Managing Care of the Client with Chronic Kidney Disease

This is another rather big topic, made more complex by the fact there are different stages that involve different
treatments. Studying tip: I have also posted a “summary table”- for the complications of later stages that
should save you some time in your test prep.

References
BC Renal Agency. (2017). Management of pruritus in patients with chronic kidney
disease. [Link]
gallery/Documents/Management%20of%20Pruritus%20in%20Patients%20with%20Chronic%20Kidney%20Disea
[Link]
Berns, J. (2023 April 6). Uremic platelet dysfunction. UpToDate.
Berns, J. (2024 March 6). Treatment of anemia in nondialysis chronic kidney disease. UpToDate.
Berns, J. & Glickman, J. (2024 January 3). Management of hyperglycemia in patients with type 2 diabetes and
pre-dialysis chronic kidney disease or end-stage renal disease. UpToDate.
Canadian Agency for Drugs and Technologies in Health. (2016). Dialysis for the treatment of end stage kidney
disease in Indigenous patients in Canada: A review of clinical
effectiveness. CADTH. [Link]
Davison, S. (2023 November 18). Management of chronic pain in advanced chronic kidney disease. UpToDate.
de Filippi, C. & Henrich, W. (2022 June 9). Cardiac troponins in patients with kidney disease. UpToDate.
Manitoba Renal Program. (2020). Guidelines for Managing Hospitalized Hemodialysis
Patients. [Link]
Jacobson, J., Ju, A., Baumgart, A., Unruh, M., O’Donoghue, D., Obrador, G., Craig, J. C., Dapueto, J. M., Dew, M.
A., Germain, M., Fluck, R., Davison, S. N., Jassal, S. V., Manera, K., Smith, A. C., & Tong, A. (2019). Patient
perspectives on the meaning and impact of fatigue in hemodialysis: A systematic review and thematic analysis of
qualitative studies. American Journal of Kidney Diseases, 74(2), 179–192.
[Link]
Kiernan, M.S., Udelson, J.E., Sarnak, M., & Konstam, M. (2022 May 10). Cardiorenal syndrome: Definition,
prevalence, diagnosis, and pathophysiology. UpToDate
Diabetes Canada Clinical Practice Guidelines Expert Committee, Lipscombe, L., Butalia, S., Dasgupta, K., Eurich,
D. T., MacCallum, L., Shah, B. R., Simpson, S., & Senior, P. A. (2020). Pharmacologic Glycemic Management of
Type 2 Diabetes in Adults: 2020 Update. Canadian Journal of Diabetes, 44(7), 575–591. [Link]
[Link]/10.1016/[Link].2020.08.001
Macdonald, D. B., Hurrell, C. D., Costa, A. F., McInnes, M. D. F., O’Malley, M., Barrett, B. J., Brown, P. A., Clark, E.
G., Hadjivassiliou, A., Kirkpatrick, I. D. C., Rempel, J., Jeon, P., & Hiremath, S. (2022). Canadian Association of
Radiologists Guidance on Contrast-Associated Acute Kidney Injury. Canadian Journal of Kidney Health and
Disease, 9, 20543581221097456. [Link]
Mann, J. (2022). Overview of hypertension in acute and chronic kidney disease. UpToDate.
McFarlane, P., Cherney, D., Gilbert, R. E., & Senior, P. (2018). Chronic kidney disease in diabetes. Canadian
Journal of Diabetes, 42, S201–S209. [Link]
Quarles, L. D. & Berkoben, M.D. (2023). Management of secondary hyperparathyroidism in adult dialysis
patients. UpToDate.
Qazi, H., Chen, H., & Zhu, M. (2018). Factors influencing dialysis withdrawal: A scoping review. BMC
Nephrology, 19(1). doi:10.1186/s12882-018-0894-5
Rickeard, D. (2023). Acute Kidney Injury and Chronic Kidney Disease. In J. Kwong, C. Reinisch, J. Tyerman, S.
Cobbett, D. Hagler, M. Harding, & R. Dottie (Eds.), Medical surgical nursing in Canada: Assessment and
management of clinical problems (5th Canadian ed., pp. 1180-1212). Elsevier Canada.
Rosenberg, M. (2022 November 10). Overview of the management of chronic kidney disease in adults.
UpToDate.
Sarnak, M., Gibson, M., Henrich, W. (2023 May 16). Chronic kidney disease and coronary heart disease.
UpToDate.

1
 Lay-out of this lesson:

• PART 1: Definition, etiology and diagnosis

• PART 2: Treatment in earlier stages

• PART 3: Consequences of late stages (4 & 5) and treatments

including RRT- (dialysis and transplant)

Because the focus of treatment varies so much between the different stages of
CKD, I have separated the presentation into these parts. Your textbooks often
present CKD as one homogenous condition, but as we move through the content,
it is important that you try to separate how the pt’s symptoms, complication risk,
and focus of treatment changes as the CKD progresses.

2
 Definition of CKD:
• The Kidney Disease Outcomes Quality Initiative (KDOQI) defines
CKD as either kidney damage or GFR <60 mL/min/1.73 m2 for 3
months or longer.

• Up to 80% of the GFR may be lost with few overt changes in body
functions due to local compensation via hyperfiltration

The definition of GFR including normal range was covered in first-year and will not be
tested in this course but being familiar with basic kidney function and how it is measured
will help you in your overall understanding of CKD. If you forget how normal kidney
physiology works, it is recommended you review this information. If you need additional
support, let me know.

We do not test the numbers on this slide! Just know that an elevated creatinine (i.e., a
decreased GFR) needs to be present for at least 3 months to be diagnosed with CKD.
Basically, if a patient were to present with a newly elevated creatinine, we will treat it as
AKI. If the Cr level does not return to normal and remains elevated for 3 months or
more, then the pt officially meets the criteria for CKD.

FYI- Manitoba has one of the highest rates of diabetic nephropathy, end stage kidney
disease, and dialysis rates in Canada. - [Link]
continues-to-have-the-highest-rates-of-kidney-disease-in-canada/

3
 4

DM: diabetic nephropathy – The CKD case studies in this course will always involve a pt who has DM
nephropathy. However, the focus will not be on the patho of its development- the pathophysiology
will be covered in detail in Patho2 and will NOT be tested in this course.

Hypertension - chronic hypertension leads to renal vascular changes, glomerulosclerosis, and

tubulointerstitial disease. Together diabetes and hypertension account for >50% of all cases of CKD
and often they occur together (Rickeard, 2023).

Dyslipidemia- accelerates glomerular and tubular damage in CKD.

These other conditions can lead to CKD but will not be covered in this course. Just know some of these
will likely be tested on the NCLEX.
Other Risk Factors
• Older adults at increased risk due to natural decline in functional nephrons
• Congenital conditions -e.g.: polycystic kidney, organ malformation
• Autoimmune disorders (connective tissue disorders) e.g.: lupus, Wegner’s granulomatosis
• Repeated incidences of kidney damage due to obstruction or other causes
• Indigenous and African Americans at greater risk

4
 SDoH…connections to CKD
• Indigenous people are more likely to develop CKD and to
progress to needing RRT.
• Ethnicity is non-modifiable but SDoH are modifiable.
• Rates of CKD and DM in the Indigenous population are more
closely linked to SDoH than to genetics
• Access to care is also an issue
• Increased focus on screening and prevention in these
populations
5

“Indigenous Canadians make up approximately 4.3% of the total Canadian

population and 17% of the population in Manitoba, however, in Manitoba,
Indigenous patients comprise 30% of the hemodialysis (HD) population. Further, one
estimate shows that Indigenous Canadians are 43% less likely to see a nephrologist
than their non-Indigenous counterparts” (CADTH, p. 14, 2016).

