NURS 3105 Medical-Surgical Nursing 2
Renal Disorders and Failure
At the end of this module, you will be able to:
1. Specify the key aspects of renal assessment
2. Describe the lab tests performed to assess renal function
3. Explain the use of imaging in renal assessment
4. Discuss age-related changes to renal function
5. Differentiate between prerenal, intrarenal, and postrenal causes of kidney disease
6. Identify different classes of renal infection, their diagnosis, and treatment.
7. Explain the causes of nephrotic syndrome and renal tract calculi
8. Discuss the treatment of renal tract calculi and implications for patients.
9. Differentiate acute renal injury/failure and chronic renal disease/failure.
10. Explain the criteria for renal injury and renal failure
11. Discuss the treatment of acute and chronic renal disease
12. Explain the nursing priorities for patients with renal disease.
13. Explain dietary changes needed with renal disease.
14. Explain the classes of drugs used to manage renal disease.
15. Discuss dialysis and differential between hemodialysis and peritoneal dialysis.
16. Clean educational needs for people undergoing peritoneal dialysis.
17. Identify the risks and complications of dialysis.
18. Explain the criteria for renal transplants.
19. Discuss patient education related to renal transplants.
20. Identify the complications of renal transplants.
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ASSESSING RENAL FUNCTION
A good history is the first step in a renal assessment. Keep in mind that many co-morbidities
can damage the kidneys, as well as many drugs. Any of the following should raise a warning
flag.
• Comorbidities: Hypertension and diabetes account for most renal diseases, but heart
failure, gout, metabolic problems, and neurologic issues (previous stroke) also
contribute.
• Medications: Many antibiotics are nephrotoxic (think the “sins:” gentamicin,
vancomycin, streptomycin, tobramycin. NSAIDs – including aspirin – if used
excessively can damage the kidneys.
The next step is a complete physical assessment. The general findings are vague; however, in
combination with other symptoms, they point to renal issues.
• General Findings: Fatigue, anorexia, headaches, blurred vision, nausea/vomiting,
chills, itching, excessive thirst, changes in weight, elevated BP
• Edema: Face, ankles, abdomen (ascites), anasarca (general edema)
• Pain: dysuria, flank or spinal pain medial to kidneys, groin or suprapubic
• Urinary pattern: nocturia (wake to urinate), increased frequency, hesitancy,
retention, incontinence (general or stress), dribbling
• Output: anuria (< 100 ml/day), oliguria (output of 100-400 ml/day), polyuria
(excessive, beyond intake, 2.5L+/day)
• Appearance of urine: Concentrated or dilute, hematuria (blood), pyuria (pus), color
(red, brown, yellow-green) – note that antacids can make urine cloudy
AGE RELATED CHANGES IN RENAL FUNCTION
Starting in middle-age, nephron function declines. This happens because there is a decreased
renal tissue as nephrons might die off and decrease the overall number. GFR also diminishes,
leading to renal insufficiency and decreased ability to secrete wastes. The loop and tubules
also decrease in functioning, meaning that electrolyte, fluid, and acid-base balance is more
problematic. (Ever notice how some older adults smell of urine? If I tell you it is probably not
due to incontinence, what do you think it might be?)
The bladder also loses elasticity and tone; consequently, older adults have decreased bladder
capacity, decreased sensation, and experience unstable bladder contractions. In men, the
prostate gland enlarges, causing benign prostatic hyperplasia (BPH) that can obstruct the
urethra and cause “dribbling” and frequency. Women will experience vaginal dryness that can
contribute to infections. (See Table 44-2 for more detail)
LABORATORY FINDINGS
Laboratory tests are essential in assessing renal function. They fall into 2 categories: blood
and urine. Specific tests of kidney function include blood urea nitrogen (BUN) and
creatinine (Cr). Because the kidneys are crucial to fluid-electrolyte and acid-base balance, we
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look at a number of electrolytes. These blood tests do not require any special handling or
fasting.
