This educational activity is credited for 4 contact hours at completion of the activity.
The purpose of this course is to provide healthcare providers with a comprehensive overview of hypertension and end-stage renal disease, including their definitions, physiological foundations, and the pathophysiological mechanisms linking the two conditions.
Commonly referred to as a silent killer, uncontrolled hypertension has emerged as the leading cause of end-stage renal disease (ESRD), the final stage of chronic kidney disease. Recognizing the connection between hypertension and ESRD is essential for healthcare professionals in delivering effective treatment, as well as educating, monitoring, and managing patients. This course offers an overview of both conditions, examining their definitions, core physiological concepts, and the pathophysiological processes that link them.
Upon completion of this course, the learner will be able to:
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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 widespread condition impacting a significant portion of the global population. The World Health Organization reports that an estimated 1.39 billion adults aged 30 to 79 are affected worldwide. In the United States, around 116 million individuals are currently living with hypertension.25 Referred to as a silent killer within the medical field, recent findings confirm that uncontrolled hypertension is the leading cause of end-stage renal disease (ESRD), the final stage of chronic kidney disease. According to the National Kidney Foundation, approximately 750,000 Americans are living with ESRD.1 The prevalence of hypertension increases with CKD progression, affecting 35% of patients in stage 1, 48% in stage 2, 59% in stage 3, and 84% in stages 4 to 5.29 These numbers are steadily increasing, presenting a significant strain on healthcare systems. Recognizing the connection between hypertension and ESRD is essential for healthcare providers, as it supports effective treatment, education, and long-term disease management. This course offers an overview of hypertension and ESRD, including their definitions, physiological foundations, and the underlying pathophysiological mechanisms linking the two conditions.
Hypertension (HTN), commonly known as high blood pressure, is a chronic condition characterized by elevated force exerted by circulating blood on the walls of the arteries. This pressure is measured using two key values:26
Systolic pressure – The force exerted when the heart contracts and pumps blood through the arteries.
Diastolic pressure – The pressure maintained in the arteries when the heart relaxes between beats.
According to the American College of Cardiology and the American Heart Association, hypertension is defined by two stages. Stage 1 is identified when the systolic reading is consistently between 130 and 139 mmHg, the diastolic reading is between 80 and 89 mmHg, or both. Stage 2 occurs when systolic pressure reaches 140 mmHg or higher, diastolic pressure is 90 mmHg or above, or both measurements meet these criteria.
The causes of hypertension involve a complex interplay between the cardiovascular, endocrine, and renal systems.12 Within the cardiovascular system, elevated peripheral vascular resistance serves as the central mechanism. This resistance arises from structural and functional changes in small arteries and arterioles. Structurally, blood vessels undergo narrowing and thickening, which limits blood flow.7 These changes may include:
Vascular hypertrophy, where smooth muscle cells in vessel walls enlarge in response to increased stress, aiding in the maintenance of vascular tone.
Vascular hyperplasia, characterized by excessive growth of smooth muscle cells, contributing to wall thickening.
Increased deposition of collagen.
Enhanced accumulation of extracellular matrix components like collagen.
These alterations contribute to fibrosis, further stiffening the arteries and decreasing their elasticity, which increases peripheral resistance.
Functional changes in small vessels also play a significant role in hypertension. These changes involve altered responses of the endothelium and vascular smooth muscle cells to substances that either constrict (vasoconstrictors) or widen (vasodilators) blood vessels. Functional changes include:21
Endothelial dysfunction.
Increased activity of the sympathetic nervous system.
Disruptions in calcium regulation in vascular smooth muscle cells.
A key feature of endothelial dysfunction in hypertension is the reduced production of nitric oxide (NO),21 a potent vasodilator. Inadequate nitric oxide levels limit vessel dilation and elevate vascular resistance. Additionally, the endothelium may produce increased levels of endothelin, a strong vasoconstrictor, which further exacerbates vessel narrowing and raises blood pressure. Oxidative stress contributes by increasing reactive oxygen species, which degrade nitric oxide and impair endothelial function, promoting both vasoconstriction and inflammation.