5
 Diagnostics: Screening for CKD
Albumin:Creatinine Ratio (ACR)

As a progressive chronic condition that is often asymptomatic in early stages, CKD meets the
criteria for a condition for which a population will be screened. The age at which this begins
will depend on a person’s cumulative risk factors.

Spot urine for albumin creatinine ratio (UACR)

• Detects small amounts of albumin that escape from the blood through the glomeruli into
the filtrate and is evidence of early glomerular damage
• Urine creatinine level is included in the ratio to determine the concentration level of the
urine to correct for diluted or concentrated amounts of albumin
• The amount of creatinine has no diagnostic relevance for this test
• Albumin is what is really being measured.

Ideal screening tests detect issues early. Therefore, the ACR is valuable in that it can give us
an indication of glomerular damage long before the eGFR is decreased, allowing for earlier
intervention to slow the progression of kidney damage.
The fact that it can be done on a spot urine test also makes it convenient. As indicated in the
graphic above, the pt would need to have 10 times the amount of protein (albumin) in their
urine for it to show up on a regular “dipstick” used with a urinalysis compared to the ACR.

New terminology: microalbuminuria is now being referred to as “moderately increased

albuminuria” in some resources. We will just use microalbuminuria in this course.

6
 Review!
Other diagnostic tests

Biochemistry tests on plasma:

• Creatinine- best indicator of GFR (calculation to determine estimated
GFR [eGFR] done using creatinine, age, gender)

• Urea- influenced by protein and fluid balance

Other investigations to determine the cause (will not be tested)

1. Plasma creatinine- creatinine is a waste produced by muscle breakdown and is

completely cleared through glomerular filtration making this test the most
rei s

blood i levelsare not

Clinically

accurate source to estimate GFR. creatininies a CR is a Best indicator for GFR

Wastepromthenormalbreakdownormuse ther
if
Kidney function declines creatinine builds up in the

leading to increased plasma creatinine level

Kidney
-HighCRmorethanmonthseas
of function
Higher Creatinine = The worse kidney function

2. Plasma urea- is the primary nitrogenous waste product of amino acid

metabolism. It is also excreted via glomerular filtration but is influenced by
things like how much protein a patient has consumed, rate of amino acid
metabolism, and sodium reabsorption from the renal tubules into the blood.
Therefore, although urea is a measure of kidney function, it is not as accurate as
creatinine for estimating GFR. Urea

High
= a waste product formed When the liver breaks down proteins into ammonia >
-

then converted intourea

urea =

Kidney disfunction or high protein diet

low urea = liver dysfunction or low protein intake

Clinical tip: Having a low creatinine or urea level is not clinically relevant. A low
creatinine is often related to having a low muscle mass and low urea may also be
seen in liver failure (recall that the liver makes urea out of ammonia) but urea levels
are not monitored in pts with liver disease. So, you never need to report low levels of
these lab results as something to be concerned about.

Other biochemistry tests–other blood tests can discover cause if not apparent (e.g.,
immunology for autoimmune conditions such as systemic lupus erythematosus [SLE])
Dx imaging/others- e.g., Renal ultrasound, biopsy, CT scan- Helps determine
possible cause of renal injury/failure by examining structures and/or histology.

7
 Stages of CKD
According to National Kidney
Foundation Kidney Disease
Outcomes Quality Initiative (NKF
KDOQI), staging of CKD should be
done according to the following:

• Cause of disease
• Five main stages of eGFR (G
stages)
• Three stages of albuminuria (A
stages)

May be referred to as “CGA”

staging.
8

• There are 5 stages based on GFR.

• Stage 3 is subdivided into 2 groups (A and B).
• This was done because the symptoms can progress quite a bit between early and
late stage 3, making the recommended treatments different.

• Albuminuria (UACR) is incorporated with the pt’s current GFR to create a “CGA” stage of
CKD.

Notice that the monitoring of albuminuria (albumin in the urine) has 2 distinct purposes-
one is for screening for CKD BEFORE the pt is diagnosed and the other is for staging CKD
and the risk for cardiovascular complications to help direct ongoing treatment AFTER the pt
has been diagnosed with CKD.

Note that most textbooks will not include these updates regarding dividing stage 3 and
albuminuria levels.

8
 PART 2: Treatment in earlier stages
Slowing progression through the stages of CKD

Targets for slowing progression of CKD

1. Preventing acute on chronic kidney injury (A/CKI)

2. Optimizing DM treatment and controlling HTN
3. Reducing proteinuria

4. Overall cardiovascular risk reduction

9

This is a list of the targets for slowing the progression of kidney disease when the
pt is in the earlier stages. Each of these targets are discussed on the subsequent
pages.

9
 1. Preventing A/CKI (our focus is on pre-renal AKI)

How can we tell this is acute?

• Elevation in baseline Cr (e.g. >25μmol in 48 h or
creatinine to ≥1.5 times in past 7 days)
• Or, acute onset oliguria

• Specific to pre-renal AKI--> High Ur:Cr ratio

• Intra-renal AKI- creatinine levels rise more than urea
(lower urea:creatinine ratio)
10

You do NOT need to memorize the numbers on this slide. Just know that an elevation in
Cr from baseline or oliguria can be used to identity AKI. We will not be covering stages of
AKI, etc.- this is covered in Acute Conditions in Adults. Also please remember that the
causes of AKI are completely different from the causes of CKD!

Note: Primary risk factor for AKI is underlying kidney disease.

• Key difference is that b/c it is an acute change, there is an acute cause! Therefore, it
should be treatable and at least partially reversible.
• Each episode of AKI in the person with CKD can accelerate the progression of the
underlying CKD, so efforts to avoid AKI are important.
• Causes of A/CKI are categorized the same as AKI

Urea is disproportionately elevated when the cause of AKI is pre-renal (i.e., related to
decreased renal perfusion). This was outlined last year and is also covered in Patho 2 this
year.
As a reminder:
• urea is reabsorbed into the blood stream when the kidneys are conserving sodium due
to the effects of aldosterone
• creatinine does not get reabsorbed in the setting of low renal perfusion
• Therefore, in pre-renal AKI BOTH creatinine AND urea are elevated, but urea is MORE
elevated than creatinine.
• If the issue is with the kidney itself (intra-renal AKI), the urea will not be reabsorbed
and the urea:creatinine ratio will be lower.
urea is
partially reabsorbed by Kidneys so When Kidneys fail it rises
more in cases of
dehydration blood
,
loss or HF

10
 1. Causes of Pre-Renal AKI
• Any condition that reduces renal blood flow (e.g. dehydration,
shock) can lead to pre-renal AKI
• Medications that make pre-renal acute kidney injury worse:
• Diuretics
• NSAIDs (relatively high dose)
• ACE-Is & ARBS

• There are optional videos posted on Learn to help you understand

this topic

11

Always remember that if we are saying a pt is experiencing ACUTE kidney injury, this
means something has ACUTELY changed for that patient. In the case of pre-renal AKI this
means there is something causing an acute decrease in renal blood flow (usually r/t
decreased cardiac output for any variety of reasons).