Electrolytes
Na+
K+
HCO3Ca2+
Phosphorus
BUN
Cr
Uric acid
GFR
Anion gap
135 - 145 mEq/l
3.5-5 mEq/l
22-26 mEq/l
8.6-10 mEq/l
2.4-4.4 mg/dl
10-23 mg/dl
0.6 -1.2 mg/dl
3-7 mg/dl M
90-125 ml/min
10-20 mEq/l
Urine Analysis
Color
Odor
Protein
Glucose
Ketones
Bilirubin
Specific Gravity
pH
RBCs
WBCs
Bacteria
Amber/light yellow
“Urine”-smelling
None or trace amount
None
None
None
1.003 - 1.020
4.0 - 8.0
0 - 4/hpf (essentially
0 - 5/hpf none)
None
Creatinine is the best indicator of renal function. Almost all creatinine that is made through
muscle movement is filtered and eliminated in urine. Very little remains unfiltered. A high
serum creatinine value indicates diminishing filtering ability. BUN can be elevated for other
reasons such as GI bleed, dehydration, or very high protein diet. When BUN/creatinine ratio is
increased, the patient does not have a renal disorder but something instead.
The anion gap is an important indicator that metabolic acidosis –
particularly diabetic ketoacidosis – has fully resolved. Because of the cellular
lysis that occurs during metabolic acidosis, the serum electrolytes – namely
K+ and Na – will not reflect the true nature of intracellular electrolytes.
As long as the anion gap is elevated, some degree of acidosis is going on.
Urine tests involve collecting and testing urine. A urine dipstick is a
simple and easy test that can be done either in a clinical setting or at
home by patients. A small sample of urine is taken and a stick is swirled
in the urine. After two minutes, different areas change color to reflect
the presence of glucose, protein, and trace blood, none of which
should be present in urine. A dipstick can also evaluate urine pH. While the patient should
clean the meatus of the urethra, a dipstick does not require a sterile sample.
When an infection or more serious condition is suspected, a urinalysis is done. Because this
test will be looking for bacteria, the manner of catching the urine is important. The patient will
be asked to clean the perineal area and the meatus of the urethra with
aseptic wipes, instructed to void part of their urine into the toilet, and
then catch the remainder. Men who are uncircumcised need to fully
retract the foreskin and clean the glans of the penis. The test must be
performed within an hour of collection. Each of these tests speaks to
different aspects of the kidney, namely is there an infection or an acute vs.
chronic issue. If WBCs are
present, the urine is discolored, and/or there is a
distinct smell, a urine culture and sensitivity may
be added. If the patient has a Foley catheter, you
can take the sample directly from the drainage
tube. You will find a port near the top of the tube. Clamp it off and wait for a few minutes,
then clean the port and draw your sample into an empty, sterile syringe.
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A 24-hour urine collection may be done to measure creatinine clearance and total composite
urine. A large collection container is use, which is marked with
the time the collection began. The patient voids the bladder
completely. Then, each time the patient urinates, they use this
container. The container must be refrigerated between samples.
Once 24-hours has gone by, the container(s) is(are) sent to the
lab and the test conducted within an hour.
If a patient has a Foley catheter, the collection bag is emptied
20
at the start. However. The collection can be done in one of two
, 20
ealth
icuH
d
e
M
ways: 1) collect the urine every 45 minutes and store it in a
refrigerator or 2) the collection bag is placed in a basin of ice
and the urine is collected each shift. The first option is
preferred; however, the urine cannot sit at room temperature
for more than an hour, so you need to be exceedingly punctual. Time considerations may lead
you to using the latter approach.
IMAGING
A kidney-ureters-bladder (KUB) XRAY is used to look at the size, shape, and position of the
kidneys. An abnormal finding may indicate some intrarenal problem. The KUB is also used to
look for kidney stones. No special preparation is needed by the patient.
Ultrasound is used to look at perfusion and to detect masses and obstructions. This is noninvasive and uses soundwaves to interpret tissue density. A gel is placed on the patient, and the
technician moves a wand around to get a computer-generated image. Because there are no dyes
and it is non-invasive, it is a safe procedure pretty much any type of patient.
CT/MRI use radiation to provide detailed images of the kidneys and locate masses and
obstructions. An iodine-based dye is sometimes used, which can lead to complications for
many patients, especially those with renal insufficiency. Patients should be asked about
allergies to iodine and shellfish, and steroids may be given to prevent a reaction.
Pyelogram is used to see the urinary tract (as opposed to the renal vasculature). It works much
like any contrast XRAY, except the contrast is excrete by the kidneys, yielding visibility of
the ducts, ureters, and bladder. There are also retrograde and
anterograde pyelograms. In the former, the contrast is put directly
into the lower tract and flows up to the kidneys. In the latter, the
contrast is injected directly into the kidneys.
