Contact Hours: 3
This online independent study activity is credited for 3 contact hours at completion.
Course Purpose
The purpose of this course is to provide an overview of chronic kidney disease, its progression to end stage renal disease, and treatment and management options.
Overview
The development of chronic kidney disease (CKD) and its progression to end-stage renal disease remains a significant source of reduced quality of life and premature mortality. In end-stage renal disease (ESRD), an individual’s kidneys permanently stop functioning, resulting in the necessity of long-term dialysis or a kidney transplant to survive. This course includes a complete overview of ESRD, its potential causes, and current treatments options for overall improved quality of life.
Course Objectives
Upon completion of the independent study, the learner will be able to:
- Identify causes of renal failure
- Review testing and assessments for renal failure
- Identify distinctions between acute renal failure and chronic kidney disease
- Recognize treatment modalities for hyperkalemia
- Summarize dialysis options, including peritoneal dialysis and hemodialysis
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.
To access End Stage Renal Disease, purchase this course or a Full Access Pass.
If you already have an account, please sign in here.
To access End Stage Renal Disease, purchase this course or a Full Access Pass.
If you already have an account, please sign in here.
| Acute Renal Failure (ARF) | A condition when an abrupt reduction in kidneys’ ability to filter waste products occurs within a few hours or a few days. |
| Alport Syndrome | A disease that damages the tiny blood vessels in the kidneys. |
| Chronic Kidney Disease (CKD) | A disease or condition impairs kidney function, causing kidney damage to worsen over several months or years, also called chronic renal failure. |
| Creatinine | A waste product that is typically filtered out of blood by the kidneys. Abnormal levels of creatinine could be a sign of kidney failure. |
| Cystic Renal Disease | Multiple diseases and conditions which all deal with cysts that develop on or around the kidneys. |
| Diabetes Mellitus | A metabolic disorder in which the body has high sugar levels for prolonged periods of time. |
| Dialysis | A life-saving therapy that can replace the work of non-functioning kidneys. |
| End-Stage Renal Disease (ESRD) | When the kidneys permanently fail to work. |
| Glomerular Filtration Rate (GFR) | A test used to check how well the kidneys are working. |
| Glomerulonephritis | Inflammation of the tiny filters in the kidneys (glomeruli). |
| High Blood Pressure | A blood pressure reading of 130/80 mm Hg or higher. |
| Nephrolithiasis | (Kidney stones) Hard deposits made of minerals and salts that form inside your kidneys. |
| Nephron | Functional unit of the kidney, the structure that produces urine in the process of removing waste and excess substances from the blood. |
| Nephrotic Syndrome | A condition results from excreting too much protein in urine due to a kidney disorder. |
| Proteinuria | A high level of protein in the urine. |
| Pyelonephritis | A sudden and severe inflammation of kidney due to a bacterial infection. |
| Renal Failure | (Kidney Failure) The condition when the kidneys do not function properly and cannot get rid of waste products in the blood. |
| Renal Replacement Therapy | Therapy that replaces the normal blood-filtering function of the kidneys. |
| Sickle Cell Nephropathy (SCN) | A type of nephropathy associated with sickle cell disease which causes kidney complications because of sickling of red blood cells in the small blood vessels. |
| Urea | An organic compound formed when nitrogen and protein break down and is the main component of human urine. |
End-stage renal disease, also called kidney failure, is a global health problem with a high prevalence rate, affecting around 10 to 12% of the population worldwide.1,3 In the United States, more than 500,000 people live with end-stage renal disease (ESRD).2 In this disease, an individual’s kidneys permanently stop functioning, resulting in the necessity of long-term dialysis or a kidney transplant to survive.4 The development of chronic kidney disease (CKD) and its progression to end-stage renal disease remains a significant source of reduced quality of life and premature mortality.2
Many chronic diseases can cause ESRD; for instance, diabetes mellitus is the leading cause of ESRD in developing countries.2 The treatment of end-stage renal disease is extremely expensive, and achieving a good long-term outcome in this group of patients is a major challenge for the nephrology community.3 Patients also face higher comorbidity and overall mortality, poor quality of life, and higher hospitalization rates.3
This course provides an overview of end stage renal disease, its potential causes, and current treatment options to improve overall quality of life.