Recall that when blood flow decreases to the glomeruli, renal autoregulation
compensates in an attempt to preserve glomerular filtration pressures. Renal
autoregulation of glomerular pressure involves:
• dilation of the afferent arteriole
• constriction of the efferent arteriole

The medications listed on this slide can interfere with this local compensatory
autoregulation and therefore can cause a decrease in GFR.

NOTE: The concept of normal autoregulation of renal blood flow was covered in
PD1. (there is a video reviewing this for those who wish to review in the recorded lesson)

Although it is an NSAID, low-dose aspirin (<100 mg OD) does NOT appear to pose a risk
for interference with afferent arteriole vasodilation and is considered safe for most
people with CKD. However, NSAIDs that are dosed at levels to treat pain or fever
WOULD potentially affect renal autoregulation and worsen pre-renal AKI (Sarnak,
Gibson, & Henirch, 2023).

11
 1. Prevention of pre-renal AKI and other complications:
SADMANS

12

A group of medications commonly taken by patients with DM type 2 have been identified by
the Diabetes Canada as needing special precautions for patients when they are ill with a
dehydrating illness. Some of these meds may increase risk for a decline in kidney function
due to interference with autoregulation as previously discussed, while others are dangerous
because they rely on renal elimination and will accumulate when GFR decreases.

All of these medications can be perfectly safe for the patient when they are euvolemic. So, if
a pt is admitted with pre-renal AKI and they are taking an ACE-I for example, the ACE-I will
be held but once pt is euvolemic, the ACE-I will usually be restarted.

*Because many of the patients at risk for AKI also have diabetes and are taking these
medications, this teaching r/t prevention of AKI should be combined with the information
about avoiding the development of DKA and HHS that was presented in our diabetes
class.

12
 1. Causes of acute INTRA-Renal AKI (intrinsic AKI)
The most common type of intra-renal AKI is call acute tubular
necrosis (ATN)

ATN is associated with:

• Aminoglycoside antibiotics (gentamicin)
• IV contrast media (radiocontrast) (See note about metformin
below)
• Sepsis
• Cardiac surgery 13

While prerenal AKI is common for patients with CKD in the community due to medications and
dehydrating illnesses, intrinsic AKI is more common in hospitalized patients.
Also, if not caught and treated, the decreased renal perfusion of prerenal AKI can progress to
ATN. Basically, if there is prolonged or severe renal ischemia this can cause destruction of the
tubular epithelium and the same thing (basically) can happen with certain nephrotoxic
medications. This damage can lead to sloughing of cellular debris, plugging the tubules. The
damage can also lead to tubular contents (filtrate) “leaking” back into the peritubular
capillaries- i.e., re-entering the bloodstream. ATN is potentially reversible if the basement
membrane is not destroyed and the tubular epithelium regenerates (Rickeard, 2023).

REMINDER: Link between renal function, metformin and CT contrast: As mentioned above,
radiocontrast can cause AKI. For this reason, patients taking metformin should hold the drug
prior to their test and for 48 hours post IV contrast. This is because the decline in GFR caused
by the CT contrast increases the risk for lactic acidosis (a type of metabolic acidosis) if
metformin is continued. Metformin is NOT nephrotoxic and does not accelerate kidney injury-
it just increases the risk for lactic acidosis if pt has a lower GFR.

FYI: Updated best practice guidelines from 2022 are less strict r/t CT contrast nephropathy.
They no longer recommend stopping metformin for patients with eGFR >30. For eGFR ≤30 or
AKI, metformin should be held at the time of, or prior to, contrast administration, and should
not be restarted for at least 48 hours. They also no longer recommend the use of N-
acetylcysteine (Mucomyst) and IV hydration pre-procedure is only recommended in certain
high-risk pts rather than routinely for most pts (MacDonald, et al., 2022).

I will not be going into the diagnostics or tx for ATN. Just know these basic risk factors and be
aware that the pt with underlying CKD is at greater risk.

13
 2. Optimizing DM and HTN Tx
The same as if your patient only had diabetes until patient reaches stage 3b
in most cases.
• goal is a BP of <130/80
• HGBA1c of <7% while avoiding hypoglycemia.
• Metformin is safe until late stage 3B/stage 4 CKD (GFR<30)
• Shorter acting sulfonylureas safer over longer ones like glyburide in CKD
• SGLT2 inhibitors are now recommended for slowing progression of CKD in
some pts

14

Metformin is still the preferred first-line oral diabetic medication. Once the pt reaches stage
3b, doses often must be adjusted (to reduce the risk for developing lactic acidosis). In the case
of drugs that are highly reliant on renal clearance, such as glyburide, it is recommended an
alternate agent be used (Lipscombe, et al., 2018).

14
 3. Preventing Proteinuria
• Known risk factor for progression of CKD

• Linked to CV events

• Treated with ACE-I (primarily)

• Moderate protein restriction

Most North Americans eat more than recommended amounts of protein.

Protein is moderately restricted in early stages of CKD and then increased
once on dialysis- this is individualized.
15

ACE-I (and ARBs) are considered “renal protective” in patients with diabetes.
• Current recommendations are to start pts on an ACE-I/ARB if they are positive for
microalbuminuria.
• While ACE inhibitors and ARBs have been shown to reduce proteinuria more than
other classes of antihypertensives, remember that they do pose important side
effects in patients with CKD such as:
• hyperkalemia
• pre-renal AKI due to the interference in renal autoregulation in hypovolemic
pts

As was mentioned, the amount of albuminuria is considered a predictor for CV

disease, so is included as part of the staging of CKD. The link between proteinuria and
cardiovascular disease is not well understood (let’s leave it at that!).

Dialysis treatment causes the loss of protein (peritoneal dialysis more so than
hemodialysis), so pts need more protein compared to before they are on dialysis.
Obviously, if the pt is no longer making urine, they cannot have proteinuria. However,
they still will have uremia which fluctuates based on protein intake. So, for the pt on
dialysis, the goal is to balance preventing protein deficit and preventing excessive
uremia.

15
4. The Patho connection between CVD and CKD
BOTH L-HF and CKD can contribute to:
• Hypervolemia
• Increased sympathetic activity
• Activation of RAAS
CKD-specific patho:
• CKD-mineral bone disorder
• Anemia

16

Cardiovascular disease is the leading cause of mortality in the pt with CKD. The connection
between kidney disease the heart disease is complex, multifactorial and reciprocal. There
are many sub-types of what is known as either “cardiorenal” or “renocardiac syndromes”.
We will try to simplify things for application in this course as a way to reinforce some basics
related to cardiovascular disease risks. Due to the complexity of resources, I decided NOT to
post a graphic showing the connections.

The basic patho connections:

• Hypervolemia- chronic FVE contributes to chronic HTN, accelerating atherosclerosis
and arteriosclerosis. The increase in preload is a primary contributor to LV dilation.
• Anemia- compensatory increase in HR contributes to LV hypertrophy.
• Increased sympathetic activity- chronic SNS activation leads to increased baseline HR
and increased contractility as well as vasoconstriction and ADH release (increased
afterload and preload) contributing to LV hypertrophy and dilation.
• Activation of RAAS- contributes to HTN (via both vasoconstriction and fluid retention)
increased afterload contributes to LV hypertrophy and increased preload contributes
to LV dilation.
• CKD-MBD- increase in arteriosclerosis and increased HTN as well as increased risk for
acute coronary syndrome.