Overactivity of the sympathetic nervous system further drives hypertension.21 This system controls vessel constriction, and its heightened activity leads to prolonged narrowing, elevated heart rate, and increased cardiac output. In hypertensive individuals, baroreceptors—sensors that detect and help regulate blood pressure—may reset to a higher pressure threshold, decreasing their sensitivity and allowing elevated blood pressure to persist unchecked. Altered calcium dynamics also contribute, as vascular smooth muscle contraction relies heavily on intracellular calcium. In hypertensive states, increased calcium influx or heightened cellular sensitivity to calcium promotes sustained contraction and vessel constriction, driving up peripheral resistance.
The renal system also plays a major role, particularly through dysfunction of the renin-angiotensin-aldosterone system (RAAS). This hormonal system regulates blood pressure and fluid balance.14 Under normal conditions, the kidneys release renin in response to low blood pressure, decreased sodium in the kidney tubules, or sympathetic stimulation.8 Renin’s functions include:
Converting angiotensinogen (a liver-produced protein) into angiotensin I, then into angiotensin II—a powerful vasoconstrictor that also stimulates antidiuretic hormone (ADH) release. ADH conserves water by reducing urinary excretion, increasing blood volume.
Stimulating aldosterone release from the adrenal glands, which promotes sodium and water reabsorption in the kidneys, contributing to increased blood volume and pressure.
In hypertension, RAAS is often hyperactive, resulting in abnormally high angiotensin II levels, which amplify vasoconstriction. Elevated aldosterone levels also drive increased sodium and water retention, further expanding blood volume and raising pressure. Chronic aldosterone elevation contributes to vascular fibrosis and remodeling, further exacerbating high blood pressure.
Uncontrolled hypertension is defined as persistently elevated blood pressure exceeding 140/90 mmHg despite adherence to antihypertensive medication regimens, dietary modifications, and lifestyle changes.10 Several contributors can lead to poor blood pressure control, including unhealthy habits, suboptimal treatment regimens, medication noncompliance, and resistant hypertension—a condition in which blood pressure remains high despite treatment with three or more antihypertensive drugs. This resistance may stem from secondary conditions that interfere with blood pressure regulation, such as kidney disorders, adrenal dysfunction, or thyroid abnormalities.6 Conditions like polycystic kidney disease, chronic kidney disease, renal artery stenosis, and glomerulonephritis disrupt the kidneys’ ability to regulate blood volume and pressure, often resulting in secondary hypertension. Adrenal gland disorders such as Conn’s syndrome, Cushing’s syndrome, pheochromocytoma, and adrenal hyperplasia influence hormone production (aldosterone, cortisol, adrenaline) involved in blood pressure regulation. Similarly, thyroid disorders—including hyperthyroidism and hypothyroidism—affect blood pressure levels. Hyperthyroidism accelerates heart rate and raises pressure, while hypothyroidism can lead to increased fluid retention and vascular resistance.
Risks Associated with Uncontrolled Hypertension
If left unmanaged, uncontrolled hypertension can cause widespread damage across multiple organ systems, notably the cardiovascular, neurological, ocular, endocrine, metabolic, and renal systems.23
Cardiovascular consequences include left ventricular hypertrophy (LVH), coronary artery disease (CAD), peripheral vascular disease (PVD), congestive heart failure, and aneurysms.13 LVH arises when prolonged high blood pressure forces the heart to work harder, thickening the muscle of the left ventricle. This leads to reduced pumping efficiency. CAD progresses when hypertension accelerates atherosclerosis—the buildup of fatty plaques in coronary arteries—restricting blood flow and increasing the risk of angina, heart attacks, and sudden death. Similarly, PVD occurs when narrowed arteries limit blood flow to extremities, often causing pain or numbness in the legs. In advanced cases, tissue death (gangrene) may occur, necessitating amputation.