The Kidney Disease Improving Global Outcomes (KDIGO) foundation guidelines define CKD using kidney damage markers that determine proteinuria and glomerular filtration rate.2 Each nephron in a normal kidney contributes to the total glomerular filtration rate (GFR).2 The decline of kidney function is gradual and may initially present asymptomatically. The natural history of renal failure depends on the etiology of the disease, but involves early homeostatic mechanisms involving hyperfiltration of the nephrons.2 The kidney maintains GFR, despite the progressive destruction of nephrons because the remaining normal nephrons develop hyperfiltration and compensatory hypertrophy. As a result, the patient with mild renal impairment can show normal creatinine values, and the disease can go undetected for some time.2
Plasma levels of substances such as urea and creatinine start to show measurable increases only after total GFR has decreased by 50%.2 The presence of both factors (glomerular filtration rate [GFR] less than 60 mL/min and albumin greater than 30 mg per gram of creatinine) along with abnormalities of kidney structure or function for greater than three months signifies chronic kidney disease.2 By definition, end-stage renal disease is defined as a GFR of less than 15 mL/min.2
There are multiple signs and symptoms associated with ESRD, such as:2,6
These symptoms start appearing in stages 4 and 5 when the GFR is less than 30 ml/min.2 Depression is also common in all ESRD patients and should be screened. Moreover, cystic renal disease or nephrotic syndrome patients may present the symptoms earlier.2
There are two kinds of renal failure; acute and chronic.5 In acute renal failure (ARF), glomerular filtration declines abruptly (hours to days) and is usually reversible.5 It is further divided into 3 classifications, depending on the site; prerenal (caused by interference with renal perfusion), intrarenal (associated with parenchymal changes caused by ischemia or nephrotoxic substances), and postrenal (occurs as the result of an obstruction in the urinary tract).5
In contrast, chronic renal failure (CRF) is defined as persistent impairment of kidney function, in other words, abnormally elevated serum creatinine for more than 3 months or calculated glomerular filtration rate (GFR) less than 60 ml per minute / 1.73m2.5 Chronic renal failure results in a progressive loss of kidney function, necessitating renal replacement therapy (dialysis or transplantation). When a patient needs renal replacement therapy, the condition is called end-stage renal disease (ESRD).5
The causes of CKD vary globally, and the most common primary diseases causing CKD and end-stage renal disease (ESRD) are as follows:5,6,7
Diabetes mellitus (DM), especially type 2 diabetes mellitus, is the most frequent cause of ESRD.5,6 In DM, excess glucose in the body damages the kidney’s filter system, resulting in the kidney’s inability to properly filter waste and extra fluid from the body.7
The first indication that diabetes is causing kidney disease is the presence of albumin, a protein, in the urine. Healthy functioning kidneys do not allow albumin to filter through blood into the urine.7
High blood pressure is the second leading cause of kidney failure in the U.S. after diabetes.8 High blood pressure damages the kidney’s blood vessels and affects their functionality.7 It narrows and constricts the blood vessels, reducing blood flow.8 As a result, the kidneys cannot remove all wastes and extra fluid from the body.8 Moreover, the extra fluid in the blood vessels can raise the blood pressure even more, creating a dangerous cycle that can lead to kidney failure.8
Other common causes of CKD and end-stage renal disease include:5,6,7
- Disorders in which the body’s immune system attacks its cells and organs, such as Anti-GBM (Goodpasture’s) disease
- Glomerulonephritis
- Heavy metal poisoning, such as lead poisoning
- Hemolytic uremic syndrome in children
- Hypertension
- Polycystic kidney disease (a genetic disorder that causes many cysts to grow in the kidneys)
- Prolonged urinary tract obstruction and nephrolithiasis
- Rare genetic conditions, such as Alport syndrome
- Recurrent kidney infections/ pyelonephritis
