Chronic Kidney Disease (FL Autonomous Practice INITIAL Differential Diagnosis)

Chronic kidney disease (CKD) is also called chronic renal failure and chronic renal insufficiency. If the disease is severe enough to require renal therapy, it is termed end-stage renal disease (ESRD). According to the U.S. Renal Data System, Medicare spent $81 billion in 2018 on beneficiaries with chronic kidney disease without end-stage renal disease. It represented about 22.3% of the Medicare fee for service spending. Medicare-related expenses related to beneficiaries with end-stage renal disease were about $51 billion in 2019. It is estimated that about 20% of the money spent on all patients 65 years or older was spent on CKD. In reality, the actual cost of CKD is much higher since Medicare only covers about 80% of the people with ESRD.

Chronic kidney disease remains a significant public health concern both nationally and worldwide. Currently, over 20 million people live with chronic kidney disease in the U.S. According to the National Center for Health Statistics, chronic kidney disease ranks the ninth leading cause of death in the United States (NCHS Health, 2016). The financial costs associated with chronic kidney disease account for 20% of the total Medicare spending budget, with most of the costs being related to end-stage renal disease (Neyra, 2021). Therefore, great importance should be placed on mitigating the incidence and diminishing the incidence and progression of chronic kidney disease.

The early identification and mitigation of modifiable risk factors for the development of chronic kidney disease are important for improved patient outcomes. Acute kidney injury is a major risk factor for the development of chronic kidney disease; it is also associated with cardiovascular disease, rehospitalization, and even an increased risk of death. Chronic kidney disease remains a public health concern, given the strong association with morbidity and mortality and its socioeconomic impact (Neyra, 2021).

The definition of chronic kidney disease was initially proposed in 2002 by the National Kidney Foundation (NKF) Kidney Disease Outcomes Quality Initiative (KDOQI). The international community later adopted it, specifically, the Kidney Disease Improving Global Outcomes (KDIGO). Chronic kidney disease is defined as kidney damage or glomerular filtration rate < 60 ml/min/1.73 m² for three months or longer regardless of the cause (KDIGO, 2012). Kidney damage in the above definition refers to renal pathology, whether established by imaging studies, renal biopsy, or deduced from urine sediment abnormalities, including increased rates of albumin excretion. Albuminuria (increased albumin excretion rate) is an indirect measure of glomerular permeability. It is defined as an albumin-to-creatinine ratio > 30mg/g in two out of three urine specimens. In effect, albuminuria reflects increased glomerular permeability to macromolecules.

The glomerular filtration rate (GFR) is the best indicator of renal function for both patients with no disease and patients with kidney dysfunction. However, it is not a perfect measure, just an estimate based on age, sex, race, and serum creatinine level. The assumption made when calculating the GFR is that the serum creatinine has been stable for several days.

Creatinine is an amino acid derivative that is freely filtered by the glomerulus. However, its secretion can be altered by certain substances such as Trimethoprim and cimetidine. Additionally, creatinine levels can be affected by dietary intake and even muscle mass. As such, a creatinine trend is much more important than a single measurement.

The difference between chronic kidney disease and acute kidney injury is the duration of the kidney damage. If the damage persists for three months or less, it is termed acute kidney injury.

Acute kidney injury is a complication that often occurs in hospitalized patients. Approximately 1 in 5 patients hospitalized experience acute kidney injury, while 1 in 2 patients in the intensive care unit experience acute kidney injury. Note that acute kidney injury is associated with chronic kidney disease and not necessarily in a sequential manner. In fact, patients with chronic kidney disease are at increased risk of acute kidney injury, with each syndrome predisposing to the other.

Prior to the Kidney Disease: Improving Global Outcomes (KDIGO) Clinical Practice Guidelines, several differing definitions for acute kidney injury were based on the different etiologies. The KDIGO Practice Guidelines aided in standardized criteria for diagnosing and managing acute kidney injury (Neyra, 2021).