Persistent high blood pressure also contributes to heart failure by overworking the heart muscle, which eventually weakens and dilates.31 Aneurysms, or abnormal bulges in weakened vessel walls, are another consequence. They can rupture and cause fatal internal bleeding, most commonly occurring in the aorta or brain. Neurologically, hypertension raises the risk of strokes, transient ischemic attacks (TIAs), cognitive impairment, and dementia.35 It is the leading risk factor for stroke, accounting for up to 90% of strokes in hypertensive men and 70% in hypertensive women.20 Stroke types include ischemic (blood flow blockage) and hemorrhagic (bleeding in the brain). High pressure may rupture delicate brain vessels, causing hemorrhages.
TIAs, or mini-strokes, result from temporary interruptions in cerebral blood flow. Though symptoms are short-lived, they indicate a heightened risk for future strokes. Hypertension also contributes to vascular dementia by limiting cerebral blood supply.32 Chronic small vessel damage may result in microinfarcts and white matter lesions, gradually leading to cognitive decline.
Ocular effects include hypertensive retinopathy and choroidopathy.23 Chronic elevation of blood pressure damages retinal vessels, leading to hypertensive retinopathy, characterized by blurry or double vision, and in advanced cases, sudden vision loss. Choroidopathy, due to fluid accumulation beneath the retina, may lead to detachment and impaired vision. Metabolic and endocrine risks include metabolic syndrome and adrenal abnormalities.11 Hypertension is frequently linked with metabolic syndrome—a group of conditions such as insulin resistance, high blood sugar, and dyslipidemia—which significantly raise the risk of type 2 diabetes. In turn, diabetes worsens cardiovascular and renal outcomes. Chronic hypertension may also overstimulate adrenal glands, prompting excess aldosterone secretion. Disorders like primary aldosteronism similarly cause secondary hypertension.9
Renal risks include chronic kidney disease (CKD) and end-stage renal disease (ESRD).18 High blood pressure injures the renal vasculature over time, diminishing the kidneys’ ability to filter waste and maintain fluid balance. As damage progresses, complete kidney failure may result.
Management of Hypertensive Crisis
A hypertensive crisis involves a sudden and severe elevation in blood pressure that endangers organ function.19 This condition is defined by systolic pressure exceeding 180 mmHg or diastolic pressure above 120 mmHg.30 Hypertensive crises fall into two categories:19
Hypertensive urgency
Hypertensive emergency
In hypertensive urgency, blood pressure is severely elevated but without signs of organ damage. Symptoms may include headache, shortness of breath, or anxiety. Although hospitalization may not be necessary, prompt treatment is required to lower pressure safely. A hypertensive emergency, or malignant hypertension, involves elevated blood pressure accompanied by acute end-organ injury. Symptoms may include chest pain, altered consciousness, shortness of breath, neurological deficits, or vision disturbances. Target organs at risk include the brain (e.g., stroke), heart (e.g., ischemia or failure), kidneys (e.g., acute injury), and eyes. This form of crisis requires immediate hospitalization and urgent blood pressure control.
The treatment goal in hypertensive crisis is gradual reduction of blood pressure to prevent or limit further organ damage.19 Rapid reduction is avoided to prevent ischemia or hypoperfusion. Intravenous antihypertensives such as nitroglycerin, nicardipine, labetalol, or sodium nitroprusside may be administered and titrated accordingly. Identifying and addressing the root cause is vital. Contributing factors may include poor medication adherence, renal artery stenosis, kidney injury, preeclampsia, drug use, or chronic disease exacerbation. Additional supportive measures may be required, such as oxygen therapy, diuretics, anticoagulants, antiplatelet agents, seizure prophylaxis, or dialysis in cases involving renal impairment or fluid overload.
Continuous monitoring of vital signs, urine output, respiratory status, cardiac rhythm, neurological function, and relevant labs is essential during crisis management. Regular cardiac and neurologic assessments help detect complications like arrhythmias, myocardial ischemia, seizures, or stroke.