Arteriogram and/or angiogram are used to look more closely at
the renal vasculature. In particular, like with the heart, we can
see if there is stenosis or arterial obstructions. In the same way
as a cardiac catheterization is done, an incision is made in the
femoral artery and a catheter is fed into the renal artery. A
dye is the injected and illuminates the vessels on XRAY.
Preparatory interventions may need to be done, such as
injected contrasts. After the procedure, the patient must remain
on bedrest, lying flat as pressure is applied to the access point.
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A cystoscopy is much like an endoscope or a colonoscope. It is a device inserted through the
urethral meatus and then moved up the urethra. It gives direct visualization of the urethra and
bladder.
RENAL DISORDERS
Anything that impedes the kidneys can cause kidney disease, and these problems fall into 3
groups based on where are the issue is: prerenal, intrarenal, and postrenal. Don’t try to
memorize all of this: when you hear/see a condition, think about how it is impacting renal
function. Then you will always be able to figure it out.
CLASSIFICATION OF RENAL DISORDERS
Prerenal causes of renal disease relate to the heart and vascular system; that is, a reduction
in systemic perfusion (including the renal arteries and veins) that results in a reduction of
renal perfusion. A prerenal issue is the most common reason for ARI. The primary causes
are:
•
•
•
Decreased vascular resistance or flow (septic, anaphylactic, or hypovolemic shock, renal
artery thrombosis/embolism).
Significant volume depletion (dehydration, hemorrhage, diarrhea/vomiting).
Decreased cardiac output (cardiogenic shock, dysrhythmias, heart failure, MI).
Intrarenal causes arise from the kidney itself, but may
be related to something else.
•
•
•
•
Drugs that cause nephrotoxicity (including
contrast dyes) and chemical exposures can lead to
loss of renal tissue.
Severe crushing
injuries (traumatic
blows, accidents) that
destroy kidney tissue.
Infections that cause
any type of
inflammation and/or
migrate to the
nephrons.
Prolonged renal
ischemia, especially
from prerenal flow, can cause intrarenal damage.
Postrenal causes involve anything that can cause a backup of urine into the system.
•
Blocked urinary flow from BPH, kidney stones, or infection.
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•
Renal Disorders
Neuromuscular and spinal injury (S2-S4 and T11-L2) that damages the parasympathetic
and sympathetic pathways to the renal system will cause urinary retention or incontinence
(neurogenic bladder).
RENAL INFECTIONS
Renal infections come in a variety of types and have different names depending on the
location/type. Most are postrenal infections but can lead to intrarenal infection and intrarenal
damage. Keep the big picture in mind when studying. Is the infection a intrarenal or
postrenal infection? How does the location change the symptoms you would expect?
Women are much more likely than men to get renal infections; however, as men age, their
risk increases.
Post-Renal Infections
Urinary tract infections (UTI) are a postrenal infection. When we think of a UTI, we
generally think of a lower tract infection (bladder or urethra). However, they can also start in
the upper tract (calyces and ureters). The vast majority of UTIs are caused by bacteria with
E. coli being the #1 cause of community-acquired UTI and in-dwelling catheters being the
#1 cause of iatrogenic UTIs in the hospital.
Urethritis is an infection of the upper part urethra, and thus is considered a lower tract
UTI. The cause is usually a sexually transmitted microbe like gonorrhea, chlamydia, or
trichomonas. However, an untreated UTI can migrate up the urethra, into the bladder, and then
ureters.
Pyelonephritis is an infection in the upper part of the urinary tract (parenchyma and
collecting ducts). It usually begins as a lower tract UTI and ascends. It is the most common
cause of urosepsis (sepsis resulting from a urinary tract infection) and hospitalization. The
bacteria that cause pyelonephritis are E. coli, Proteus, Klebsiella, and Enterobacter.
Cystitis refers to an infection of the bladder itself. Like other post-renal infections, cystitis is
caused by an infection that has migrated from the lower urinary tract.
Intra-Renal Infections
Glomerulonephritis is an intrarenal infection of the glomerulus. There are many causes, but
the most common is a previous UTI or a systemic infection (there is a specific diagnosis for
post-streptococcal glomerulonephritis). These infections have a sudden onset and then a
temporary remission. They are very dangerous, can lead to chronic damage, and result in
kidney failure.