The period of transition from acute kidney injury to chronic kidney disease is known as acute kidney disease, and this was rarely mentioned or fully characterized in clinical practice. As such, the Acute Disease Quality Initiative (ADQI) 16 Workgroup put forth a consensus definition of acute kidney disease to encourage its widespread application in clinical practice.

The definition for acute kidney injury varied significantly based on practice variations and etiologies. Also, for years the association between acute kidney injury and chronic kidney disease remained unclear. To help clarify the relationship between these syndromes and the definition of acute kidney injury, the Kidney Disease: Improving Global Outcomes (KDIGO), Clinical Practice Guidelines were put forth to standardize the criteria for the management and diagnosis of acute kidney injury. The transition period from acute kidney injury to chronic kidney disease, known as acute kidney disease, was not well defined and rarely designated in clinical practice. The Acute Disease Quality Initiative (ADQI) Workgroup suggested a consensus definition of Acute Kidney Disease to encourage more widespread clinical implementation.

If acute kidney injury persists for more than 90 days, it is considered an incident or progressive chronic kidney disease.

As detailed above, acute kidney injury affects up to 20% of hospitalized and 50% of patients in the intensive care unit. Acute kidney injury is associated with increased hospital stays overall, particularly intensive care unit stays. As such, it is associated with increased healthcare costs. Common complications associated with acute kidney injury include hypertension, cardiovascular disease, development of chronic kidney disease, and eventually end-stage renal disease.

According to Heung et al., an episode of acute kidney injury is associated with a ten-fold increase in the risk of chronic kidney disease and a three-fold increase in the risk of end-stage renal disease (Heung et al., 2016). It is important to recognize and treat acute kidney injury early to reduce the risk of further kidney damage.

Traditionally, the management of acute kidney injury has been based on the KDIGO recommendations focusing primarily on fluid management, hemodynamic support, avoiding nephrotoxic agents, and renal replacement therapy when appropriate.

In 2012, KDIGO published a clinical practice guideline for the evaluation and management of Chronic Kidney disease, which sought to provide guidance in the evaluation, management, and treatment of patients with chronic kidney disease. They recommended a new method of staging chronic kidney disease based on its cause, the GFR and albuminuria categories (KDIGO, 2012).

Risk factors for chronic kidney disease can be divided into demographic and clinical factors. Demographic factors include male sex, older age, African American race, and Hispanic ethnicity. Clinical factors include a family history of CKD, diabetes, hypertension, hyperlipidemia, cardiovascular disease, smoking, and obesity.

They also noted that the risk of CKD increased significantly with age, estimating that almost 50% of all cases of CKD in the United States occurred in patients over the age of 70. Overall, they determined that women were at greater risk for CKD than men. However, fewer women progressed to ESRD compared to men.

Diabetes Mellitus is the most significant contributor to CKD in the United States and worldwide. Cardiovascular disease is the number one cause of morbidity and mortality in patients with CKD (at every stage). Other comorbidities include depression, sexual dysfunction, calciphylaxis, and malnutrition, to name a few.

The medical management of patients with CKD can be very challenging, considering the multiple comorbidities and the potential for damaging effects if mistakes are made in their care. This is compounded by the fact that patients with CKD may experience deleterious effects from standard medication therapy used to treat the very same comorbidities in non-CKD patients. Therefore, it is imperative to provide appropriate care to these patients taking all of their comorbidities into consideration.

When discussing the management of CKD patients, the patient population can be divided into two groups: patients with CKD and patients with end-stage renal disease (ESRD). Nurses and other health care practitioners caring for patients with CKD must be cognizant of the perils of applying standard therapy to this patient group.

Angiotensin-Converting Enzyme (ACE) inhibitors and Angiotensin Receptor Blockers (ARBs) are commonly used together to manage hypertension in patients with CKD. There is, however, a greater incidence of acute kidney injury and adverse cardiac events with the use of medications in these drug classes. Common adverse events reported with these drug classes include anaphylaxis and hyperkalemia. At the same time, ACE inhibitors are associated with cough and angioedema.