End-stage renal disease (ESRD) represents the terminal stage of chronic kidney disease.18 At this point, nephrons—the kidney’s filtration units—are extensively damaged and have lost nearly all capacity to regulate fluid, electrolyte, and waste elimination. Clinically, ESRD is defined by a glomerular filtration rate (GFR) of less than 15 mL/min/1.73 m², in contrast to the normal GFR of 90–120 mL/min/1.73 m².15 Diagnosis is supported by renal ultrasound, complete blood count (CBC), urinalysis, basic metabolic panel (BMP), and kidney biopsy. The inability of the kidneys to excrete potassium leads to hyperkalemia, while phosphate accumulation results in hyperphosphatemia. Impaired sodium and water handling contributes to fluid retention, hypertension, and peripheral edema. These disturbances form a cycle of dysfunction, accelerating renal deterioration.
As GFR declines, surviving nephrons attempt to compensate through hyperfiltration, which increases intraglomerular pressure—a phenomenon known as glomerular hypertension—further damaging glomerular structures and promoting sclerosis.15 Ongoing nephron injury also affects renal tubules and the surrounding interstitium, inducing fibrosis and an overaccumulation of extracellular matrix proteins. These changes disrupt the kidney’s structure and function, leading to worsening renal impairment. In advanced ESRD, secondary renal functions are also lost. These include regulation of blood pressure via the renin-angiotensin-aldosterone system (RAAS), erythropoietin production for red blood cell synthesis, and conversion of vitamin D to its active form, calcitriol, which is essential for calcium absorption.
ESRD is most commonly the result of chronic conditions such as hypertension, diabetes mellitus, and proteinuria. Other contributing factors include glomerulonephritis, polycystic kidney disease, and long-term urinary tract obstructions.3 Additional risk factors include prolonged dehydration, exposure to nephrotoxic agents such as non-steroidal anti-inflammatory drugs (NSAIDs), and tobacco use. Individuals with ESRD frequently present with symptoms such as profound fatigue, generalized edema, dyspnea, and uremia—a condition marked by toxic waste buildup in the bloodstream.15 Without interventions like dialysis or renal transplantation, patients are at risk of life-threatening metabolic imbalances, cardiovascular complications, and mortality.3
Chronic hypertension ranks as the second leading cause of chronic kidney disease and kidney failure.⁵ The underlying pathophysiology of hypertension-induced kidney damage encompasses a variety of mechanisms.⁶ Persistent high blood pressure exerts sustained stress on the kidneys’ delicate vascular system, resulting in structural changes such as arteriolar sclerosis, hyalinosis, and fibrosis.⁴ These alterations impair perfusion to the nephrons, limiting their ability to filter waste and manage fluid balance efficiently. Long-term elevation in blood pressure compromises the kidney’s vascular architecture, initiating a chain of pathological events that gradually reduce renal function. Elevated intraglomerular pressure from hypertension contributes to glomerular hypertrophy, increased filtration activity, and subsequent injury to the glomeruli. Activation of the renin-angiotensin-aldosterone system (RAAS) and the sympathetic nervous system further worsens renal injury through inflammation, oxidative stress, and fibrotic changes in renal tissue. If hypertension remains unregulated, these cumulative effects lead to hypertensive nephropathy and ultimately end-stage renal disease.
Consequences of Kidney Failure
The systemic consequences of kidney failure are far-reaching and affect numerous body systems, resulting in serious metabolic, cardiovascular, hematologic, gastrointestinal, and neurological issues.¹⁵ When the kidneys fail to eliminate excess fluids, patients may develop edema in areas such as the face, lower extremities, and ankles. In severe cases, fluid buildup may progress to pulmonary edema, which hinders respiratory function. The kidneys’ inability to maintain proper electrolyte levels leads to imbalances—particularly in sodium, potassium, and calcium—that can reach dangerous levels. Hyperkalemia, for example, may cause life-threatening cardiac arrhythmias. Additionally, the failure to excrete hydrogen ions and reabsorb bicarbonate contributes to metabolic acidosis, manifesting as fatigue, confusion, and respiratory distress. Cardiovascular issues are especially prominent, with hypertension remaining a consistent concern due to the kidneys’ central role in regulating fluid volume and blood pressure.¹⁸ The kidneys also produce hormones vital to this regulation through the RAAS pathway.
