebral aneurysm). Neurological Risks of hypertension include strokes, transient ischemic attacks, cognitive decline, and dementia.35 Hypertension is the foremost risk factor for stroke, with a likelihood of 90% in hypertensive men and 70% in hypertensive women.20 Strokes may be hemorrhagic, where bleeding is seen in or around the brain, or ischemic, where blood clots block blood to the brain. The increased pressure can also cause vulnerable blood vessels in the brain to rupture.
Transient ischemic attacks, also known as “mini-stroke,” are temporary periods of stroke-like symptoms and occur when blood flow is briefly interrupted to part of the brain. These attacks are warning signs of future strokes. Uncontrolled hypertension can give way to cognitive decline and dementia.32 Vascular dementia results from reduced blood to the brain, essentially depriving brain cells of oxygen and nutrients. High blood pressure can also cause small vessel disease, leading to white matter lesions and microinfarcts that cumulatively impair cognitive function.
Ocular risks of hypertension include hypertensive retinopathy and choroidopathy.23 Chronic hypertension can damage the blood vessels in the light-sensitive tissue at the back of the eye, known as the retina. This leads to conditions called hypertensive retinopathy, which is characterized by blurred vision, double vision, and sudden loss of vision if not managed. Choroidopathy results from excessive fluid buildup under the retina. It may cause retinal detachment and vision loss. Metabolic and endocrine risks of hypertension include metabolic syndrome and adrenal disorders.11 Hypertension is often associated with metabolic syndrome, a cluster of conditions including insulin resistance, hyperglycemia, and dyslipidemia. These conditions increase the risk of developing type-2 diabetes. The combination of diabetes and hypertension also significantly raises the risk of more serious cardiovascular and renal complications. Chronic hypertension can exacerbate adrenal gland dysfunctions, triggering the adrenal glands to produce excess aldosterone. Conversely, conditions like primary aldosteronism, which have a similar effect, can lead to secondary hypertension.9 Renal risks of hypertension include chronic kidney disease and end-stage renal disease.18 Chronic high blood pressure damages the renal blood vessels, diminishing their ability to effectively filter waste from the blood. This can lead to the kidneys gradually losing their function. In severe cases, complete loss of function may occur.
Management of Hypertensive Crisis
A hypertensive crisis refers to a severe elevation in blood pressure that poses an immediate threat to organ function and patient health.19 It is characterized by systolic blood pressure readings greater than 180 mmHg, diastolic blood pressure readings greater than 120 mmHg, or both.30 Hypertensive crises are classified into two categories: 19
- Hypertensive urgency
- Hypertensive emergency
Hypertensive urgency is severely elevated blood pressure without acute end-organ damage. Patients may experience symptoms such as severe headaches, shortness of breath, or anxiety. While hypertensive urgency requires prompt medical attention and blood pressure management, it does not typically necessitate immediate hospitalization. Hypertensive emergency, also known as malignant hypertension, is severely elevated blood pressure with acute end-organ damage. This often includes symptoms such as chest pain, dyspnea, confusion, visual disturbances, neurological deficits, or signs of organ damage such as acute kidney injury, hypertensive encephalopathy, or acute heart failure. Hypertensive emergencies require urgent, management and hospitalization to prevent further damage to organs and life-threatening complications.
For a patient presenting with a hypertensive crisis, the chief goal of treatment is to reduce blood pressure to reduce the risk of organ damage.19 However, this must be done gradually over hours to days rather than abruptly, as rapid reductions may precipitate ischemic events or dysfunction. Intravenous antihypertensive medications, such as nitroglycerin, labetalol, nicardipine, or sodium nitroprusside, are often titrated to achieve controlled blood pressure reduction. During management, it is critical to identify and treat underlying causes contributing to the hypertensive crisis. This may include addressing factors such as medication non-adherence, renal artery stenosis, acute kidney injury, preeclampsia/eclampsia, illicit drug use, or exacerbation of chronic medical conditions. As such, additional interventions may be indicated. This may include supplemental oxygen, diuretics, antiplatelet agents, anticoagulation, seizure prophylaxis, or renal replacement therapy in cases of acute kidney injury or fluid overload. The patient’s vital signs, together with cardiac rhythm, respiratory rate, oxygen saturation, neurological status, urine output, and laboratory parameters, are monitored closely throughout management. Continuous cardiac monitoring and frequent neurologic assessments help detect and manage complications such as myocardial ischemia, arrhythmias, stroke, or seizures.