You are a nurse for a primary care physician who is seeing a 23 year old who was recently diagnosed with CKD and is also hypertensive. He was started on Lisinopril 3 weeks ago and has reported a chronic nonproductive cough since then. He denies any other signs and symptoms of a cold. He reports no other complaints and is dismissive of the cough but continues to clear his throat during your assessment.

You are a dialysis nurse working at an outpatient clinic, and part of your clinic’s policy is to review each patient’s medication list each month. Ms. C. is a 38-year-old female with a history of CKD, HTN, and Diabetes. She recently visited her parents, and while she was there, she felt dizzy at a family function. Her mom checked her glucose level and noted that her blood glucose was 478. Her mom insisted she sees the family doctor who had been taking care of her before she left for college. He noted that she had been taken off Metformin, which she had previously been on, and instead was prescribed glipizide. He then added Metformin 1000mg PO daily. Of note, she neglected to tell the doctor she was now diagnosed with ESRD. She has been taking Metformin and glipizide for a total of 3 weeks.

With hemodialysis, specific complications occur acutely during the dialysis process that dialysis nurses must be cognizant of, including hypotension, cramps, nausea and vomiting, headache, chest pain, back pain, itching, fever, and chills. We will focus on a few commonly occurring complications during dialysis.

Often, dialysis nurses are expected to manage these acute dialysis complications independently, given the acuity and frequency of their occurrence. As such, they are expected to be well versed in managing these complications.

It occurs in 25-55% of hemodialysis treatments. Variations in blood pressure are caused by a decrease in blood volume induced by the process of ultrafiltration coupled with the fact that patients with ESRD tend to have abnormal compensatory response systems to fluid removal.

Repetitive episodes of intra-dialysis hypotension have been associated with asymptomatic myocardial ischemia, which induces myocardial stunning and eventually irreversible cardiac death.

Dialysis-associated hypotension should be managed acutely by discontinuing ultrafiltration, administration of 100-250 ml of isotonic saline, 10 ml of 23% saturated hypertonic saline, administration of a low salt albumin solution. Other methods proposed for limiting the occurrence of hypotension during dialysis include careful evaluation and monitoring of the patient’s dry weight. The estimated dry weight is defined as the patient’s baseline weight without the weight of the fluid accumulated in between dialysis treatment sessions. The corresponding measure in a non-ESRD patient will be the weight the patient weighs after urinating. Cooling the dialysate during dialysis and refraining from eating heavy meals during and immediately before dialysis are also used to prevent hypotension.

Finally, decreasing inter-dialysis weight gain, promoting greater sodium to water restriction, and correcting severe anemia have all been beneficial in managing hypotension occurring during dialysis.

Muscle cramps are a complication of unclear etiology, which are relatively common in dialysis patients occurring in 5-20% of dialysis treatments. Changes in muscle perfusion secondary to extremely rapid volume removal often precipitate dialysis-associated cramps.

Cramps can be treated by decreasing the ultrafiltration rate either by reducing the volume to be removed during dialysis or increasing the dialysis time. Another method is ultrafiltration profiling; sodium modeling profiles and the administration of hypertonic saline have been reported as beneficial. In non-diabetic patients, using D50W solution is helpful, particularly towards the end of the dialysis session, especially since glucose is metabolized without the effects of hyperosmolality and intravascular volume expansion. Diazepam has also been shown to treat dialysis-associated muscle cramps effectively, but it may also cause hypotension. Quinine is also very effective in preventing muscle cramps if administered 1-2 hours before the hemodialysis session. However, a significant side effect is the risk of thrombocytopenia. Vitamin E and L-Carnitine have also been shown to be weakly effective.

DDS is a syndrome characterized by various acute neurologic symptoms, ranging from benign to very severe. DDS usually affects dialysis patients when they first start dialysis, and it is thought to be secondary to cerebral edema.

Risk factors for DDS include CKD as a reason for initiating dialysis rather than Acute Kidney Injury (AKI), first dialysis treatment, very high urea concentrations in the blood prior to initiating dialysis, older age, and pediatric patients.