16
 4. Reducing Cardiovascular Risk- Diabetes Canada
According to Diabetes Canada:

• ACE-I (previously discussed r/t proteinuria)

• SGLT2 inhibitor with proven CV benefit may be considered to reduce

the risk of major CV events

Other recommendations are similar to risk reduction in the general

population:

• BP tx, statins, ASA (secondary prevention only), weight loss, physical

activity.
17

You may have learned that troponin levels can be chronically elevated in the pt with CKD.
This is even more so now that we use high-sensitivity troponin assays. However, just as
with the general population, an increased troponin level is the primary diagnostic test for
MI in pts with CKD and is used in the same way, examining for elevations over time. Note
that increased troponin levels in stable, asymptomatic CKD patients predict worse long-
term cardiovascular outcomes and poor survival which implies this is not an entirely
benign laboratory artifact (de Filippi & Henrich, 2022).

17
 Part 3: Consequences of CKD, stages 3B-5 and the
treatments

Because complications and treatments in CKD vary depending on the stage, especially when
the pt begins dialysis treatments, it is important for you to be clear about these differences. I
will do my best to make it clear when information is specific to the patient on dialysis so you
can better make these associations when studying. As mentioned, textbooks often lump it all
together so be careful when reading about interventions in CKD- they vary GREATLY
depending on what stage the pt is in.

Once the patient is in stage 3b and in stages 4 they will begin to suffer from more overt
symptoms of CKD and require change from prior treatment. In stage 5, the patient may have
renal replacement therapy (dialysis or transplant) or they may choose conservative medical
management. Guidelines from the Canadian Society of Nephrology recommend that patients
with an eGFR <15 ml/min should be closely followed by their nephrologist and dialysis
deferred until symptoms of uremia, volume overload, hyperkalemia or acidosis become an
issue or the eGFR drops below 6 ml/min.

This section refers to effects we expect to see in patients nearing the need for dialysis and also
those already receiving dialysis treatments. Look for the HD icon for specific references to
dialysis patients in the notes. It was recommended that you review the general information
related to renal replacement therapy prior to this class. Although that information is not
tested directly, it will help you make sense of some of the information specific to dialysis in
this part of the lesson.

18
 Stages 3B-5- Complications primarily result from the failure for
the kidney to perform these functions:
1. Urine formation (filtration, reabsorption and excretion)

2. BP regulation
3. Hormone production (EPO and calcitriol)

Consider the Potential Complications the patient would be at risk for.

See posted table for a short-cut!
19

Each of these points are expanded upon in the upcoming slides. I left in the colour-
coding of the topics in case you wanted to print in colour and keep track of the
associations. You can always choose “grey scale” when printing to not use your
colour ink.

You should see some correlation to the various Potential Complications as we

discuss the patho, treatments, and nursing responsibilities related to CKD.
1. Physical injury (altered mobility, delirium, high-risk meds)
2. Malnutrition
3. Impaired oxygenation (ventilation, perfusion, transport)
4. Fluid imbalances (total body water, electrolyte, and acid base imbalances)
5. Infections and sepsis

19
 1. Failure of urine formation
A. Fluid retention
B. Build up of wastes including:
i. Creatinine and urea
ii. Hydrogen ions
iii. Certain electrolytes
▪ potassium
▪ magnesium
▪ phosphate
C. Decreased medication clearance

20

When your kidneys no longer produce enough normal urine, there are negative
consequences. This list of the primary consequences of oliguria and anuria will be
expanded on in the upcoming slides.

20
 A. Fluid imbalance

• Reminder! In stages 1-3 the pt is usually producing adequate

urine and we want to avoid AKI r/t FVD, so fluids are not
restricted. FVE can still be treated with diuretics.

• Stages 4-5= fluid restriction will depend on how much urine they
are producing and will be an MD order
Fluid restriction: Urine output +500-1000 ml/24h
Sodium restriction: MD or renal dietician order
21

Fluid balance can usually be maintained via homeostatic mechanisms until the eGFR falls
below 10 to 15 (when RRT is necessary). However, the renal “handling” of sodium is
impaired, increasing the risk fluid retention. Therefore, most pts with CKD who still produce
urine are treated with diuretic therapy (usually loop) and sodium restriction of usually <2
g/day unless contraindicated (Rosenberg, 2022).

Once in ESKD and requiring RRT, diuretics will no longer be effective, and the excess fluid is
removed via dialysis. Pts on hemodialysis will require fluid restriction but this is most often
not needed in pts getting peritoneal dialysis. It is very important to maintain the sodium
and fluid restrictions between HD treatments.

21
 A. Preventing FVE- Nursing interventions
• Maintain fluid and sodium restriction
• Track all input and check total a few times/day
• DO-NOT keep water at the bedside
• Educate client and other care givers
• Post sign indicating total amounts allowed
• Teach pt about sources of sodium

Strategies to diminish thirst/dry mouth

• ice chips (include as input)
• sugar-free gum, candy
• moistened toothettes/brushing teeth
• avoid high-sodium foods (see note below) 22

Weights:
The pt will be weighed in the HD department if on HD, and on the unit prior to PD treatments
if on PD.

Fluid restriction
• All pts on HD will be on a fluid restriction between treatments
• Thirst and dry mouth are serious discomforts and can be the main reason for failing to
maintain the restrictions.
The nurse:
• Ensures the pt understands the reason for the restriction and the consequences of not
adhering to it.
• Teaches about common sources of HIDDEN sodium are important- such as canned soups,
bottled sauces, cured and smoked meats, and processed cheeses.
• Most patients know to avoid table salt and salty snacks but may not realize how
high some of these other foods are in sodium.
• Involves pt in tracking fluid and sodium intake if possible.
• intake should be monitored a few times a day in case adjustments need to be
made if the pt is in excess of allotted totals.
• Monitors for the need to adjust the restriction. For example:
• If experiencing fluid loss though other mechanisms such as diarrhea or vomiting
track these losses and notify the MD for any adjustments required to the fluid
restriction.

22
 A. Preventing FVE- Assessing Weight

Daily weight is the only relevant measure of total body

water

Terminology related to the pt receiving HD:

• Pre-treatment weight
• Post-treatment weight
• Inter-Dialytic weight gain
• Goal weight Edema?

Remember your principles of fluid movement!

23

Keep in mind that the scales we are using to weigh pts are not able to tell use WHERE the water
weight is located. ALL fluid in the body whether in the IV, interstitial, or intracellular spaces will
contribute to the total weight of the pt.