Prolonged fluid retention and persistent hypertension increase cardiac workload, potentially resulting in left ventricular hypertrophy and congestive heart failure. Mineral metabolism disturbances and the buildup of uremic toxins contribute to accelerated vascular calcification and atherosclerosis, raising the risk of heart attacks and strokes.¹⁸ Hematological complications stem from reduced erythropoietin production, which causes anemia—marked by low red blood cell counts and symptoms like fatigue and decreased tissue oxygenation. Uremia also interferes with platelet function and coagulation, leading to increased susceptibility to bleeding, bruising, and infection. Gastrointestinal symptoms, including nausea, vomiting, and appetite loss, are common as retained toxins irritate the GI tract and hinder nutrient absorption, increasing the risk of malnutrition.³ Neurological consequences include peripheral neuropathy, characterized by numbness, tingling, or weakness due to nerve damage from toxins. Severe uremia may impair cognitive functions, causing memory issues, confusion, or even seizures and coma in extreme cases.¹⁸
Dermatological signs of advanced kidney failure may include pruritus and the presence of uremic frost, a condition where crystallized urea appears on the skin. Endocrine-related dysfunctions such as hyperphosphatemia may lead to secondary hyperparathyroidism and reduced vitamin D activation, which, in turn, contribute to bone pain, increased fracture risk, and vascular calcification.
As kidney function declines into end-stage renal disease, timely and comprehensive treatment becomes necessary to maintain and improve patient well-being. Available options include kidney transplantation and dialysis.¹⁵ Although kidney transplantation generally leads to more favorable outcomes, dialysis remains the predominant treatment modality for most patients.²⁴
Kidney Transplantation
Kidney transplantation involves surgically placing a healthy kidney from a compatible donor into a patient with renal failure, thereby restoring proper kidney function.¹⁵ Several transplant types are offered to those with ESRD, including deceased donor, living donor, paired exchange, preemptive, and non-directed (altruistic) transplants.¹⁷ Deceased donor transplantation involves obtaining kidneys from individuals who have passed away, often due to brain death, but who had previously agreed to organ donation. Allocation is determined by donor-recipient compatibility, availability, and priority on the transplant list. Living donor transplantation is performed using a kidney from a living person—typically a relative or close acquaintance. Both donor and recipient can maintain normal physiological balance with one healthy kidney. Living donations typically result in shorter wait periods, higher graft success rates, and more favorable long-term outcomes.
For donor-recipient pairs who are biologically incompatible, paired exchange transplantation serves as an alternative.²⁷ In this approach, mismatched pairs join a registry that facilitates compatible matches among multiple participants, enabling transplants that would otherwise be unfeasible. Preemptive transplantation takes place before the patient begins dialysis and offers advantages such as maintaining residual renal function, avoiding dialysis-related complications, and improving post-surgical prognosis. Nonetheless, thorough medical evaluation is essential to determine eligibility. Non-directed or altruistic transplantation is when a donor gives a kidney to a stranger without a specific recipient in mind. While kidney transplantation offers patients the possibility of living without dialysis, it presents potential risks such as surgical complications, immune rejection of the organ, and the necessity for lifelong immunosuppression.
Dialysis Types
Dialysis comes in two main forms:⁴
Hemodialysis uses a dialysis machine to remove excess fluids and waste from the blood via vascular access.² Common access methods include arteriovenous fistulas (AVFs), arteriovenous grafts (AVGs), and central venous catheters (CVCs). During treatment, two needles are inserted: one draws blood to the machine, and the other returns filtered blood to the body. Blood enters the dialyzer through the arterial needle and interacts with a specialized fluid called dialysate.