- Renal vascular diseases
- Vesicoureteral reflux (a condition in which urine backs up into the kidneys)
The first step in the evaluation of end-stage renal disease is establishing chronicity.6 Chronic kidney disease is diagnosed when there is evidence of kidney damage for at least three months or in any patient with a GFR of less than 60 mL/min for that same amount of time.2,6
When a GFR of less than 60 mL/min is detected, attention needs to be paid to the previous blood and urine test results and clinical history to determine whether this is a result of ARF or CKD that has been present but asymptomatic.6
The relevant history and physical examinations associated with ESRD include:5
Medical History
- Any use of a contrast agent or any procedure performed
- Detailed present medical illness history
- Family history of kidney diseases
- History of diabetes mellitus and hypertension
- Medications, especially start date, drug levels of nephrotoxic agents, NSAIDs
- Previous renal function
- Review of hospital records
Physical examination
- Hemodynamics, including blood pressure, heart rate, and weight
- Volume status, look for edema, jugular venous distention, lung crackles, and S3 gallop
- Skin: check for any diffuse rash or uremic frost
- Look for signs of uremia: asterixis, lethargy, seizures, pericardial friction rub, peripheral neuropathies
- Abdomen exam: check for bladder distention, and note any suprapubic fullness
Suppose the distinction between ARF and CKD is unclear as the cause of low GFR. In that case, kidney function tests should be repeated within 2 weeks of the initial finding of low eGFR below 60 ml/min/1.73 m2.6 Chronic kidney disease is confirmed if previous tests confirm that the low eGFR is chronic or the repeat blood test results over 3 months are consistent.6 However, if eGFR based on serum creatinine is known to be less accurate, other markers like cystatin-c or an isotope-clearance measurement can be undertaken.6
Further evaluation of renal failure includes the following laboratory tests and assessments:5,6,7
- Complete blood count (CBC) – CBC shows normochromic normocytic anemia).
- Kidney imaging – If an ultrasound examination of kidneys shows small kidneys with reduced cortical thickness, increased echogenicity, scarring, or multiple cysts, this suggests a chronic process.
- Radiology – Plain abdominal radiography can detect radio-opaque stones or nephrocalcinosis.
- Renal biopsy – Percutaneous ultrasound-guided renal biopsy is indicated when the diagnosis is unclear after an appropriate workup.
- Urinalysis – A spot urine protein/creatinine ratio can be used to quantitate albuminuria.
Specific tests include:2,6
- Anti–glomerular basement membrane (anti-GBM) antibodies for Goodpasture syndrome
- Antinuclear antibodies (ANA), double-stranded DNA antibody levels for systemic lupus erythematosus
- Casts: Pigmented granular/muddy brown casts-ATN; WBC casts-acute interstitial nephritis; RBC casts-glomerulonephritis
- Cytoplasmic and perinuclear pattern antineutrophil cytoplasmic antibody (C-ANCA and P-ANCA) levels for granulomatosis with polyangiitis (Wegener granulomatosis) and microscopic polyangiitis
- Dipstick for blood and protein; microscopy for cells, casts, and crystals
- Hepatitis B and C, human immunodeficiency virus (HIV), and venereal disease research laboratory (VDRL) serology
- Serum and urine protein electrophoresis for multiple myeloma
- Serum complement levels
An accurate diagnosis will help the healthcare team create an effective course of action to treat or manage the underlying disease.6 Moreover, certain diseases carry a higher frequency of recurrence in the kidney after transplantation, and accurate diagnosis influences later management.6
Management and treatment of end-stage renal disease largely depend on the kidneys’ underlying cause and failure.5 Thus, it is broadly divided into two groups; treating the cause of renal failure in acute states and replacing the renal function in acute or chronic conditions.5
In acute renal failure, the underlying cause is often reversible such as infection, drugs that reduce the GFR, hypotension caused by shock, and hypovolemia caused by vomiting and diarrhea.6