End-stage renal disease (ESRD) is the final phase of chronic kidney disease. 18 In ESRD, the nephrons, the functional elements of the kidneys responsible for filtration, have suffered extensive damage and have lost nearly all their ability to maintain the body’s balance of fluids, electrolytes, and waste product function. Clinically, the glomerular filtration rate (GFR) in ESRD is less than 15 mL/min/1.73 m² as compared to the normal range of 90–120 mL/min/1.73 m2.15 Renal ultrasound, complete blood count (CBC), urinalysis, basic metabolic panel (BMP), and kidney biopsy are also used to confirm ESRD. At this stage, the kidneys are unable to efficiently excrete potassium, which results in hyperkalemia. The kidneys are also unable to excrete phosphate, which results in hyperphosphatemia. The kidneys cannot balance sodium or water, leading to retention, thus elevating blood pressure further and causing edema. All these impairments create a vicious cycle, which further accelerates the loss of kidney function.
With declining GFR, the remaining nephrons compensate by hyperfiltration, which increases the pressure within the glomeruli (glomerular hypertension), leading to further damage and sclerosis of structures.15 Chronic injury to the nephrons also affects the renal tubules and interstitial tissue, resulting in fibrosis and the accumulation of extracellular matrix proteins. The elevated levels of proteins disrupt the architecture and function of the renal tissue, exacerbating kidney failure. In ESRD, the kidneys cannot execute their secondary functions, which include regulating blood pressure through the RAAS-producing erythropoietin, a hormone that stimulates red blood cell production and vitamin D conversion to its active form, calcitriol, which helps calcium absorption.
Damage to the kidneys is typically caused by underlying conditions, most commonly hypertension, diabetes, and proteinuria, as well as chronic issues such as glomerulonephritis, polycystic kidney disease, and prolonged obstruction of the urinary tract.3 Prolonged dehydration, use of nephrotoxins like non-steroidal anti-inflammatory drugs (NSAIDs), and smoking can also cause renal injury. Patients with ESRD exhibit symptoms such as severe fatigue, edema, shortness of breath, and uremia; the accumulation of waste products in the blood.15 Without effective treatments like dialysis or kidney transplantation, these imbalances can lead to severe metabolic disturbances, cardiovascular complications, and ultimately death.3
Chronic hypertension is the second most common cause of both chronic kidney disease and failure.5 The precise pathophysiology of kidney damage induced by hypertension involves various mechanisms.6 The sustained elevation of blood pressure places excessive strain on the delicate structures of the kidneys, inducing alterations in the renal vasculature.4 This includes arteriolar sclerosis, hyalinosis, and fibrosis, all of which compromise the blood flow to the nephrons and impair their ability to effectively filter waste products and regulate fluid balance. Prolonged elevation of blood pressure also disrupts the intricate network of blood vessels within the kidneys, leading to a cascade of pathological changes that progressively diminish renal function. Hypertension causes increased intraglomerular pressure, which leads to glomerular hypertrophy, hyperfiltration, and increased glomerular injury. Hypertension-induced activation of the renin-angiotensin-aldosterone system (RAAS) and sympathetic nervous system exacerbates renal damage by promoting inflammation, oxidative stress, and fibrosis within the renal parenchyma. If left uncontrolled, the pathological processes collectively contribute to the development of hypertensive nephropathy, culminating in end-stage renal failure.