The dialysate closely resembles the electrolyte and acid-base composition of normal plasma.²² It contains sodium, potassium, bicarbonate, and calcium, among other components, mixed in sterile water. Inside the dialyzer, blood and dialysate flow in opposite directions, creating a concentration gradient for the diffusion of solutes like urea, creatinine, and electrolytes through a semipermeable membrane. Ultrafiltration removes excess fluid by using hydrostatic pressure across the membrane. Hemodialysis usually lasts between three and five hours and occurs three times per week, although this may vary depending on the patient’s condition and treatment goals.
Possible complications from hemodialysis include low blood pressure, unstable hemodynamics, vascular access problems, and dialysis-related amyloidosis.² Rapid fluid removal can result in symptoms such as dizziness, cramps, or nausea due to volume depletion. Electrolyte shifts—particularly with potassium—may trigger cardiac arrhythmias or cardiovascular instability. Access-related complications like infections, thrombosis, narrowing (stenosis), or aneurysms require close monitoring. Long-term use of dialysis membranes can trigger inflammation and lead to β₂-microglobulin accumulation, which causes dialysis-related amyloidosis and musculoskeletal issues. Despite these risks, hemodialysis is a crucial intervention for patients awaiting transplantation or requiring ongoing renal support.
Peritoneal dialysis utilizes the body’s peritoneal lining as a semipermeable membrane to exchange solutes and remove fluid.³⁴ Before starting therapy, a soft catheter is surgically placed in the lower abdomen. This catheter is used to introduce and remove dialysate from the peritoneal cavity. In the inflow phase, dialysate is infused into the abdominal cavity. Its composition and volume are tailored to individual patient needs and treatment objectives. While the dialysate remains in place, solutes and fluids cross the peritoneal membrane: toxins and waste from the bloodstream diffuse into the dialysate, and electrolyte levels are adjusted to maintain balance. After the dwell period, the fluid is drained via the catheter. Peritoneal dialysis may be performed manually (continuous ambulatory peritoneal dialysis) or automatically overnight using a mechanical cycler (automated peritoneal dialysis).
This method provides advantages such as increased independence, preserved kidney function, and avoidance of vascular access issues, making it suitable for certain ESRD patients. However, complications include peritonitis, infections at the catheter site, abdominal hernias, and fluid overload.³⁴ Peritonitis—caused by bacterial contamination—is a severe complication that demands immediate antibiotic treatment. Exit-site infections, including cellulitis and tunnel infections, necessitate meticulous hygiene and sterile technique during exchanges. Pressure fluctuations from repeated fluid exchanges can lead to abdominal hernias requiring surgical correction. Lastly, fluid overload—whether from inadequate ultrafiltration or excess intake—can cause swelling, elevated blood pressure, and heightened heart failure risk.
Antihypertensive medications frequently prescribed for individuals with kidney failure include angiotensin-converting enzyme (ACE) inhibitors, angiotensin II receptor blockers (ARBs), calcium channel blockers, beta-blockers, and diuretics.²⁸ ACE inhibitors, such as lisinopril and enalapril, function by blocking the conversion of angiotensin I to angiotensin II, resulting in vasodilation and reduced aldosterone secretion. These agents are especially useful for kidney failure patients due to their renoprotective properties, which help slow the advancement of proteinuria and chronic kidney disease. ARBs, including valsartan and losartan, prevent angiotensin II from binding to its receptors, also promoting vasodilation and decreasing aldosterone levels. ARBs provide similar renoprotective advantages and are often selected for patients who cannot tolerate ACE inhibitors or have contraindications to their use.