• Pre-treatment weight- immediately before treatment begins (done in the HD department)

• Post-treatment weight- the pt’s actual wt immediately after treatment (done in HD
department)
• Inter-dialytic weight gain- difference between the end of one dialysis and the start of the
next. Ideally kept under 2.5 kg in order to have successful treatment. In excess of this=
difficult to remove adequate fluid.
• Goal weight- sometimes referred to as “dry weight” this is the weight the MD would like the
pt’s post-treatment to be
Fluid can only be removed via HD if it is in the INTRAVASCULAR space.
• If a pt has a large amount of edema prior to treatment, it is more likely the post-treatment
weight will be higher than the goal weight since this fluid in the interstitial spaces could not
be removed (issues like low albumin, or venous insufficiency can contribute to chronic
edema).
• This pt may NOT have been in an excess of total body water and therefore, their pre-
treatment weight may have been within the recommended 2.5 kg.
• The issue was that too much of that water was not in the IV space. After dialysis, fluid will
generally move from the interstitial space back into the intravascular space due to the
reduction in intravascular hydrostatic pressure.
If the pt exceeds the prescribed fluid and/or sodium restriction, this will place them in overall
total body water excess- FVE. In this case, the pt’s pretreatment TBW and weight will be higher
than it should be. This will also make it more difficult to achieve the goal weight because the
pt’s BP may drop when they attempt to pull of that excess fluid during HD, making it unsafe to
get them to the goal weight.

23
 B. Build up of wastes
• Creatinine and Urea=
azotemia, “uremic”
• Hydrogen ions=
**acidosis
• Electrolytes:
• K+
• PO4
• Mg
• Medications

24

Azotemia-having elevated Ur and Cr levels (so is a lab finding)

Uremic syndrome- constellation of symptoms that develops when nitrogenous wastes accumulate.
We usually just say the pt is “uremic”.

**Acidosis: Generally, acidosis in CKD is mild as phosphate levels tend to be elevated and
phosphate is a buffer, offsetting the excess H+ present. Serum bicarbonate concentration TCO2)
tends to stabilize between 12 and 20 mEq/L and rarely falling below 10 mEq/L (Rosenberg, 2022).

• The low-grade chronic metabolic acidosis in CKD may accelerate kidney damage and protein
and muscle loss as well as exacerbate CKD-MBD.
• Alkali therapy may be used for some patients.
• For those on HD, sodium bicarb can be used during treatment.
• Most common oral alkali therapy is sodium bicarbonate or sodium citrate (citrate is rapidly
metabolized to bicarbonate)
• Because most forms contain sodium, risk for increased fluid retention needs to be considered.

Electrolytes and Medications are discussed on the next few slides.

24
 B. Build up of wastes: Avoiding excess K+

• Hyperkalemia is a greater issue in AKI compared to CKD

When on dialysis, it is rare to need treatment for hyperkalemia
between treatments IF restricting intake of high K+ foods such
as:
Avocados
Bananas
Potatoes
Citrus fruits
25

In CKD the body compensates for chronic low-grade elevations in potassium through excess
aldosterone and increased renal secretion. However, once a person is oliguric, aldosterone
cannot be effective.

Once on dialysis, K+ is balanced through dialysis treatments.

Subtle increases (<5.5) close to the time a pt will be getting treatment are not significant as it
will be corrected during that treatment.
For

Per MB renal program: NEVER give hemodialysis patients citrus juices - orange and
grapefruit, prune or tomato (may cause increased K+). Cranberry juice is OK. If using juices to
treat hypoglycemia, pay attention to grams of sugar per volume…remember the goal is 15-
20g of simple CHO.

25
 B. Hyperkalemic Emergency

• Hyperkalemic emergency is defined by a combination of

• Degree of elevation
• ECG changes
• Risk for complicated treatment
Treatment:
• Calcium IV if ECG changes present or K+ > 6.5
• 10 units of regular insulin IV and 25g IV dextrose
• Oral or PR cation exchanger
• Loop diuretic

26

Patients with hyperkalemic emergency include:

• Those with clinical manifestations or ECG changes.
• Those with serum potassium of >6.5 meq/L.
• Those with serum potassium of >5.5 meq/L plus kidney function impairment and ongoing
tissue breakdown or potassium absorption.

Treatment:
• If ECG changes present and/or serum potassium >6.5 meq/L: Give calcium IV to stabilize
cardiac
• For ALL hyperkalemic emergencies: Give insulin and glucose to shift K+ intracellularly
(only give glucose if serum glucose is <13.9 mmol/L).

• Remove potassium from the body

**Hemodialysis for pts with significant kidney dysfunction- only way to remove
K+ effectively.
• Oral or PR cation exchanger- sodium zirconium cyclosilicate (SCZ/Lokelma) or
patiromer orally- are Ok for pt with severe CKD waiting for STAT HD. Sodium
polystyrene sulfonate (SPS/ Kayexelate) only if other exchangers are not
available.
• Loop diuretics (in hypervolemic patients) or saline infusion with IV loop diuretics
can be administered to nonoliguric patients without severe kidney function
impairment. So not ideal in pre-renal AKI and completely ineffective in ESKD!

Mount, D. (2024 February 5). Treatment and prevention of hyperkalemia in adults.

UpToDate.

26
 B. Other electrolytes of concern
• Magnesium- may be high, normal, or low. Risk for
elevations associated with magnesium-containing antacids
or laxatives (Maalox, Milk of Magnesia).
• Phosphate- found in many foods especially dairy and
processed foods

27

Magnesium: should be assessed periodically as there are factors that result in

hypomagnesemia and hypermagnesemia. We will only focus on the risk for
hypermagnesemia.

Hypermagnesemia: not usually an issue unless pt is taking meds with magnesium in them.
• Avoid magnesium containing antacids and laxatives (e.g., Magnolax, Milk of Magnesia) .
• Use aluminum-based OTC antacids instead, but limit use as which is associated with
increased risk for bone disease.
• Emergent elevations in Mg can result in respiratory depression and cardiac
dysrhythmias.
• Hypermagnesemia can be treated with IV calcium gluconate and/or dialysis.

Hyperphosphatemia: found in dairy, nuts, processed foods, and many other protein-rich
foods including meats.
• It is very difficult to achieve the needed restriction of <1000mg/day as phosphate is in so
many foods so pharmacological treatment usually needed (discussed in the section on
CKD-MBD later).

Although comprehensive dietary teaching will be done be a dietician, nurses should be

aware of some of the most common sources of potassium, magnesium, and phosphate as
you will need to reinforce the dietary restrictions in practice.

27
 C. Altered medication clearance

Patients with chronic kidney disease have decreased elimination and often take
numerous different medications for a variety of coexisting conditions putting them
at increased risk of adverse medication events.

Many but not ALL medications require dose adjustment.

Stages 1-4- trying to preserve renal function while preventing adverse

effects

Stage 5- no renal function to preserve. Focus is on other adverse effects.

Timing of medications related to hemodialysis treatments depends on how
the drug is eliminated (consult unit resources in practice)
28

As GFR decreases, some medications and their metabolites accumulate and will require
dose adjustment- this is not true for all medication.

NOTE! Once pt in ESKD nephrotoxicity is not an issue, BUT other adverse effects are! For
example, it does not matter that gentamicin is nephrotoxic anymore, but it can still cause
ototoxicity…and more likely so due to having no renal clearance!

Specific to HD:
• Many medication administration times need to be altered if they will be removed by
hemodialysis.
• The Manitoba Renal Program has created guidelines to advise GDRN caring for inpts. I
have posted this document on Learn: Medication Administration Times-Guidelines for
Hospitalized or Long-Term Care Patients receiving (Chronic) Hemodialysis, available on
Learn.
• You do not have to memorize this list for the course but please access it for guidance in
your clinical settings.