Oliguric patients should have a fluid restriction of 400 mL + the previous day’s urine output.5 But, if there is no volume overload noted, a fluid challenge may be appropriate with diligent monitoring.5 Moreover, if obstructive etiology is present, it should be treated accordingly, and if bladder outlet obstruction is secondary to prostatic hypertrophy, the patient may benefit from Flomax or other selective alpha-blockers.5
Many causes can result in the progression of kidney disease and thus, should be managed early on, such as hypertension, proteinuria, metabolic acidosis, and hyperlipidemia. Hypertension should be managed in kidney disease by establishing blood pressure goals.2,6 The blood pressure goal should be a systolic blood pressure of less than 130 mmHg and diastolic blood pressure of less than 80 mmHg in adults with or without diabetes mellitus whose urine albumin excretion exceeds 30 mg for 24 hours.2
For diabetic patients with proteinuria, an angiotensin-converting-enzyme inhibitor (ACEI) or angiotensin 2 receptor blocker (ARB) should be conisdered.2 These drugs slow the disease progression, particularly when initiated before the GFR decreases to less than 60 mL/min or before plasma creatinine concentration exceeds 1.2 mg/dL in women and 1.5 mg/dL in men.2
Other management tips to reduce the progression of ARF to CKD involve general lifestyle recommendations such as smoking cessation and dietary restriction, bicarbonate supplementation to treat chronic metabolic acidosis, tight glycemic control, and cardiovascular risk reduction.2,6 Moreover, intensive glucose control in diabetics has also been shown to delay the development of albuminuria and the progression of albuminuria to overt proteinuria.6
Hyperkalemia – Medications to Reduce Potassium Levels
Hyperkalemia is a common finding in patients with CKD.9 It is defined as an increase in potassium levels and is associated with decreased renal ion excretion, medications to reduce the progression of CKD, and control of associated diseases such as diabetes mellitus and heart failure.9 If not controlled, hyperkalemia increases the mortality rate and the risk of cardiac arrhythmia episodes and sudden death.9 Management involves reducing potassium levels through lifestyle changes and medication.9
The serum level of potassium is maintained by the daily excretion of a quantity close to that ingested, approximately 100 mEq/day.9 The ion elimination occurs through the skin, gastrointestinal tract, and kidneys.9 The incidence of hyperkalemia varies between 2-35% of CKD patients and is caused due to multiple factors, such as disorderly distribution between the intra and extracellular compartments, increased intake of foods rich in potassium, and abnormalities in potassium excretion.9
Acute renal failure and hyperkalemia caused by blood transfusion also contribute to the elevation of potassium ions, which increases the risk cardiac arrhythmia and sudden death, and is one of the most common indications for emergency dialysis treatment.9
Treatment for acute hyperkalemia includes the use of potassium-lowering medications, such as:
Insulin and dextrose effectively decrease the serum potassium level through activation of Na+/K+ ATPase after insulin fixation to its receptor.10 Using insulin and dextrose decreases the potassium level by ∼0.5–1 mmol/L.10 The main side effects are glycemic variations, including hyperglycemia and hypoglycemia. 10 According to a recent review, a high dose of dextrose 50% (50g) and 10 units of regular insulin reduced the risks of hypoglycemia occurring when treating hyperkalemia. 10
According to multiple studies, sodium bicarbonate is also efficient in decreasing potassium levels.10 In a recent randomized controlled trial (RCT), the authors observed a significant decrease in serum potassium levels in patients receiving sodium bicarbonate 4 h after the beginning of the perfusion.10 The sodium bicarbonate dose varies between 3-5 grams per day and is indicated only in patients with metabolic acidosis and hypovolemia.9,10 It is worth noting that this measure is poorly tolerated in patients with CKD in advanced stages due to increased blood pressure and fluid retention risk and should be taken in combination with other medications, such as insulin glucose.9,10