Nephrotic syndrome is another intrarenal disease of the glomerulus that you need to familiar
with from a big-picture perspective. Nephrotic syndrome has either a primary cause
(something just happens in the glomerulus) or a secondary cause (something else like the
infections mentioned above, systemic disease, diabetes, allergic reactions, drugs, or cancers).
Diabetes and systemic lupus account for over 1/3 of all cases of nephrotic syndrome.
Classically, patients will present with peripheral edema and complain of “foamy” urine.
They will be found to have proteinuria, hypertension, hyperlipidemia, and
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hypoalbuminemia. Hypercoagulability is also a complication of nephrotic syndrome, with
patients at significant risk for thromboembolism.
SYMPTOMS OF RENAL INFECTIONS
While there are some differences in presentation and clinical management, all renal infections
have a common approach. See Appendix A for distinguishing characteristics.
Common symptoms experienced are abdominal or flank pain and dysuria. In addition, all
patients will have changes in their urinary pattern, including hesitancy, frequency,
urgency, incontinence, and nocturia. A decreased urine production (anuria, oliguria,
retention) is a sign of late disease and may indicate acute renal injury or failure
(ARI/ARF).
Patients with UTIs have generalized pain, while those with pyelonephritis will experience
unilateral pain.
Those with pyelonephritis will also experience fever, chills, and vomiting.
For urethritis, the classic symptom is a discharge from the urethral meatus, along with
dysuria, urgency, and frequency. They will also have fever and chills, as well as emesis.
DIAGNOSIS OF RENAL INFECTIONS
Diagnosis is done with a urine dipstick, which is a quick measure for blood, pH, and glucose.
A urinalysis will find abnormal color, often pungent smell, WBCs, and bacteria. If a
urinalysis is positive, a urine culture will be done to identify the cause of the infection.
Infections can be caused by bacteria, viruses, fungi, and yeast and are treated with the
appropriate antibiotic or antimicrobial drug.
Pain is managed with either a local analgesic or a systemic agent, depending on the severity.
Complications include advancing to a more serious condition (lower UTI becomes urethritis
or pyelonephritis) and urosepsis. If left untreated or with recurrent infections, the patient may
experience chronic kidney disease (CKD).
METABOLIC ACID-BASE BALANCE
Metabolic acidosis is a common finding with renal disease, and
those with chronic renal disease can develop chronic metabolic
acidosis. Consider the distribution of filtration, reabsorption, and
secretion, and you can see how different areas can result in
different acid-base imbalances. If the glomerulus is not
functioning, then filtration is poor, resulting in retention of
cations. The proximal convoluted tubules and the collecting
ducts are responsible for balancing H+ and HCO3-. The distal
convoluted tubules are responsible for secreting K+, and if not
enough is secreted, excess H+ can result (K+ pushes it out of the
cells).
Excessive aspirin intake is a common drug-related cause of metabolic acidosis (remember,
aspirin is actually called acetylsalicylic acid).
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Metabolic alkalosis can occur if there is a loss of K+ in the ICF (H+ moves into the cells to
takes its place). Many loop diuretics cause the loss of K+, so nurses should be mindful of this
in their assessments. Excess oral intake of antacids, especially with renal disease, can
increase serum HCO3-. Volume loss will impede the function of the tubules and collecting
ducts, leading to metabolic alkalosis. GI volume loss through emesis creates a unique type of
metabolic alkalosis: hypochloremic metabolic alkalosis. Remember that the active substance
in the stomach is an acid: HCl (H+ - Cl-), so a loss of HCl will result in a loss of H+, and the
kidneys may not be able to respond adequately.
KIDNEY STONES
Urinary tract calculi, officially called nephrolithiasis
and commonly called kidney stones, are a common renal
disorder. There are many factors that contribute to the
formation, but in all cases, urine crystalizes in to a stone
that then gets lodged in the calyx, or less commonly,
the ureter or bladder.
The exact pathogensis is not well established, but
appears to be related to urine saturation due to
dehydration and the formation of mucoproteins. When pH increases (and the urine becomes
more alkaline), metals can percipitate. Kidney stones are composed of calcium oxate, calcium
phosphate, uric acid, or cystine. UTIs can result in stuvite stones.