A note about insulin in CKD: One favourite tidbit for NCLEX prep tool questions specific to
HD patients is regarding the possible decrease in insulin needs once pt starts on dialysis. This
is thought to be related to dialysis decreasing the degree of uremia (a cause of insulin
resistance). However, there is also less clearance of insulin in ESKD, so predicting best dosing
can be difficult. Frequent monitoring and adjustments are often needed (Berns & Glickman,
2024).

28
 2. Alteration in BP regulation
The role of renal regulation of BP (RAAS) was discussed earlier.

Also, once in ESKD pts show a widening pulse pressure- aortic stiffness
with greater elevations in systolic compared to diastolic BP.

120/80= pulse pressure of 40

180/70 = pulse pressure of 110

NOTE: The previously discussed connections between kidney and

heart disease continue once pt on HD.
29

Specific to HD:
Once on dialysis, BP fluctuations related to treatment can also be an issue. “Patients with
end-stage renal disease are more likely to have an increase in central pulse pressure and
isolated systolic hypertension. Why this occurs is incompletely understood, but increased
aortic stiffness probably plays an important role” (Mann, 2022). This is why many dialysis
patients often have greater elevations in systolic levels compared to diastolic- i.e., a wide
pulse pressure.

Note that once on HD, the benefits of the ACE-I or ARB related to proteinuria is no longer
relevant. Current best practice recommends use of a beta blocker or calcium channel blocker
in most patients, but treatment is individualized.

29
 3. Decreased Hormone Production
1. Lack of EPO (and other factors=Anemia)

30

As renal mass decreases, the endocrine role of the kidney is affected with the primary hormones
being reduced being EPO and calcitriol.

Contributing factors to anemia:

• EPO deficit is the primary reason for anemia
• Hemolysis 2° HD
• Platelet dysfunction: The most common cause of bleeding in uremia is platelet dysfunction (note
this is NOT the same as thrombocytopenia. The pt has normal PLT count, but the plts are less
“functional”). The primary prevention is the treatment of uremia through regular dialysis. If the
pt is actively bleeding, they may be given desmopressin (DDAVP) which partially reverses platelet
dysfunction. We treat active bleeding depending on the reason for that bleeding. Vitamin K will
NOT work for platelet dysfunction and desmopressin would not reverse an INR. Plt dysfunction
alone does not cause anemia but increases the risk for both acute and chronic blood loss (Berns,
2023).
• Chronic inflammatory state: uremia shortens RBC lifespan
• Increased GI acid and decreased motility= irritation to GI mucosa- at increased risk for ulcer
formation and pts are at risk for chronic and acute GI blood loss
• Malnutrition: discussed later in the notes

There are MANY reasons for fatigue in the pt with CKD so it should not be attributed solely to chronic
anemia. And remember, if your pt’s symptoms are far worse all of a sudden, you cannot blame a
stable, chronic pathology.

30
 3. Treatment of Anemia in CKD

[Link] supplements (ideally between meals, not with calcium)

• If causes GI upset, may be given with meals
• Can contribute to constipation, dark stools
[Link] iron - given in HD (if pt on HD!)
[Link] subq injection NOTE: EPO not effective if insufficient iron
levels present. Iron is required in order for bone marrow to
create adequate numbers of RBCs.
[Link] transfusions?
31

“Anemic patients who are iron deficient should be treated with iron before the administration
of erythrocyte stimulating agents” (Berns, 2024). Sufficient iron is needed for RBC synthesis so
response to EPO will be poor until iron deficiency is corrected.

Hemodialysis patients should receive parenteral rather than oral iron therapy because of the
dosing required and the fact that iron is poorly absorbed from the GI tract and generally poorly
tolerated. The preparations ferric gluconate or ferumoxytol are preferred over iron dextran as
iron dextran carries the highest risk for anaphylaxis

EPO is started in hemodialysis patients who have a HGB<100 g/dL and are not iron deficient
with a maintenance target HGB of 110-115.
• Therefore, the goal is not to get the HGB within normal laboratory range. This is because
higher HGB levels in pts with CKD is associated with an increase in thrombotic events,
especially MI.
• Note that is takes several weeks to months before the RBC level will be increased enough
for the pt to notice a relief of anemia-related symptoms. (Berns, 2023).

Patients receiving HD often do require blood transfusions- decision is made on risk vs benefit.
Blood is almost always transfused in the HD department.

Q-Why might blood transfusions be avoided… esp. in younger pts?

When we transfuse patients with someone else’s blood, we introduce foreign proteins which
promotes the production of antibodies. This increases the risk for organ rejection should the pt
receive a kidney transplant in the future.

31
 3. Lack of active Vit D (calcitriol)= CKD-MBD

Secondary hyperparathyroidism

Figure 49-4

32

Chronic Kidney Disease Mineral and Bone Disorder (CKD-MBD)

Three main contributors to the patho processes:
1. Decreased phosphate excretion
2. Less vitamin D is converted to its active form
3. Increased levels of parathyroid hormone (PTH)

• Active forms of vitamin D are needed to absorb calcium from the GI tract,
• Low levels of serum calcium activates the parathyroid gland to release PTH
• PTH stimulates bone demineralization with the release of calcium from the bones.
• Phosphate is released as well, leading to further elevated serum phosphate levels
• Phosphate binds with calcium in the bloodstream, leading to the formation of insoluble
calcifications that are deposited in the vascular walls and other soft tissues
• Calcifications contribute to cardiovascular disease

Note that the patho of this is more complex than we will cover in this class. We just want to
reach the point of understanding why the condition matters and connect the treatments. You
may get greater detail in the Patho 2 course.

32
 Treatment of CKD-MBD

• Dietary restrictions- see earlier discussion

• Phosphate binders -CaCO3 most common, sevelamer (non-
calcium containing binder).
• NOTE: Give all phosphate binders WITH meals.
• Active Vit D (calcitriol)- not started until PO4 levels under
control
• Parathyroidectomy is done as a tx of last resort if
medications are not achieving targets.
33

Hey! Do not memorize the numbers on this page- they are for illustration purposes only! You
will never need to include the numbers when responding to test questions.

Phosphate control is the initial target of treatment via dietary restriction and phosphate
binders.
• Similar to the goals when treating anemia, the goal is not to reach normal lab levels but to
lower phosphate enough to prevent calcifications = <1.78 mmol/L (N= 1.0-1.5 for non-CKD
pts).

Preventing hypercalcemia
• Not all pts with ESKD have low calcium levels
• hypercalcemia from calcium-based PO4 binders increases cardiac calcifications.
• calcium-based phosphate binders are generally limited to a maximum of 1500
mg/day.
• calcium levels are monitored and a goal short of the upper end of normal is the
target…i.e., should not exceed 2.37 mmol/L (N=2.10-2.50 mmol/L)
• Non-calcium based PO4 binders such as sevelamer may be used

Active form of vitamin D, “calcitriol” may be started if hypocalcemia or vitamin D deficiency

persist even when serum phosphate levels are controlled and supplemental calcium is given.
• It is important to lower the phosphate level before administering calcitriol supplements
• may contribute to soft tissue calcification by increasing calcium levels while
phosphate levels highly elevated.