β2-agonists decrease the serum potassium level through two different pathways: first, by increased secretion of endogenous insulin and second, by the activation of Na+/K+ ATPase after stimulation of the β2-receptors in the muscle and liver.10 However, some patients may be resistant to β2-agonists.10 Therefore, insulin and dextrose or an association of insulin/glucose and β2-agonists should be considered first-line therapy in patients treated with β-blockers or patients with life-threatening hyperkalemia.10 Albuterol in a dose-dependent manner is efficient in decreasing the serum potassium level.10 Other medication options include diuretics and exchange resins like patiromer, sodium zirconium cyclosilicate, calcium polystyrene sulfonate, and sodium polystyrene sulfonate.9
As ESRD progresses, based on health condition and in consultation with their healthcare provider, patients must discuss treatment options, including dialytic or non-dialytic treatment. If dialysis is the best option, dialysis modality selection and the preferred timing of dialysis initiation is considered.11
Even in early detection of ESRD, patients should have a plan of care that considers disease progression.2 Advanced preparation enables patients to be prepared for dialysis, when necessary.11 When other comorbid conditions are present and symptoms are non-specific, it may be difficult to determine whether symptoms would improve with dialysis initiation rather than with other method, but with a plan in place, the patient and healthcare provider is better equipped to make decisions with the best outcome and quality of life.11
Peritoneal dialysis is a treatment for ESRD and is used to remove the waste products from the blood when the kidneys are unable to function adequately.12 It forces the abdomen’s inner lining and peritoneum to function as a natural filter and uses dialysate fluid to cleanse the blood.12
A soft catheter carries the dialysate fluid, which is a mixture of salt and other additives, into the abdomen lining. Once the fluid is completely transferred, patients can remove the fluid bag, put a cap over the catheter, and continue their routine activities.12 The dialysate inside the belly lining absorbs water and extra fluid from the blood.12 Solutes like creatinine, urea, and potassium also diffuse from the bloodstream into the dialysate, whereas the blood absorbs glucose from the dialysate.15
The toxin removal in peritoneal dialysis is based on the diffusion of uremic toxins out of the blood through the peritoneal membrane into the peritoneal fluid.14 This process is accelerated when the fluid is fresh, but as time passes, the filtration process is slowed down, and the solution is emptied into another bag and drained.12 This cycle is repeated around 4 to 6 times a day and is called an exchange.12
The rate of solute transfer varies from person to person and depends on the concentration gradient and degree of peritoneal vascularity.15 The type of dialysate fluid used determines the time period through which the fluid will remain in your abdomen lining, also known as dwell time.15
There are two types of peritoneal dialysis; continuous ambulatory peritoneal dialysis (CAPD) and automated peritoneal dialysis.12,13 Both differ in their administration and the schedule of exchanges.12,13 For instance, CAPD is a machine-free dialysis process in which the exchange is done by hand.12,13 It is a continuous procedure that enables patients to continue their routine activities, such as reading, watching tv, and going to school.12,13 Exchanges are frequent and are required around 4 to 6 times a day; each exchange can take 30 to 40 minutes and is usually done at mealtime or bedtime.12,13
On the other hand, automated peritoneal dialysis is done by a machine and is also known as continuous cycler-assisted peritoneal dialysis or CCPD.12,13 A machine, called a cycler, automatically fills and empties the dialysate throughout the night, so the patient has fresh dialysate when they wake up.12 Patients can do one exchange during the day or leave the dialysate for the whole day inside their belly. Automated peritoneal dialysis is done by a machine and is also known as continuous cycler-assisted peritoneal dialysis or CCPD.