Consequences of Kidney Failure
Kidney failure has widespread effects on the body and can lead to serious metabolic, cardiovascular, hematologic, gastrointestinal, and neurological complications.15 Failing kidneys are unable to excrete excess fluid, leading to swelling in the face, ankles, legs, and feet. If left untreated, severe fluid retention can cause pulmonary edema, which impairs breathing. Essential electrolytes like sodium, potassium, and calcium become imbalanced, increasing to life-threatening levels. For example, hyperkalemia (elevated potassium) can lead to cardiac arrhythmias and sudden death. The kidney’s inability to excrete hydrogen ions and reabsorb bicarbonate can lead to metabolic acidosis. This condition results in fatigue, confusion, and difficulty breathing. Cardiovascular complications are also prevalent in kidney failure. Hypertension is a frequent problem as the kidneys aid in blood pressure regulation.18 Not only do the kidneys control the fluid balance of the circulatory system, but they also produce critical hormones via the RAAS.
Chronic fluid overload and hypertension increase the workload on the heart, potentially leading to left ventricular hypertrophy and congestive heart failure. Uremia and dysregulated mineral metabolism accelerate atherosclerosis and the calcification of blood vessels, heightening the risk of myocardial infarction and stroke.18 Hematologic issues arise due to decreased production of erythropoietin by diseased kidneys, leading to anemia. This causes fatigue, weakness, and decreased oxygen delivery to tissues. Uremic toxins can impair platelet function, coagulation pathways, and immune function, increasing the risk of bleeding, bruising, and infection. Gastrointestinal problems, such as nausea, vomiting, and loss of appetite, are common due to the accumulation of waste products irritating the gastrointestinal tract, leading to poor nutrient absorption and malnutrition.3 Neurological effects may include peripheral neuropathy, where uremic toxins damage peripheral nerves, and causes tingling, numbness, and weakness in the limbs. Severe uremia can cause cognitive impairment, difficulty concentrating, and confusion. In extreme cases, severe uremia can cause seizures and coma.18 Dermatologic manifestations may also be present. In advanced kidney failure, conditions such as pruritus (itchy skin) and uremic frost, where crystallized urea deposits on the skin, are also seen. Endocrine dysfunctions like hyperphosphatemia contribute to secondary hyperparathyroidism and the decreased activation of vitamin D, which can lead to bone pain, fractures, and vascular calcification.
As kidney failure progresses to end-stage renal disease, prompt and comprehensive interventions are needed to sustain and improve quality of life. Treatment options include kidney transplantations and dialysis.15 While kidney transplantation typically yields better patient outcomes, most patients are treated with dialysis.24
Kidney Transplantation
Kidney transplantation involves the surgical implantation of a healthy kidney from a biocompatible donor into the recipient’s body, effectively replacing the failed kidneys and restoring renal function.15 There are several transplant options available for individuals with ESRD. These include deceased donor transplants, living donor transplants, paired exchange transplants, preemptive transplantation, and non-directed or altruistic donor transplants.17 Deceased donor kidney transplantation involves the retrieval of kidneys from individuals who have died and consented to organ donation. The kidneys are typically procured from those who have suffered brain death but have otherwise healthy kidneys. Deceased donor transplants are allocated based on a variety of factors, including recipient compatibility, organ availability, and waiting list priority. Living donor kidney transplantation involves the donation of a kidney from a living individual, often a family member or friend. Both the recipient and the donor will be able to maintain fluid balance, electrolyte homeostasis, acid-base balance, and waste excretion with a single healthy kidney. Living donor transplants offer several advantages over deceased donor transplants, including shorter wait times, better graft survival rates, and potentially superior long-term outcomes.