Calcium channel blockers such as amlodipine and diltiazem inhibit calcium influx into vascular smooth muscle cells.²⁸ This action facilitates vasodilation and lowers peripheral vascular resistance. These medications are typically preferred for patients who concurrently have coronary artery disease or peripheral vascular disease. Beta-blockers, including metoprolol and carvedilol, block the effects of catecholamines at beta-adrenergic receptors, leading to a decrease in heart rate and myocardial contractility. Although beta-blockers are not commonly used as first-line antihypertensive agents in kidney failure, they are indicated for individuals with coexisting cardiovascular conditions like heart failure or ischemic heart disease. Diuretics, such as furosemide and hydrochlorothiazide, work by inhibiting sodium reabsorption in the renal tubules, thereby reducing blood sodium levels. They are frequently used in combination with other antihypertensives to manage blood pressure and address volume overload in kidney failure patients with fluid retention.
In individuals with kidney failure, impaired renal clearance can lead to drug accumulation and increased toxicity.³⁶ Therefore, medication dosages often require adjustment based on the patient’s estimated glomerular filtration rate (GFR) and creatinine clearance. Close monitoring is essential, as diuretics may disrupt electrolyte levels and increase the risk of hyperkalemia, hypokalemia, hyponatremia, and hypercalcemia, all of which can result in serious complications. Patients with kidney failure frequently have comorbid conditions such as diabetes, hyperlipidemia, and cardiovascular disease, and they may be on various medications to manage these issues. Antihypertensive drugs can interact with other treatments, especially phosphate binders, erythropoiesis-stimulating agents, and immunosuppressants. It is vital for healthcare providers to evaluate potential drug interactions and customize therapeutic strategies to ensure safe and effective management.
Once OCD behaviors have been significantly reduced or eliminated through initial treatment with medication and psychotherapy, the focus shifts to long-term maintenance to sustain treatment gains and prevent relapse.⁴ Given that OCD is a chronic condition with a high relapse rate, consistent follow-up care is essential. Monthly visits are typically advised during the first six months following the completion of initial therapy, and continued monitoring is recommended for at least a year before tapering medications or discontinuing therapy. Ongoing assessments help track symptom severity, insight, and functional limitations, enabling timely intervention if symptoms return. Many individuals benefit from continued psychotherapy, which can be individualized or conducted in a group setting. The frequency of sessions may vary depending on progress and the person’s need for support, but maintaining therapy helps reinforce learned coping skills, address lingering symptoms, and manage triggers.
Medication regimens may also need adjustments based on how well the individual responds and tolerates treatment.¹⁸ In cases where significant symptom improvement or remission occurs, providers might explore the gradual discontinuation of medications. The standard tapering process reduces the dose by 25% at a time, with a two-month observation period between each adjustment to monitor for relapse. This slow withdrawal strategy minimizes the risk of symptom recurrence. However, for those with multiple severe relapses or several milder episodes, long-term or even lifelong medication may be needed to maintain symptom control and functional stability.
Healthy lifestyle habits play a vital role in long-term OCD management.⁷ Physical exercise is known to reduce co-occurring anxiety and depression. Consistent, quality sleep is crucial to mental health and helps prevent worsening of OCD symptoms. Stress-reduction practices such as deep breathing, mindfulness, and relaxation exercises help manage the distress that often accompanies OCD. A nutrient-rich, balanced diet supports brain function and emotional regulation. In addition, engaging in hobbies, meaningful activities, and social relationships contributes to emotional resilience. These activities provide a sense of fulfillment and help distract from obsessive thoughts, interrupting the cycle of compulsions and reducing anxiety. Strong social support from friends, family, or support groups can also be instrumental in offering encouragement and emotional reinforcement during ongoing treatment.
In pediatric OCD cases, family involvement is a key component of successful long-term management.²¹ ²³ Parents and caregivers should participate in therapy, help implement behavioral strategies at home, ensure that prescribed medications are taken correctly, and offer emotional support. Promoting healthy routines such as physical activity, sufficient sleep, proper nutrition, and stress-management practices can help children maintain emotional and physical balance. Cooperation with educators is also important in fostering a supportive school environment. Accommodations like extended time on assignments, reduced workload, or access to school counselors can enhance a child’s ability to function academically while managing OCD. Because a child’s OCD symptoms and treatment needs often change over time, healthcare providers should routinely reevaluate the child’s progress and make necessary modifications to the treatment plan to support long-term success.