In the United States, only a small percentage of ESRD patients, around 7%, are on peritoneal dialysis.14 Many observational studies and national registries from different parts of the world have reported better survival with peritoneal dialysis than hemodialysis.14 Peritoneal dialysis also has a higher survival advantage over hemodialysis, but it is not considered for patients with abdominal adhesions, uncorrected abdominal wall hernia, or a pleuroperitoneal shunt.14
Complications Related to Peritoneal Dialysis
Complications regarding peritoneal dialysis can be infectious or non-infectious.15
There are different techniques used for catheter placement, such as surgical or percutaneous.14 Determining one technique’s advantages over another is difficult as the process depends on multiple factors and the patient’s overall condition.14 However, research shows that there are multiple complications associated with open-surgical catheter placement, such as:14
One of the most serious complications of peritoneal dialysis is infections. These can occur on the catheter site or in the abdominal cavity.14,15,16 Catheter-site infections cause pus-like drainage from the area and lead to redness, firmness, and tenderness of the skin around the catheter.16 These infections can be treated with oral or cream antibiotics and skin cleaning within 2 to 3 weeks; if not, catheter removal may be required.16
A common peritoneal infection is fungal peritonitis, which increases the risk of peritoneal dialysis failure, requires urgent catheter removal, and is life-threatening to the patient; mortality from peritoneal dialysis-related peritonitis ranges from 3 to 10%14,15 It is an infection of the abdominal cavity and is caused when bacteria enter the abdomen through the catheter.16 According to the International Society for Peritoneal Dialysis, the benchmark episode for this infection is one every two years.15 Patients are required to remove the catheter if peritonitis fails to resolve in five days and all cases of fungal peritonitis.15
If the white blood cell count in the peritoneal fluid is above 100 WBC/mL and there are more than 50 percent neutrophils in the fluid, a peritonitis diagnosis can be assumed.15 Other signs of peritonitis include nausea, diarrhea, mild or severe abdominal pain, fever, and cloudy used dialysate fluid.16 It can be treated through antibiotics, catheter removal (in severe cases), or temporarily changing the dialysate or dwell time.16 During catheter removal, the patient might be shifted to hemodialysis until the infection is resolved.16
Patients undergoing peritoneal dialysis can also develop a hernia, which is a term used to define abdominal muscle weakness.16 It is caused by increased stress and opening due to the catheter and can develop in the groin (inguinal hernia), near the belly button (umbilical hernia), or the catheter site (incisional hernia).16
Other complications include catheter malfunction, fluid leakage around the catheter, metabolic complications secondary to hyperglycemia, and hypokalemia.15
In the United States, there are currently 400,000 patients with ESRD on maintenance hemodialysis (HD).17 It is a form of renal replacement therapy that removes waste and extra fluid from the blood by using an external filter called a dialyzer, also known as an artificial kidney.18,19 The dialyzer consists of a semipermeable membrane that creates a counter-current flow gradient to separate the waste, where blood flow is in one direction and the fluid of the dialyzer is in the opposite direction.19
The hemodialysis machine uses the principle of diffusion of solutes across a semipermeable membrane.19 The blood enters the machine through one side of the filter and is passed through thin, hollow fibers. Metabolic waste products, such as creatinine and urea, diffuse down the concentration gradient from the circulation into the dialysate.18,19 The particles’ size determines the rate of diffusion across the membrane. For instance, the larger the size of the solute particle, the slower the diffusion rate across the membrane.19
A hemodialysis machine helps control blood pressure and the concentration of various minerals in the blood, such as calcium, potassium, and sodium.18 The procedure is usually performed at a dialysis center and is typically conducted three times per week, where each session lasts about four to five hours.20
Hemodialysis is initiated in acute illness associated with the following diseases:21
Complications Related to Hemodialysis
There are some disadvantages and mild to severe complications associated with hemodialysis, including:
Hemodialysis is usually conducted in a dialysis center. Thus, frequent visits can be burdensome for patients.20 Moreover, the hemodialysis procedure is long and complex. It only works when the right type of passageway is created through surgery, in which an artery and a vein are connected in the forearm to create a blood short-circuit, called an arteriovenous fistula or a shunt.20 This causes a slightly larger blood vessel to form for easy insertion of dialysis cannulas.20 The fistula takes some time to develop and heal and could lead to typical complications as well, such as inflammation or blockage of the new blood vessel from a blood clot.20
Oxidative stress is developed in patients undergoing hemodialysis.19 During dialysis, the semipermeable membrane faces an immunological response and makes it permeable to granulocytes.19 The activated granulocytes in the blood stimulate the release of reactive oxygen species (ROS) and exaggerate oxidative stress.19 The affected and non-functioning kidney further increases oxidative stress by activating macrophages, vascular cells, and various glomerular cells to produce free radicals.19 All of this combined leads to sequential changes in organs, resulting in multiple organ failures and death.19
Hypotension is a common outcome of these changes and increases mortality.21 A nadir systolic BP lower than 90 mmHg strongly correlates with mortality.21 It has subtle symptoms and can also include light-headedness, dizziness, and nausea. When hypotension occurs, a nurse may consider placing the patient in Trendelenburg position and administering a 100 mL bolus of normal saline through the bloodline as quickly as possible.21 The ultrafiltration rate should be reduced, and the patient should be kept under surveillance until vitals have stabilized.21
Other risk factors include hyperlipidemia, anemia, and the calcification of coronary arteries.19
Vascular access is also a common complication in patients undergoing hemodialysis.18 The access site can become infected or be blocked by a blood clot and have poor blood flow.18 In the vascular access process, death may also occur from cardiac arrhythmias, pulmonary edema, or contrast medium reaction.21 To avoid such occurrences, the following are suggested:21
- Avoid sleeping on the arm or carrying heavy items.