In cases where a potential living donor is incompatible with the intended recipient due to blood type or human leukocyte antigen (HLA) mismatch, paired exchange transplantation offers a solution.27 In a paired exchange, incompatible donor-recipient pairs are matched with other pairs in a kidney exchange program, allowing for compatible matches to be made and transplants to proceed. Paired exchange programs aim to maximize the number of kidney transplants performed while ensuring optimal donor-recipient compatibility. Preemptive transplantation refers to kidney transplantation performed before initiating dialysis. Preemptive transplantation offers several benefits. It preserves the residual renal function, avoids dialysis-related complications, and improves post-transplant outcomes. However, candidates must undergo comprehensive medical evaluations to assess their suitability. Non-directed or altruistic donor transplantation involves a kidney donation by an individual who is not biologically related to the recipient and does not specify a particular recipient for the donated organ. While kidney transplantation offers freedom from dialysis, it comes with certain risks, such as surgical complications, organ rejection, and the need for lifelong immunosuppressive therapy to prevent rejection.
Dialysis Types
There are two forms of dialysis:4
- Hemodialysis
- Peritoneal dialysis
Hemodialysis uses a specialized dialysis machine to filter both waste and excess fluid from the blood through vascular access.2 Common access sites include arteriovenous fistulas (AVFs), arteriovenous grafts (AVGs), and central venous catheters (CVCs). The patient is connected to a hemodialysis machine via two needles inserted into the vascular access site: one for blood withdrawal (arterial needle) and the other for blood return (venous needle). Blood flows from the patient’s vascular access through the arterial needle into the dialyzer, where it is exposed to the dialysis solution (dialysate) and undergoes filtration.
The dialysate is carefully tailored to mimic the electrolyte and acid-base balance of normal plasma.22 It is composed of specific electrolyte concentrations and has a controlled pH. Dialysate is prepared using sterile water and specialized dialysis solutions containing sodium, potassium, bicarbonate, and calcium, among other components. Within the dialyzer, blood and dialysate flow in opposite directions, creating a concentration gradient that promotes the diffusion of solutes, such as urea, creatinine, and electrolytes, across the semipermeable membrane. 2 Excess fluid is removed from the blood through the process of ultrafiltration, driven by hydrostatic pressure gradients across the membrane. Hemodialysis sessions typically last three to five hours and are performed three times a week to maintain adequate fluid balance and clearance of waste products. However, the duration and frequency of hemodialysis may vary based on individual patient characteristics, residual kidney function, and treatment goals.
Complications of hemodialysis include hypotension, hemodynamic instability, vascular access complications, and dialysis-related amyloidosis. 2 Rapid fluid removal during hemodialysis can lead to intravascular volume depletion and hypotension, resulting in symptoms such as dizziness, nausea, and muscle cramps. Hemodialysis-induced shifts in electrolyte concentrations, particularly potassium, can predispose patients to cardiac arrhythmias and hemodynamic instability. Complications associated with vascular access include infection, thrombosis, stenosis, and aneurysm formation. Vigilant monitoring and appropriate intervention is necessary to optimize access function and longevity. Long-term exposure to dialysis membranes and repeated inflammatory responses can lead to the accumulation of β2-microglobulin protein fragments in the joints and soft tissues, resulting in dialysis-related amyloidosis and musculoskeletal complications. Despite potential issues, hemodialysis remains a vital and lifesaving therapy for individuals with ESRD, providing symptomatic relief and prolonging survival while awaiting kidney transplantation, or as a long-term renal replacement option.
Peritoneal dialysis utilizes the peritoneal membrane lining the abdominal cavity as a semipermeable membrane for solute exchange and fluid removal.34 Prior to initiating peritoneal dialysis, a soft, flexible catheter is surgically embedded into the abdominal cavity, typically through a small incision in the lower abdomen. The catheter serves as the conduit for the introduction and drainage of dialysate into and out of the peritoneal cavity. In the inflow phase, dialysate is infused into the peritoneal cavity through the catheter. The volume and composition of the dialysis fluid are predetermined based on individual patient health needs and treatment goals. The dialysate remains within the peritoneal cavity for a specified period, during which solutes and fluid move across the peritoneal membrane – waste products and toxins from the bloodstream diffuse into the dialysate, while electrolytes and other solutes are exchanged to maintain osmotic balance. Once the exchange is complete, the dialysate is drained from the peritoneal cavity via the catheter. Peritoneal dialysis may be performed manually, with exchanges conducted by the patient or caregiver multiple times daily, or via automated peritoneal dialysis (APD) using a mechanical cycler device that automates dialysis exchanges overnight while the patient sleeps.