When providing care for individuals diagnosed with both hypertension and end-stage renal disease (ESRD), nurses play a pivotal role in delivering comprehensive care aimed at enhancing health outcomes and preserving quality of life.²⁵ Nursing responsibilities include care coordination, ongoing assessments, treatment monitoring, patient education, and emotional support. Due to the complex nature of these chronic conditions, nurses collaborate closely with interdisciplinary team members, including cardiologists, nephrologists, dietitians, and social workers, to formulate individualized care plans. They facilitate timely referrals to specialized services, such as transplant evaluations and physical rehabilitation, based on patient condition and progression. In hospitalized individuals with ESRD or during hypertensive crises, nurses are responsible for administering medications as prescribed and closely monitoring for any adverse reactions, intolerance, or interactions—especially those involving nephrotoxic agents.³³ Routine assessments include evaluations of renal function, fluid and electrolyte balance, vital signs, and overall patient status. Laboratory markers such as serum creatinine, blood urea nitrogen (BUN), electrolyte levels, and urine output are closely monitored to detect complications early. Observations of fluid overload, electrolyte disturbances, persistent hypertension, or anemia are essential for initiating timely interventions.
Nurses are integral in supporting patients undergoing hemodialysis or peritoneal dialysis.¹⁶ They educate patients thoroughly on dialysis procedures, promote adherence to proper self-care practices, and teach strategies to minimize infection risks. In individuals receiving hemodialysis, nurses inspect vascular access sites regularly for signs of infection, clot formation, or mechanical failure, thereby preserving access viability. Throughout dialysis sessions, nurses monitor patient vital signs and remain alert to complications such as hypotension, muscle cramps, or bleeding at the access site. Immediate intervention is essential to ensure patient safety and to optimize dialysis effectiveness. Nutritional management is also a core nursing responsibility. In partnership with dietitians, nurses help create individualized meal plans that consider limitations on sodium, potassium, phosphorus, and protein intake. They guide patients in implementing heart-healthy and kidney-friendly dietary habits, providing instruction on portion control, food label interpretation, and meal preparation that aligns with dietary restrictions.
Educational outreach is another vital component of nursing care for patients with hypertension and ESRD.¹⁶ Nurses ensure that patients and their caregivers understand the pathophysiology behind both conditions, available therapeutic options, self-management techniques, and methods to control disease progression. Emphasis is placed on the importance of lifestyle changes, including regular physical activity, smoking cessation, and reduced alcohol consumption. Nurses stress adherence to prescribed medications by educating patients on dosage instructions, possible side effects, and the necessity of attending routine medical appointments. In addition to clinical education, nurses offer emotional support and counseling, helping to establish a therapeutic environment built on trust and empathy. When needed, they connect patients to mental health services or support groups to extend psychosocial support. By promoting open dialogue, nurses empower patients to voice their preferences, questions, and concerns. This fosters shared decision-making and strengthens the patient’s sense of autonomy and engagement in their treatment plan.
Exploring the interplay between hypertension and end-stage renal disease (ESRD) reveals a cyclical relationship wherein each condition aggravates the other. Hypertension often precedes ESRD and, when left unmanaged, causes progressive damage to the kidney’s fragile structures. This ongoing damage hastens the decline of renal function, which in turn amplifies hypertension, creating a feedback loop that heightens the risk of health deterioration and hypertensive crises. Breaking this cycle demands timely and effective intervention aimed at stabilizing blood pressure and slowing renal decline. Although treatment strategies such as antihypertensive therapy, dialysis, and kidney transplantation offer pathways for management, each presents limitations and potential complications. Therefore, coordinated care among multidisciplinary healthcare professionals is essential. Through proactive monitoring, prompt clinical decisions, and patient-centered support, healthcare providers play a vital role in enhancing outcomes and maintaining quality of life for individuals impacted by this dual burden.
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