Kidney stones are more common among men than women, except when 2° to a UTI. A genetic
component appears at play, as a family history increases individual risk. Being sedentary or
immobilized (i.e. hospitialized) incrases risk, as does GI/GU surgery. Diet also appears to be a
factor.
Acute, sudden, unilateral flank pain is a hallmark symptom. This is called renal colic and
arises from the ureter responding to the lodged stone: the
stretching, dilation, and spasms. Groin pain is
common. Both men and women experience genital
pain: Men: testicular pain, women: labial pain. People
suffering from renal calculi often do the “kidney stone”
dance, where they cannot settle down, shift weight from
one foot to the other, forward then back, sit then stand, etc.
It is not uncommon to find trace amounts of blood (trace,
not a urinary tract bleed).
In severe cases, patients may have nausea and vomiting and present with “mild shock,”
where they are diaphoretic, and their skin is cool to the touch. These are serious presenting
symptoms.
DIAGNOSTIC TESTING
The first test that is done is usually a urine dipstick, followed by a full urinalysis. Ruling out
UTI is critical. The urinalysis will find hematuria, crystalluria, and elevated pH. A
comprehensive metabolic panel is also draw to look for electrolyte imbalances. A CBC is
drawn to look for indications of an infection.
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Once a stone is suspected, an ultrasound or non-contrast CT scan is done to locate the stone
and measure its size. Ask yourself why the CT is non-contrast – it relates to how the die is
removed from the body.
In the acute phase, treatment revolves around pain management (usually opioids), fluid and
electrolyte balance, and prevention of infection. Antibiotics may be given to prevent a
secondary infection. The location and cause of the stone must be identified, as this will help
guide treatment options. If there is a partial obstruction or tamsulosin (Flomax) or terazosin
(Hytrin) is given to gently increase urine output (and maybe push the stone out).
Treatment is either conservative or invasive. If the stone is small, the patient may be sent home
to “pass” the stone naturally. This can take a long time and “passing the stone” is incredibly
painful. Patients are encouraged to consume large amounts of water to increase urine (2 – 3
liters/day) and take an OTC pain medication. Medications like Flomax or calcium channel
blockers can be used to relax the smooth muscle and facilitate passage.
Large kidney stones that cannot pass through the urinary tract require surgical intervention.
Other indications are signs of a serious complication related to the obstruction, such as an
elevated Cr, bacteria in the urine, persistent nausea and vomiting, or a paralytic ileus.
The most common surgical approach is through extracorporeal shockwave lithotripsy
(ESWL or just lithotripsy). This is a non-invasive procedure where a sound waves are
directed at the stone(s) and smash them. The smaller stones are then passed out through
the urine. While non-invasive, patients usually experience discomfort afterwards, and a
small amount of bleeding is to be expected.
Cystoscopies and ureteroscopies use flexible scopes that are passed through the urethral
meatus, up the urethra and into the bladder, and then into the ureters. The stones can
then be broken up using a laser or extracted (lithotomy).
If neither lithotripsy nor ureteroscopy are viable, a percutaneous lithotripsy or lithotomy can
be done. These are surgical procedures that access the stone through the abdomen and either
crush or remove the stone. As a final option, open surgery may be necessary, especially if the
kidney is threatened. This is a major surgery, using general anesthesia, and involves all the
risks associated with such.
After any procedure involving the kidneys, urine output must be closely monitored, as renal
failure is a possibility. Patients should also be educated on differentiating the presence of minor
blood from a hemorrhage (where the urine will look like blood). In addition, this phenonmenon
should decrease and resolve over time.
RENAL INJURY & FAILURE
Renal failure is not a primary diagnosis, rather it is a syndrome that results from some other
kidney pathology. Anything that can disrupt renal function can cause renal damage and failure.
Urinary tract infection (UTI) is the leading cause of kidney problem, especially in young girls,
older women, and anyone with urinary retention (like older man with BPH).
Renal failure is the partial or complete loss of renal function. The end result is the inability to
excrete wastes and to maintain fluid, electrolyte, and acid-base balance. If not corrected or
managed, renal failure will quickly lead to death.