33
 Ca and phos binding in GI=GOOD! Stays in GI.

PO4 + Ca+= Calcium carbonate

Phosphate with meal*
PO4 Ca3(PO4)2
GI Tract
PO4
Ca3(PO4)2

Bloodstream
Too much phosphate in blood= BAD! Binds with Ca creating
calcifications. 34

The MOA of phosphate binders relies on their ability to be in physical contact with phosphate.
This is why they must be administered with meals.
• The phosphate is introduced in the FOOD the pt eats.
• We introduce calcium carbonate (CaCO3) to the GI tract at the same time the food is
ingested so the CaCO3 can create a chemical reaction with the phosphate
• The chemical reaction creates a new substance that cannot leave the GI tract.
• Reduces the serum phosphate level by sequestering it to be eliminated via bowel.

So, the same chemical attraction that causes calcium and phosphate to bind in the bloodstream
and leads to calcifications in soft tissues is being applied pharmacologically to trap the
phosphate in the GI tract.

Testing tip: There is always at least one or two questions on a test related to CKD-MBD (either
its patho or the tx, - and often a combination of these things tied to a nursing decision!)

34
 Causes deposits of calcifications in soft tissues

Medial and Intimal Calcification in Chronic Kidney Disease: Stressing the Contributions - Scientific Figure on ResearchGate. Available from:
[Link]

Calciphylaxis
35

The difference between atherosclerosis and arteriosclerosis is indicated in the image above.
In atherosclerosis, there is a deposit of calcifications in the intimal lining while in calcification
due to CKD-MBD, the deposits are deeper, in the medial layer. This makes the vessel stiff and
noncompliant which further increases the risk for MI and other CV complications.

Calciphylaxis – also known as calcific uremic arteriolopathy (CUA).

• life-threatening complication that needs to be identified early.
• should be suspected in pts with painful subcutaneous nodules or “lumps”; nonhealing
ulcers; and/or evidence of skin necrosis.
• Higher fat areas like abdomen, thighs, and buttocks are often affected, but lower legs also
a common site.
• Some common treatments in CKD (or its comorbidities) increase the risk for CUA such as
warfarin, calcium carbonate, corticosteroids, iron, and active vitamin D supplements.

It seems counter-intuitive that the meds used to TREAT CKD-MBD could increase the risk of
this complication, but this is related to the fact that the perfect balance of PTH, calcium, and
phosphate levels is very hard to achieve.

35
 Speaking of Infections…
Impaired
Frequent Immuno-
immune
hospitalization suppressive meds
response

Additional risk Chronic

factors- DM, age Acute wounds
infection
Fluid and Invasive lines
nutritional for HD/PD
imbalances Increased
risk for
Remember to consider clinical context when using
sepsis sepsis screening tools
36

Infections are the second leading cause of death in the pt undergoing dialysis. If the pt has a
VAS cath, line infections should always be suspected when general signs of infection are
present. Pts receiving peritoneal dialysis are at increased risk for peritonitis. So, all forms of
dialysis increase the risk for infections.

Considering clinical context related to sepsis screening

- May have very high baseline systolic pressure (wide pulse pressure). In pts with high
baseline BP, we cannot use criteria based on a normal baseline. Therefore, a drop of
more than SBP drop >40 mm Hg from the pt’s recent baseline BP should make you
suspect a serious complication.

Considering clinical context related to sepsis treatment

- IV fluid therapy may need to be modified due to risk for FVE- esp if pt also has L-HF
- If still has SOME renal function, some antibiotics may increase risk for AKI (e.g.,
vancomycin, gentamycin), greater risk for other adverse effects r/t decreased (or no)
renal clearance
- May have to coordinate for transfer to ICU for continuous renal replacement therapy
(CRRT) or HD department for management

Clinical reasoning tip: Be prepared to identify and intervene for potential complications that
can cause acute drop in BP in a pt with ESKD HD.

36
 Other PC that affect HRQoL in pts with CKD:
Malnutrition, Pain and other discomforts, Psychosocial

Malnutrition
• Replavite
• Anti-emetics, appetite stimulants, GI motility meds
• Dietician consult, calorie counts
• Weights not necessarily reliable r/t nutrition due to fluctuating fluid
volumes-need to monitor labs (renal dietician)
• Dietary supplements specially designed for pts with DM/CKD (such as
Nepro)
37

Risk factors for malnutrition is multifactorial and individual (requires a focused

assessment.) Some common factors:
• GI upset/nausea/vomiting
• Constipation
• Dietary restrictions
• Protein loss via dialysis

Replavite is a vitamin supplement designed for people with kidney disease. It

contains water-soluble vitamins: vitamin C and B vitamins including folic acid that
may be lost during dialysis and that are important for the production of RBCs.
Because it is water soluble, it must be given after HD treatments.

Due to decreased GI motility r/t uremia, pts often feel bloated and have increased
incidence of GERD (gastroesophageal reflux disease). GI motility medications such as
metoclopramide may be prescribed.

As mentioned, a dietician specializing in renal disease needs to be involved and the

RN’s role is to reinforce the importance of the restrictions and recognize when the
plan may need revision (poor intake, pt not able to maintain restrictions, etc.)

Due to dietary restrictions, you should not provide stock supplements to pts with
CKD/ESKD without making sure it is appropriate for that patient. For example, the
supplement Boost has 3x the amount of potassium and phosphorus compared to
Nepro, a supplement made for pts with CKD.

37
 Pain and other discomforts
[Link] (discussed earlier)
[Link]/anxiety
[Link] mouth (discussed earlier)
[Link] disturbance
5.*Constipation/GI issues- (constipation discussed below)
[Link] dysfunction
Discussed on next slides:
[Link]
[Link] management

38

Careful assessment including patient interview should be done to address these

common discomforts as much as is reasonably possible. While medical treatment is
often needed, there are often non-pharmacological, low-tech interventions the nurse
can perform to help the pt be more comfortable. This is highly individualized as it is
based on pt preference but minimizing these issues can have a big impact on pt
outcomes. For example, dry mouth due to medications/fluid restrictions can promote
tooth decay, dysphagia, poor nutrition, and many other complications. Sometimes the
“little things” really do still matter.

*Constipation- often related to medications (calcium, others), fluid restriction,

decreased activity but uremia may also play a role (decreased GI motility).
• Constipation must be managed aggressively in the pt receiving peritoneal dialysis as it
can interfere with performing the dialysis exchanges.
• Non-pharm interventions such as increased dietary fiber is tricky due to restrictions
of electrolytes prevalent in some typical high fiber foods and the fact the pt is on a fld
restriction.
• Note that we cannot increase fluid intake if pt on a fld restriction and increasing
activity can be challenging.
• We also have to avoid laxatives that contain magnesium if pt has elevated Mg levels.

Tx usually:
-stool softeners or senna regularly
-laxatives PRN- osmotic (lactulose), simulant (bisacodyl)

38
 Pruritus
• Often a more distressing symptom than pain for the person with ESKD
and nurses plays a major role in assessing, treating and evaluating
effectiveness

Is linked to:
• Inadequate dialysis
• Elevated PO4 level, hyperparathyroidism, and calcifications
• Xerosis (dry skin caused by sweat gland atrophy)
• Elevated serum magnesium and aluminum concentrations
Tx includes
• Basics for itchy skin
• Emollients (topical tx)
• Antihistamines
39

Management of Dry Skin - General Measures

In addition to the usual recommendation for dry, itchy skin such as:
• avoiding harsh detergents
• wearing breathable clothing
• keep fingernails short and clean and try not to rub or scratch due to the risk for injury
and infection.
• Other strategies include keeping the environment cool and humid (difficult in the
hospital!).