Peritoneal dialysis offers advantages such as flexibility, preservation of remaining renal function, and avoidance of vascular access-related complications, making it a preferred option for select individuals with ESRD. However, it comes with its own complications, including peritonitis, exit-site infection, hernias, and fluid overload.34 Peritonitis is the inflammation of the peritoneal membrane following bacterial contamination. It represents a serious and potentially life-threatening complication of peritoneal dialysis. Prompt recognition and treatment with antimicrobial therapy is essential to mitigate the risk of peritonitis-associated morbidity and mortality. Infections at the catheter exit site, including cellulitis and tunnel infections, can occur following peritoneal catheter placement, necessitating meticulous catheter care and adherence to sterile technique during dialysis exchanges. Chronic intra-abdominal pressure fluctuations associated with peritoneal dialysis may predispose patients to the development of abdominal wall hernias, necessitating surgical intervention in severe cases. Inadequate ultrafiltration or excessive fluid intake during peritoneal dialysis exchanges can lead to fluid overload. This manifests as peripheral edema, hypertension, and a heightened risk of heart failure.
Antihypertensive medications commonly prescribed for patients with kidney failure include angiotensin-converting enzyme (ACE) inhibitors, angiotensin II receptor blockers (ARBs), calcium channel blockers, beta-blockers, and diuretics.28 Angiotensin-converting enzyme inhibitors, such as lisinopril and enalapril, inhibit angiotensin I conversion to angiotensin II, leading to vasodilation and decreased aldosterone secretion. They are particularly beneficial in patients with kidney failure due to their renoprotective effects, meaning they slow the progression of proteinuria and renal disease. Angiotensin II receptor blockers, such as valsartan and losartan, block the action of angiotensin II at its receptor sites, resulting in vasodilation and decreased aldosterone release. Like ACE inhibitors, ARBs offer renoprotective benefits and are commonly used as alternative antihypertensive agents in patients who are intolerant of ACE inhibitors or with contraindications to their use.
Calcium channel blockers, including amlodipine and diltiazem, inhibit the inflow of calcium ions into vascular smooth muscle cells.28 This causes vasodilation and reduces peripheral vascular resistance. Calcium channel blockers are often preferred for those with simultaneous coronary artery disease or peripheral vascular disease. Beta-blockers, such as metoprolol and carvedilol, antagonize the effects of catecholamines on beta-adrenergic receptors, resulting in decreased heart rate and myocardial contractility. While beta-blockers are less commonly used as first-line agents in patients with kidney failure, they may be indicated in those with coexisting cardiovascular conditions, such as heart failure or ischemic heart disease. Diuretics, such as furosemide and hydrochlorothiazide, inhibit sodium reabsorption in the renal tubules, thereby decreasing their levels in the bloodstream. They are often used adjunctively with other antihypertensive medications to achieve blood pressure control and mitigate volume overload in patients with kidney failure and fluid retention.
In patients with kidney failure, the use of antihypertensive medications can lead to drug accumulation and toxicity.36 Dosages may need to be adjusted frequently based on estimated GFR and creatinine clearance. Careful monitoring is also crucial because diuretics can alter electrolyte balance and predispose patients to hyperkalemia, hypokalemia, hyponatremia, and hypercalcemia, which can cause several complications. Patients with kidney failure often have multiple comorbidities, such as diabetes mellitus, hyperlipidemia, and cardiovascular disease, and may be taking medications to manage these conditions. Antihypertensive medications may interact with other medications, especially if they include phosphate binders, erythropoiesis-stimulating agents, or immunosuppressants. It is crucial that healthcare professionals take potential medication interactions into account and tailor treatment plans accordingly to achieve optimal outcomes.