Clinical manifestations of DDS include nausea, vomiting, headache, restlessness, blurred vision, asterixis (the hand's tremor when the wrist is extended due to the inability to actively maintain position secondary to metabolic encephalopathy), confusion, seizures, comas, or death.

The best course for management of DDS is to establish slow urea removal either by reducing the duration of the first few dialysis sessions or by alternating ultrafiltration with hemodialysis. Also, starting with a low blood flow rate and slowing building up to the target blood flow rate during sessions has been shown to be beneficial.

Allergic reactions to the dialyzer

Although uncommon, anaphylactic reactions to the dialyzer can occur, especially on the first use. Reactions will be divided into three types in this article.

• Type 1 reactions are attributed to an IgE mediated hypersensitivity reaction to ethylene oxide used to sterilize new dialyzers. Type 1 reactions usually occur within a few minutes and may progress to full anaphylaxis if the offending stimulus is not removed (i.e., stopping the dialysis treatment). Treatment is usually with epinephrine and steroids. Dialysis should be stopped immediately, and the patient’s blood should not be returned.
• Type 2 reactions occur from complement activation and cytokine release. This reaction usually occurs several minutes (usually 20-40 minutes) into the dialysis treatment and will typically resolve with continued dialysis. They usually present as nonspecific symptoms such as chest and back pain.
• Type 3 reactions are pyogenic reactions that can occur at any time. They usually occur from endotoxin or bacterial contamination. Treatment is to stop hemodialysis immediately if hypotension is present, collect blood cultures, and administer antibiotics and antipyretics.

The most common complications occurring with peritoneal dialysis include peritonitis, catheter-associated infections (non-peritonitis infections), metabolic disturbances, and residual uremia. Peritonitis usually occurs secondary to a lack of sterile technique during peritoneal fluid exchange procedures. Clinically, peritonitis is diagnosed by an elevated peritoneal fluid with a blood cell count greater or equal to 100/uL (at least 50% of those being neutrophils). Of note, the bacterial count cut-off is lower than that established for the diagnosis of spontaneous bacterial peritonitis because the peritoneal dialysis solution contains sugars in the form of dextrose. The clinical presentation is usually a cloudy dialysate fluid with abdominal pain and fever. The common organisms involved are gram-positive cocci and other skin flora.

Treatment is either with intraperitoneal or oral antibiotics, and most patients can be managed on an outpatient basis. If the infection does not respond to antibiotic therapy, the dialysis catheter may be removed. In catheter-associated infections not related to peritonitis, management may be limited to silver nitrate administration or antibiotic therapy, and on rare occasions, the catheter may have to be removed.

Peritoneal dialysis patients are prone to multiple metabolic complications. For example, albumin and other proteins could be lost across the peritoneal membrane. There is a smaller chance of potassium and phosphorus accumulation with peritoneal dialysis than with hemodialysis.

Drugs that are primarily eliminated by the kidneys, have a narrow therapeutic index, or have active metabolites primarily eliminated by the kidneys should be closely monitored for adverse side effects. These dose adjustments are necessary to avoid toxicity in patients with CKD.

Medication errors are a huge factor contributing to morbidity in patients in general, especially in patients with CKD. Many medication errors occur in patients with CKD due to prescribing standard doses to patients who should be receiving reduced doses or prescribing medications to ESRD patients that should never be prescribed.

Most drug doses have to be adjusted in dialysis patients. This section will focus on understanding why and how doses must be adjusted in patients with CKD and patients with dialysis. First, we must understand the bioavailability of drugs, defined as the percentage of a drug that reaches the bloodstream. Note that bioavailability is 100% in the IV administration of drugs.