- Avoid wearing tight clothes or anything that causes additional trauma to the access site.
- Examine the site for any signs of infection, such as redness, pain, or warmth.
- If the access site is bleeding, seek medical assistance or call 911.
The exact reason is unknown, but a combination of hypotension, hypovolemia, and high filtration rate can lead to cramps.21 These factors trigger vasoconstriction and muscle hypo-perfusion, with secondary impairment of muscle relaxation.21 If muscle cramps occur simultaneously with hypotension, forced stretching of muscle and treatment with 0.9% ;may be effective.21
A dialyzer can cause allergic reactions in ESRD patients. There are two types of reactions, type A and type B.22 Type A reactions are more severe than type B and are mediated by preformed immunoglobulin E. Type A reactions are triggered after a few minutes to around 30 mins of dialysis initiation and result from hypersensitivity to ethylene oxide used to sterilize dialyzers.21,22 Type A reaction symptoms include:21
Management involves using steroids, epinephrine, and intravenous antihistamines.21 Type B reactions are less common and severe and do not require dialysis termination.22 Type B reactions cause chest or back pain 20 to 40 minutes after dialysis initiation.21 Treatment involves using a different dialyzer membrane.21 Other complications include hemolysis, aim embolism, nausea, vomiting, dialysis equilibrium syndrome, and headache.21
End-stage renal disease is a progressive disease, necessitating renal replacement therapy to survive.2 The disease is associated with frequent hospitalizations, high-cost treatments, and metabolic changes that increase mortality rates and lead to life-long lifestyle changes associated with dialysis and medication use.2 If patients become unresponsive to medications, dialysis is recommended.2 Planning of dialysis should be made in advance with the help of healthcare professionals who review patients and identify potential barriers to peritoneal dialysis, including physical, visual, cognitive, psychological, and social problems.11 Healthcare professionals should also offer assistance in overcoming such barriers by educating patients, providing adequate care, offering psychological counseling, and providing dialysis assistance.11
Although there is no cure, short-term treatments are available.2 However, the only way to prevent long-term complications related to CKD and ESRD is to prevent the disease’s progression.2 The disease is best managed by an interprofessional healthcare team involving a specialized pharmacist, nurse educator, nutritionist, social worker, primary care provider, and a trained nephrologist.2,4
A patient should be educated on the progression of the disease and the lifestyle modifications, such as healthy eating, regular exercise, discontinuing tobacco, and avoiding alcohol to prevent disease progression and improve the overall quality of life.2,4
- Calderon-Margalit R, Golan E, Twig G, et al. History of Childhood Kidney Disease and Risk of Adult End-Stage Renal Disease. New England Journal of Medicine. 2018;378(5):428-438. doi:10.1056/nejmoa1700993
- Benjamin O, Lappin SL. End-Stage Renal Disease. Nih.gov. Published 2019. https://www.ncbi.nlm.nih.gov/books/NBK499861/
- Cobo G, Lindholm B, Stenvinkel P. Chronic inflammation in end-stage renal disease and dialysis. Nephrology, Dialysis, Transplantation: Official Publication of the European Dialysis and Transplant Association – European Renal Association. 2018;33(suppl_3):iii35-iii40. doi:10.1093/ndt/gfy175