Once OCD behaviors are eliminated or considerably reduced following an initial course of medication and psychotherapy, long-term management focuses on maintenance treatment to keep the gains achieved during active treatment, and prevent relapse.4 This is especially important because OCD is a chronic disorder, and relapse is common. Healthcare providers recommend monthly follow-up visits for at least the first six months after completing a successful course of treatment. The follow-up care should continue for at least one year before considering the discontinuation of medications or psychotherapy. Regular monitoring is critical for tracking symptom severity, insight, and functional impairment over time, allowing for timely intervention if symptoms worsen or relapse occurs. For a majority of individuals, continued psychotherapy is beneficial, though the frequency of sessions depends on the individual’s progress, stability, and ongoing need for support. Whether individualized or in a group setting, maintaining psychotherapy sessions can help individuals maintain the skills learned during active treatment, reinforce adaptive coping strategies, and address any residual symptoms or triggers.
Long-term management also involves healthcare providers adjusting medication dosages or changing medications based on individual response and tolerability.18 In some cases, individuals may experience noteworthy improvement in symptoms or achieve stable remission while on medication. In such instances, healthcare providers may consider gradually discontinuing medication. The general protocol for medication discontinuation involves reducing dosages by 25% at a time, with waiting periods of two months to monitor responses before further adjustments. A gradual approach helps minimize the risk of relapse and allows healthcare providers to closely monitor individuals for signs of symptom recurrence. However, for individuals who experience repeated episodes of OCD, such as 2 to 4 severe relapses or 3 to 4 milder relapses, long-term or even lifelong medication management may be necessary to prevent symptom exacerbation and maintain stability.
Adopting a healthy lifestyle can expressively contribute to long-term well-being.7 Regular exercise has been shown to reduce symptoms of anxiety and depression, which often coexists with OCD. Adequate sleep is vital for overall mental health, as sleep disturbances can exacerbate symptoms of OCD. Stress management practices such as deep breathing, mindfulness meditation, and relaxation exercises can help individuals cope with the anxiety and distress associated with OCD. Maintaining a balanced diet rich in nutrients also supports brain function and overall well-being. Engaging in meaningful activities, hobbies, and social connections can also play a vital role in managing OCD symptoms. Participating in deeds that bring joy and fulfillment can provide a sense of purpose and accomplishment, thereby reducing obsessive thoughts and compulsive behaviors. Social support from friends, family, or support groups can offer emotional support, encouragement, and understanding, which are invaluable in navigating the challenges of living with OCD. Distracting oneself from obsessive thoughts through enjoyable activities and interactions can help break the cycle of rumination and alleviate distress.
Family involvement plays a crucial role in the long-term management of OCD in children.21,23 Parents and caregivers should be actively engaged in a child’s treatment, participating in therapy sessions, implementing behavioral interventions at home, ensuring medication regimens are followed, and providing emotional support. Encouraging children to maintain a healthy lifestyle can support their overall well-being and help manage OCD symptoms. This includes promoting regular exercise, adequate sleep, nutritious eating habits, and stress-reduction techniques. Collaborating with school personnel is important to create a supportive environment for children. School accommodations, such as modified assignments, extra time for tasks, and access to support services can help children manage their symptoms effectively while participating in school activities. A child’s needs and experiences with OCD are known to change frequently over time, requiring flexibility and adaptation in their treatment approach. Healthcare providers should regularly reassess the child’s progress and modify treatment strategies accordingly to ensure continued symptom management and overall well-being.