In patients with ESRD, multiple factors affect drug availability, including:

• decreased gastrointestinal absorption
• co-administration of drugs with phosphate binders that form complexes, making them insoluble and, therefore, nonabsorbable
• impaired plasma protein binding results in more free drugs available for metabolism through the liver
• uremia has been shown to alter drug pharmacokinetics and pharmacodynamics

The volume of distribution of a drug is not an actual physical volume; instead, it is a theoretical volume obtained from the ratio between the dose of a drug present within the body and the plasma concentration. Once the drug concentration within the tissues and plasma has reached equilibrium, the ratio is calculated. Therefore, lipid-soluble drugs tend to have a higher volume of distribution while lipid-insoluble drugs have a low volume of distribution.

ESRD patients with uremia may have decreased protein binding of drugs, affecting the amount of free (active) drugs available. Also, drug metabolism by non-hepatic oxidation is delayed in patients with renal disease, thereby affecting the plasma concentration.

A few drug classes have a narrow therapeutic range, making it necessary for clinicians to monitor drug ranges due to the risk of drug toxicity. Antibiotics are a commonly used drug class, and we will review a few drug classes and how their metabolism is affected in patients with CKD. Frequently, dialysis patients have poor vascular access options; therefore, dialysis nurses are asked to draw multiple labs to check for specific drug levels. It is crucial to understand when these drug levels may be drawn. Often, the clinicians requesting the labs are not nephrologists, and in such cases, dialysis nurses should be able to educate and properly communicate with non-dialysis specialized personnel. This section will focus on two common examples.

Aminoglycosides, e.g., Gentamicin (peak of 5-8 mg/L and a trough of 0.5-2 mg/L). The peak is usually drawn 30 min after a 30 -45 min infusion. The trough is generally drawn immediately prior to the dose. Both are drawn around the third dose.

Digoxin has a therapeutic dose range of 0.8-2.0 ng/mL, and the lab is usually checked 5-7 days after the first dose in patients with normal renal function and 15-20 days in anephric patients. The lab sample should be drawn 12 hours after the maintenance dose is administered in all patients.

Most drug dosing must be adjusted in patients with ESRD, and some drugs may be avoided altogether. In today’s healthcare climate laden with polypharmacy and over-prescription, nurses must understand which drugs place their patients at increased risk for experiencing toxic side effects. We will examine a few common drugs and review how the doses change depending on the GFR.

Acetaminophen can be administered at standard doses as often as every 4 hours in patients with a GFR > 50 mL/min. In patients with a GFR between 10-50 mL/min, the standard 4-hour doses should be administered at 6-hour intervals. And in patients with a GFR < 10mL/min, the standard dose should be administered at 8-hour intervals. Patients on hemodialysis and peritoneal dialysis should also receive their dose reduced to 8-hour intervals.

Acetazolamide is a carbonic anhydrase inhibitor commonly used as a diuretic or for the treatment of glaucoma. In patients with a GFR > 50 mL/min, the standard dose should be administered every 6 hours. If the GFR is between 10-50 mL/min, the dose should be prolonged to q12h, and if the GFR is less than 10 mL/min, the dose should be prolonged to q24h. In patients receiving hemodialysis and peritoneal dialysis, the dose should be administered q24h.

Acetylsalicylic acid (Aspirin) can be administered q4h in patients with a GFR > 50 mL/min. The dose should be prolonged to q4-6h in patients with a GFR between 10 - 50 mL/min. It should be avoided entirely in patients with a GFR < 10 mL/min. Patients on hemodialysis and peritoneal dialysis may receive standard doses as patients with a normal GFR because it is appropriately cleared during dialysis.

When administering Atenolol in patients with CKD, the dose must be decreased by 50% in patients with a GFR between 10 - 50 mL/min. In patients with a GFR < 10 mL/min, the dose should be decreased to 33% of the daily dose administered every 24 hours.

Cefazolin is typically administered q8h in patients with GFR > 50 mL/min. In patients with a GFR between 10 -50 mL/min, the dose should be prolonged to q12h. If the GFR is < 10mL/min, the dose should be halved and administered q24-48h. In hemodialysis patients, the dose should be weight-based at 15-20 mg/kg.