- End-Stage Renal Disease (ESRD) | CMS. www.cms.gov. Published December 1, 2021. https://www.cms.gov/Medicare/Coordination-of-Benefits-and-Recovery/Coordination-of-Benefits-and-Recovery-Overview/End-Stage-Renal-Disease-ESRD/ESRD#:~:text=End%2DStage%20Renal%20Disease%20(ESRD)%20is%20a%20medical%20condition
- Bindroo S, Challa HJ. Renal Failure. PubMed. Published 2020. https://www.ncbi.nlm.nih.gov/books/NBK519012/
- Vaidya SR, Aeddula NR, Doerr C. Chronic Renal Failure (Nursing). PubMed. Published 2021. https://www.ncbi.nlm.nih.gov/books/NBK568778/
- NIDDK. Causes of Chronic Kidney Disease | NIDDK. National Institute of Diabetes and Digestive and Kidney Diseases. Published October 2016. https://www.niddk.nih.gov/health-information/kidney-disease/chronic-kidney-disease-ckd/causes
- High Blood Pressure & Kidney Disease | NIDDK. National Institute of Diabetes and Digestive and Kidney Diseases. https://www.niddk.nih.gov/health-information/kidney-disease/high-blood-pressure#HBPKidneys
- Watanabe R. Hyperkalemia in chronic kidney disease. Revista da Associação Médica Brasileira. 2020;66(suppl 1):s31-s36. doi:10.1590/1806-9282.66.s1.31
- Coutrot M, Dépret F, Legrand M. Tailoring treatment of hyperkalemia. Nephrology Dialysis Transplantation. 2019;34(Supplement_3):iii62-iii68. doi:10.1093/ndt/gfz220
- Segall L, Nistor I, Van Biesen W, et al. Dialysis modality choice in elderly patients with end-stage renal disease: a narrative review of the available evidence: Table 1. Nephrology Dialysis Transplantation. Published online December 15, 2015:gfv411. doi:10.1093/ndt/gfv411
- NIDDK. Peritoneal Dialysis | NIDDK. National Institute of Diabetes and Digestive and Kidney Diseases. Published June 5, 2019. https://www.niddk.nih.gov/health-information/kidney-disease/kidney-failure/peritoneal-dialysis
- National Kidney Foundation. Peritoneal Dialysis: What You Need to Know. National Kidney Foundation. Published February 3, 2017. https://www.kidney.org/atoz/content/peritoneal
- Sachdeva B, Zulfiqar H, Aeddula NR. Peritoneal Dialysis. PubMed. Published 2022. https://www.ncbi.nlm.nih.gov/books/NBK532979/
- Roberts JR. InFocus: Diagnosing Peritoneal Dialysis Complications in the ED. Emergency Medicine News. 2022;44(2):12. doi:10.1097/01.EEM.0000820888.02744.b6
- UpToDate. Uptodate.com. Published 2019. https://www.uptodate.com/contents/peritoneal-dialysis-beyond-the-basics
- Saha M, Allon M. Diagnosis, Treatment, and Prevention of Hemodialysis Emergencies. Clinical Journal of the American Society of Nephrology. 2016;12(2):357-369. doi:10.2215/cjn.05260516
- NIDDK. Hemodialysis | NIDDK. National Institute of Diabetes and Digestive and Kidney Diseases. Published June 5, 2019. https://www.niddk.nih.gov/health-information/kidney-disease/kidney-failure/hemodialysis
- Vadakedath S, Kandi V. Dialysis: A review of the mechanisms underlying complications in the management of chronic renal failure. Cureus. 2017;9(8). doi:10.7759/cureus.1603
- Dialysis in chronic kidney disease. Nih.gov. Published March 8, 2018. https://www.ncbi.nlm.nih.gov/books/NBK492979/
- Murdeshwar HN, Anjum F. Hemodialysis. PubMed. Published 2020. https://www.ncbi.nlm.nih.gov/books/NBK563296/
- UpToDate. www.uptodate.com. Accessed January 20, 2023. https://www.uptodate.com/contents/reactions-to-the-hemodialysis-membrane#H3
To access End Stage Renal Disease, purchase this course or a Full Access Pass.
If you already have an account, please sign in here.
To access End Stage Renal Disease, purchase this course or a Full Access Pass.
If you already have an account, please sign in here.