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ACUTE RENAL INJURY
Acute renal injury (ARI) has a sudden onset and is potentially reversible. There is some
underlying acute process, usually and infection that has cause tubular necrosis. Loss of
function can range from mild (slight rise in Cr) to severe (azotemia – buildup of nitrogen
wastes in the body).
Acute renal injury (ARI) is staged using the RIFLE system. The first 3 stages are based on
increasing serum Cr and decreasing GFR. Acute renal failure (ARF) occurs when the Cr is 3x
greater than normal or the GFR drops by 75%. Urine output also goes down. Note, however,
that an acute process can result in end-stage renal disease (ESRD).
RIFLE Classification of Acute Renal Injury
Stage
Criteria
Risk
slight increase in Cr (x 1.5) or decrease in GFR (25%),
with slight drop in urine output
Injury
increased Cr x 2 or decrease in GFR by 50%. More
marked drop in urine output.
Failure
increased Cr x 3 or decrease in GFR by 75%, oliguria
or anuria
Loss of Function Persistent acute kidney failure, complete loss of
function for 4 weeks
End-Stage Renal Complete loss of kidney function for 3+ months
Disease (ESRD):
Acute renal injury progresses through 4 phases:
•
•
•
•
Initiation: urine output diminishes
Oliguria: urine output drops to almost nothing
Diuresis: large volume of output (after underlying cause is gone/nephrons resume work)
Recovery: back to normal.
CHRONIC RENAL DISEASE
Chronic kidney disease (CKD) develops gradually over years (its distinguishing characteristic
from acute renal injury). It is usually related to diabetic nephropathy, a complication of
uncontrolled diabetes or hypertension. Diabetes and hypertension damage the blood vessels
and tubular system in the kidneys, leading to intrarenal and postrenal damage. In addition,
they are affecting the prerenal circulation. There are other causes (see below), but we focus on
these because of the potential for significant control through clinical management.
In CKD, there is a significant drop in GFR (< 60 ml/min from 125) for 3 months, or long-term
renal damage. Chronic kidney disease is progressive and irreversible, and patients usually die
from cardiovascular disease.
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Causes of chronic renal failure
Diabetes (chronic)
Hypertension (chronic)
Glomerulonephritis (acute leading
to chronic)
Systemic lupus
Polycystic kidney disease
Renal Disorders
Causes of acute renal failure
Low cardiac output
Renal stones
Blocked urinary catheter
Burns
CT contrast dye, vancomycin,
ketorolac
Initial clinical management is to change life-style and control the underlying pathology. A
healthy diet, exercise, and adherence to medication regimes is important. By the time patients
reach Stage III, they are generally showing symptoms and more aggressive treatment is
needed. Eventually, CKD will advance to Stage IV and V, where patients will die if there is
nothing done to replace the kidneys. This includes dialysis and/or kidney transplantation.
CKD also progresses through an organized, almost predictable set of stages. The National
Kidney Foundation has defined the criteria for the 5 stages of CKD.
National Kidney Foundation Stages of Chronic Kidney Disease
Stage
Description
GFR
Clinical Action Plan
1
Kidney damage with
≥90
Diagnosis and treatment CVD risk
normal or ↑ GFR
reduction Slow progression
2
Kidney damage with
60-89
Estimation of progression
mild ↓ GFR
3a
Moderate ↓ GFR
45-59
Evaluation and treatment of
complications
3b
Moderate ↓ GFR
30-44
More aggressive treatment of
complications
4
Severe ↓ GFR
15-29
Preparation for renal replacement
therapy (dialysis, kidney transplant)
5
Kidney failure
<15 (or
Renal replacement therapy (if uremia
dialysis) present and patient desires
treatment)
CLINICAL MANAGEMENT OF RENAL FAILURE
Patients with ARI/ARF and CKD/CRF have many of the same symptoms, the difference
being the speed of onset. Patients will have complaints related to multiple body systems as all
body systems are affected. Oliguria and/or anuria are common symptoms shared by both
acute and chronic processes. Fatigue, lack of concentration, and confusion are also common.
GI distress is seen in both, though food intolerance is noticed more in chronic disease.
Neuropathy, or a lack of feeling and/or pain due to nerve loss, is usually seen only in chronic
disease. Calcium and uric crystals can lead to sore muscles. Underlying all of this is the loss
of fluid, electrolyte, and acid-base balance and inability to filter out metabolic waste.