Digoxin dose should be decreased by 10 – 25% of the standard dose administered to patients with a normal GFR. And in patients with a GFR < 10 mL/min, the dose is decreased to 10-25%, and the timing is prolonged to q24-48h.

Rivaroxaban (Xarelto) and Triamterene should be avoided in patients with a GFR < 50 mL/min, including dialysis patients.

Hemodialysis access can be either short-term access or long-term access for hemodialysis. There are three options for long-term hemodialysis access: arteriovenous fistulas (AVF), arteriovenous grafts (AVG), and a tunneled venous catheter. Note that these are listed in the order of decreasing preference.

When considering options for short-term dialysis access, the focus is to provide access that can be used immediately and has minimal complications in the short term. Ideally, an arteriovenous fistula should be placed at least six months prior to initiating dialysis. A dialysis graft should be placed 3-6 weeks prior to the initiation of dialysis. A peritoneal dialysis catheter should be placed at least two weeks prior to the initiation of peritoneal dialysis.

Note that not all venous access catheters are equal. Specific catheters must be used when intending to perform dialysis. Dialysis catheters tend to have larger lumens to withstand the high blood flow rates. Ideal access has to withstand flow rates of up to 600 ml/minute. The basic dialysis catheter has at least two ports: red and blue. The red port removes blood away from the patient, and the blue port corresponds to the venous return port. Some catheters include a third port used for lab draws that some dialysis patients may require as frequently as once a week.

Some have termed dialysis access as “the patient’s lifeline,” and as such, patients are very protective of their access. Dialysis nurses are skilled at assessing the dialysis access for potential complications. Still, sometimes non-dialysis nurses are taking care of patients and are faced with the ordeal of assessing a patient’s dialysis access. Assessing dialysis access will be discussed by reviewing the following case studies.

You are a medical/surgical nurse working in a hospital setting, and you have a newly assigned patient. Mrs. T. is a 55-year-old female admitted with congestive heart failure. This is her 3rd admission in the past six weeks. She recently had her arteriovenous fistula on her left forearm fail and had an arteriovenous graft placed four weeks ago on her right upper arm. She also has a tunneled dialysis catheter on her right chest. Upon physical assessment, you notice that all the accesses are uncovered, and the access on her left forearm has pus oozing out of an open wound overlying the access. Upon questioning, the patient reports that she was picking at the scabs on her AVF access when she noticed pus oozing out about a week ago. She also reports that her catheter exit site was occasionally itchy, which is why the dressing fell off.

Mr. P. is a 45-year-old male with a right forearm AVF admitted for pneumonia and respiratory failure necessitating intubation. You are an ICU nurse caring for this patient who is currently extubated. He gets dialysis on Mondays, Wednesdays, and Fridays, and you are working on a Sunday. You cared for him the previous day, and this morning you are performing your nursing physical assessment. You notice a faint thrill but do not hear a bruit. What do you do next?

Caring for patients undergoing dialysis comes with special challenges for physicians, mid-level providers as well as nurses, and other allied healthcare providers, including social workers and hemodialysis technicians. The challenges faced by the patients undergoing dialysis are very unique because initiating dialysis is usually reserved for patients with end-stage renal disease (ESRD). Implying that the majority of patients initiating dialysis usually remain on dialysis indefinitely or until they get a kidney transplant which may take years.

In addition, they reported that depression in patients with CKD has been linked to poorer outcomes. The challenge of making the diagnosis in this patient group is the fact that depression is confounded by the overlap in symptoms with multiple comorbidities.

The nutritional restriction imposed by the disease processes is bound to cause some degree of emotional distress. Not being able to drink as much water as one pleases can be frustrating in and of itself. Not to mention the innumerable dietary restrictions.

CKD patients, especially those on dialysis, face many challenges and often times have limited emotional support systems because their families may experience caregiver burnout, or they may be reclusive in forming relationships given the chronicity of their disease. However, as nurses caring for patients with dialysis, we could always show empathy because our emotional support may be the only source of support our patients receive on any given day.

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