Some topical treatments include emollients (e.g., fragrance-free baby oil). If topical
measures do not provide relief, antihistamines such as hydroxyzine or diphenhydramine
can be prescribed, but both are sedating.

39
Pain Management
NOCICEPTIVE PAIN
WHO ladder- start with non-opioid
• Acetaminophen better for pts with CKD than NSAIDS
• Tramadol (synthetic) preferred over natural opioids and codeine is not
recommended.
• If opioids must be used, choose those will few or no active metabolites such
as: Methadone, fentanyl
• If these are not a good match for the individual (or due to cost/other factors),
hydromorphone is next best choice

NEUROPATHIC PAIN
• Gabapentin (after HD- usually at HS)
• Tricyclic antidepressants
40

General pain management principles are the same for the pt with CKD as in the general
population (using non-pharmacological tx, avoiding opioids, if possible, etc.) Choice of
opioid when required will depend on the client’s preference, risk factors, and whether
they are on dialysis (Davison, 2022).

Uremia can result in encephalopathy as well as peripheral neuropathies.

• Neuropathy is common in clients with ESKD secondary to uremia which differs from
diabetic neuropathy (but patients may have both).
• Restless leg syndrome (RLS) and neuropathic pain are both prevalent.
• Note that gabapentin is used to treat these peripheral conditions and this medication
gets dialyzed out so for pts on HD, administration has to be post treatment.
• As with other pts, TCAs can also be used for resistant neuropathic pain.

40
Psychosocial and HRQoL Issues

Suicide rates are higher in pts with CKD than the general population.

Choosing to withdraw from dialysis is considered a treatment choice

(not suicide).

For pts requiring HD, death usually occurs within days or weeks of
stopping treatment.

41

• Although maximizing HRQoL can help reduce depression and suicidal ideation, pts
with terminal chronic illnesses and a large symptom burden will have greater
incidence of these issues.
• As the nurse, you have to accept that treatment refusal is not a “right or wrong”
option, nor is it considered a type of suicide. It is a personal healthcare decision.
• Advance care planning is now part of the standard care plan and part of an
ongoing dialogue with the pt and family. When making the decision to start
dialysis treatments, the plan for discontinuing treatments should also be
discussed.
• As with other invasive treatments, the pt and family experience distress when
having to make these decisions when health conditions change, made worse if it
is the first time it is being discussed.

Qazi, H., Chen, H., & Zhu, M. (2018). Factors influencing dialysis withdrawal: A
scoping review. BMC Nephrology, 19(1). doi:10.1186/s12882-018-0894-5

41
 GDRN Responsibilities for in-pts getting HD
As the GDRN, you are for responsible for caring for clients in-between
their dialysis treatments

Some key responsibilities:

• Maintenance of fluid and dietary restrictions
• Medication management (all those NOT given in HD)
• Ensuring pt eats prior to HD
• Report to/from HD
• Line and dressing maintenance
• Fistula/graph assessment

42

Fluid restrictions:
• May be necessary to alter usual practices related to IV medications. The minimum fluid
necessary should be used (e.g., do not use a primary infusion when infusing intermittent minibag
medications- check with policy).
• Remember, the pt on HD cannot have their fluid restriction simply discontinued! It has to be
maintained or the pt will develop extreme FVE between HD treatments!
• Strategies to help pt adherence were covered earlier in the notes.
Medication management:
Almost all routine meds are administered once the pt returns to the unit after treatment. They are
not given in HD.
When you are unsure of what you should do r/t holding and giving meds consult the MRP’s -
Guidelines for Managing Hospitalized Hemodialysis Patients. If the medication in not listed, ask for
guidance.
Common medication management info you should know for testing purposes:
• If a once daily medication is dialyzed out, it should be given at HS if possible (HD tx times can get
changed, so this is the best time to schedule the med).
• Some pts may have reduced basal insulin dosing on their HD days. This is because the reduction
in uremia makes the pt more sensitive to insulin, so there is a risk for hypoglycemia if taking the
same dose as on non-HD days. This is individualized based on the pt’s trends.
• There is a misconception that nurses should hold all antihypertensives before HD and that you
need to remove the pt’s nitropatch if they are wearing one- this is NOT true…treatment is
individualized. The nephrologist should write order specific to pt’s needs- if in doubt ask.
• You should NOT send any scheduled routine meds to HD (they will not be given).
Ensuring pt eats:
• Typical HD times are 0800, 1300 and 1800.
• This means you often have to arrange for earlier meal trays to ensure the client has a meal prior
to HD.
• One reason the client should not have a meal during the hemodialysis treatment is that it has
been found to increase the risk of hypotension due to splanchnic vasodilation.
Anytime a pt moves between departments, the risk for error increases. It is essential that you
offer a relevant and accurate report to the nurse in the HD unit and receive report prior to the pt
returning to your unit.

42
 Caring for the VAS cath or AV fistula

VAS cath
Dressing: Same as other CVADs- Transparent semipermeable (e.g., Tegaderm, IV3000) changed
in HD weekly. However, you should assess the drsg q shift and PRN. The GDRN can change the
dressing if it is compromised (e.g., lifting, moisture, drainage or blood is present; or signs and
symptoms of infection are present).

Accessing: The VAS cath can be accessed for blood sampling or as CVAD access, but this should
only be if absolutely necessary.
• Routine bloodwork should be collected in HD department.
• Note that accessing a VAS cath is very different from accessing a standard central line like
you have learned about in techniques. There are different caps, different heparinization
method, etc. Be sure you know what type of line your patient has and if you are allowed to
access it.
• Also, if a pt has a VAS cath, but is not going for regular HD (this is often the case in pts who
needed HD for AKI), you need to check on policy r/t routine heparinization, etc. for line
maintenance.

AV fistula
• NO BP or venipuncture on fistula arm (post sign at bedside, ensure pt knows this as well).
• No constrictive clothing, armbands, or watches should be worn on the fistula arm.
• Should be assessed q shift using stethoscope for a “bruit” and palpation for turbulent flow
and charted- “Audible and palpable”
• Some patients will need a topical anesthetic cream (e.g., EMLA) applied about one hour prior
to treatment.

Because the fistula needs time to mature, the pt may have BOTH a fistula and VAS cath but we
will only be using ONE of these for HD.

43
 Comparing pros and cons of HD vs PD

This information related to comparing the pros and cons of HD vs PD is testable.

Note that this refers to HD in an HD clinic, but some patients CAN arrange from
home HD as well. It is important to remember that although pts receiving HD are
at increased risk for infection due to invasive access, the same it true for pts getting
PD as this is also an invasive line- a catheter into the peritoneum and these pt are
at increased risk for peritonitis.

44
 Potential Complications
Using the knowledge you gathered, are you able to link the risk
factors for potential complications and appropriate interventions
to pts at the various stages of CKD?
1. Physical injury (altered mobility, delirium, high-risk meds)
2. Malnutrition
3. Impaired oxygenation (ventilation, perfusion, transport)
4. Fluid imbalances (total body water, electrolyte, and acid base
imbalances)
5. Infections and sepsis
Test your understanding using the learning activity!
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As always, our test questions will be limited to the content and concepts in our
posted notes, but we will assess your ability to apply these in a clinical practice
situation. Study the content with this in mind!

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