When caring for patients with hypertension and end-stage renal disease (ESRD), nurses play a crucial role in providing holistic care to promote optimal health outcomes and quality of life.25 Nursing considerations encompass various aspects of care, including coordination, treatment management, continuous assessments, patient education, and support. Given the complex nature of both these conditions, nurses work closely with interdisciplinary healthcare team members, such as cardiologists, nephrologists, dietitians, and social workers, to develop plans tailored to each patient’s needs. Nurses facilitate referrals to specialty services, such as transplant evaluation and rehabilitation, as indicated by the patient’s condition. For hospitalized patients with ESRD or in hypertensive crisis, nurses ensure the timely administration of prescribed medications and monitor for signs of intolerance, adverse effects, and drug interactions, especially with nephrotoxic medications.33 Nurses routinely assess renal function, fluid and electrolyte balance, vital signs, and overall health status. This includes monitoring laboratory values such as serum creatinine, blood urea nitrogen (BUN), electrolytes, and urine output to identify any potential complications. Nurses also monitor for signs and symptoms of fluid overload, electrolyte imbalances, hypertension, anemia, and other issues commonly associated with ESRD. Assessments are crucial for early detection and intervention to promote optimal health outcomes for patients with ESRD.
Nurses are central to educating and supporting patients undergoing hemodialysis or peritoneal dialysis.16 This involves providing comprehensive education on proper dialysis techniques, self-care measures, and infection prevention strategies to empower patients in managing their treatment effectively. In patients receiving hemodialysis, nurses regularly evaluate vascular access sites for any signs of infection, thrombosis, or dysfunction to prevent complications and ensure the longevity of access. During dialysis sessions, nurses monitor vital signs closely and gauge the likelihood of potential complications such as hypotension, muscle cramps, or access site bleeding. They must intervene promptly as needed to maintain patient safety and optimize treatment outcomes. Nutritional support is another component of care for patients with both hypertension and renal disease. Nurses collaborate closely with dietitians to develop personalized dietary plans that align with each patient’s unique requirements and restrictions, considering factors such as sodium, potassium, phosphorus, and protein intake limitations. Nurses educate patients on the importance of adhering to a heart-healthy, renal-friendly diet, emphasizing its significance in managing their condition effectively. This includes providing guidance on meal planning, portion control, and reading food labels to help patients make informed and healthy dietary choices.
Nurses engage in comprehensive education efforts, ensuring patients and their families comprehend the underlying reasons for hypertension and ESRD, available treatment options, self-care measures, and strategies for managing both conditions. 16 Nurses also provide information on lifestyle modifications, emphasizing the benefits of exercise, smoking cessation, and moderation of alcohol intake. Nurses reinforce the importance of medication adherence, educating patients on proper dosage, potential side effects, and the significance of attending regular follow-up appointments, and offer counseling and emotional support, lending a compassionate ear and fostering a therapeutic environment. They facilitate connections to support groups or mental health professionals when necessary, ensuring patients have access to additional resources. By encouraging open communication, nurses give patients the space to voice concerns, preferences, and goals regarding treatment and care. This, in turn, enables patients to be actively involved in decision-making processes, thereby promoting patient autonomy and a sense of control.
Examining the connection between hypertension and end-stage renal disease (ESRD) reveals a compelling cycle of mutual influence. Hypertension not only stands as a precursor to ESRD, but when uncontrolled, further damages the delicate structures of the kidney. This perpetuates the progression of kidney failure, which in turn exacerbates hypertension, accelerating the deterioration of health and increasing the likelihood of a hypertensive crisis. In navigating this complex scenario, it is critical to intervene effectively and break this cycle to forge a path toward controlled blood pressure and improved kidney function. While treatment avenues exist, ranging from antihypertensive medications to dialysis and transplantation, they are limited in their effectiveness and carry substantial risks. Ultimately, a collaborative effort of dedicated healthcare providers becomes indispensable. Through constant vigilance and swift actions, healthcare providers can provide expertise and support to optimize well-being and quality of life for those affected.
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