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In acute renal injury, patients may be too ill to report symptoms. If NH3 levels are excessive or
metabolic acidosis/alkalosis advanced, patients may have encephalopathy or be confused. The
course of ARI depends on the nature and extend of the underlying pathology.
The primary clinical goal in ARI/ARF is to cure the underlying cause. Fluid and dietary
restrictions are put into place. Fluids are usually limited to 600 ml/day, protein may need to be
increased, but phosphorus producing foods are avoided. Electrolyte imbalances and metabolic
acidosis need to be monitored and addressed. In severe cases, dialysis (renal replacement
therapy) may be needed.
In CKD, patients may have compensated metabolic acidosis and chronic electrolyte
imbalances. Patients with CKD are chronically tired and may report sleep disturbances.
Urinary output should be closely monitored because it is an indication of worsening function.
Diet is also important because many foods result in waste products like NH3 and phosphate,
particularly protein metabolism. Anemia and bleeding are found due to the lack of
erythropoietin production.
Management of CKD involves controlling contributing factors, such as diabetes and HTN,
addressing electrolyte imbalances, and controlling anemia. Diet is crucial for CKD patients, as
limiting Na+, K+, protein, and phosphate intake can mitigate electrolyte imbalances and excess
metabolic wastes. Fluids also need to be monitored.
PHARMACOLOGIC MANAGEMENT
Drug therapy is different for acute and chronic renal patients. With acute renal patients,
the goal is to simply manage complications. Diuretics, like furosemide (Lasix), are used to
stimulate kidney function and offload fluids. IV insulin, sodium bicarbonate, or calcium
gluconate may be given to address hyperkalemia. Insulin shifts K+ into the cells, but IV
glucose is needed to prevent hypoglycemia. Sodium bicarbonate (NaHCO3) corrects
metabolic acidosis (do you see why?) and helps shift K+ into cells. Calcium gluconate is used
when hyperkalemic cardiac dysrhythmias are present because it reduces the excitability of
the cardiac muscle.
Oral medications are also used. For hyperkalemia, sodium polystyrene sulfonate
(Kayexalate) is given because it causes a K+-Na+ exchange in the bowels. It is frequently
given as an enema to create a potassium-rich “evacuation” of the bowels.
In chronic disease, potassium is often managed with patiromer (Veltassa), a potassiumbinding drug that is then passed in the stool. Kayexalate is also used. ACE inhibitors and
ARBs (angiotensin II receptor blockers) are given to control HTN by attenuating the RAAS.
Phosphate-binders are used with meals to control phosphate levels, such as sevelamar
carbonate (Renvela). Epoetin alpha (Epogen, Procrit) is an artificial erythropoietin that is
given IV or SQ to treat anemia.
RENAL REPLACEMENT
Once renal function is down to 15%, the patient is in Stage V end-stage renal failure (ESRD)
and uremia can no longer be managed by conservative interventions. The patient now needs
renal replacement therapy: dialysis or a transplant. The time from onset of CKD to ESRD can
take many, many years, during which time patients cope with the gradual loss and adapt to
their disease, and many see dialysis as just another step.
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Dialysis works by diffusion and ultrafiltration. Electrolytes and waste products (solutes)
move from the blood through a semipermeable membrane that acts like the capillary walls
and into a dialysate (dialysis fluid). This movement occurs because the dialysate is less
concentrated than the blood (diffusion). Excess fluid is removed because the dialysate has a
high concentration of glucose that creates a higher osmotic pressure than in the blood and pulls
the water and fluid across the membrane (ultrafiltration). Don’t worry about the technical
details. Remember that dialysis works by pulling solids and fluids across a membrane.
Diffusion for the solids and ultrafiltration for the fluids.
HEMODIALYSIS
Hemodialysis works like an artificial
kidney. Blood is pumped out of the
artery and into a dialyzer, filtered by
the dialysate, and then returned to the
patient through a vein.
The dialyzer consists of pathways
made of a porous layer (semipermeable membrane) that are
surrounded by dialysate. Blood goes
through the pathways and the dialysate removes wastes, electrolytes, and fluids. The dialysate
is continuously pulled through another filtration system so that it is refreshed. Heparin is also
used during the process to prevent clots while the blood is outside the body.
The entire process takes 3-5 hours and is done about 3 times a week. While the patient is
awake and can be somewhat active, they are tied to the machine and cannot just get up and
leave. In addition, they must go to a dialysis center.
ACCESS FOR HEMODIALYSIS
For hemodialysis, a vascular access device is needed. The
most commonly used device is an arteriovenous fistula,
also called an AV fistula. This is a surgically created fistula
between a large artery and large vein. The most common
locations are the cephalic or basilic artery and vein in either
the forearm or upper arm. The fistula allows arterial blood
to flow into the vein, but it takes about 3 months before it
can be used. An AV fistula has a thrill that can be palpated
(feels like a buzzer) and a bruit that can be auscultated (sounds like a pulsating, rushing sound).
Absence of a thrill or bruit means the fistula is not working.
The finding needs to be reported to the nephrologist and the
fistula should not be used until assessed.
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An arteriovenous graft, or AV graft, is similar to an AV fistula. A synthetic graft is made
to bridge between an artery and a vein. The most common location is the brachial artery
and the antecubital vein. AV grafts can be used sooner than an AV fistula.
A temporary HD vascular access device may be inserted and used until an AV fistula or graft
are ready, or as a temporary measure for patients in acute renal failure who need dialysis. This
is essentially a tunneled central line. It can be place at the
bedside and used as soon as its placement is verified.
Access is usually the internal jugular vein, and the device
has two lumens, one for withdrawing blood and one for its
return.
Important rules:
•
•
•
Never perform BPs or blood draws on the arm with an
AV fistula or AV graft.
Only a trained dialysis nurse should handle a HD access
device.
During dialysis, the patient’s weight and blood pressure are frequently monitored.
PERITONEAL DIALYSIS
Peritoneal dialysis uses the peritoneal cavity as the
semipermeable membrane. A major benefit is that
patients can do this on their own at home; however, it
is not as effective as hemodialysis. A catheter is
surgically placed into the peritoneal space through the
abdomen, with a port extending out of the abdomen.
Dialysate is instilled and removed via this drain.
Peritoneal dialysis is done in exchanges, with three
phases.
•
•
•
First, the dialysate is instilled (inflow phase).
Second, the fluid remains in place for a specified period
of time (dwell phase).
Third, the fluid is removed (drain phase).
Continuous peritoneal dialysis involves patients doing
multiple exchanges during the day.
Between exchanges, the patient is free to do their normal
activities. There are usually 4 exchanges during the day,
and the last dwell occurs overnight as the patient sleeps.
Patient education is important regarding hand hygiene and
gloves for exchanges, and to monitor for infection. Also,
patient need make sure the amount of drain matches the inflow. If not enough fluid is
drained, the patient should move around from side to side. This may shift fluid to allow it to
drain. If it does not fully drain, they should contact their provider as this can lead to serious
complications and infections.
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Automated peritoneal dialysis is done overnight. At bedtime, the patient hooks up their
catheter to a machine that is itself connected to dialysate and drain bags. As the patient sleeps,
the machine performs 2-3 exchanges. However, automated peritoneal dialysis is usually not
adequate by itself, so patients need to perform 1 or 2 exchanges during the day.
RISKS AND COMPLICATIONS OF DIALYSIS
Complications to hemodialysis are disequilibrium syndrome and anemia. Disequilibrium
syndrome will happen when the patient first starts dialysis. Toxins are removed too quickly
and fluid can shift rapidly into brain cells, resulting in the patient becoming delirious. They
may have seizures. Anemia will become more pronounced with dialysis due to blood
removal, so erythropoietin is given to patients during dialysis. There is a risk for bleeding
due to the use of anticoagulants. Patients may have elevated temperatures due to the use of
warmed up dialysate, but it is not a problem until it reaches over 38.5° C. Lastly,
hypotension can occur if fluid is taken off to fast.
Many drugs are not given prior to dialysis because they will be “dialyzed out,” meaning they
will be filtered and therefore useless. If a patient is having dialysis performed, you should
check all their medications before administration and give only those that will not be filtered or
there is a specific order for. Checking with the dialysis nurse is always a good idea. Anti-HTN
medications should not be given prior to dialysis. If the patient’s BP is too low, dialysis cannot
be done
There are many complications that can occur with peritoneal dialysis, peritonitis being the
most common. The high sugar concentration that sits in the peritoneal cavity makes a very
favorable environment for many bacteria, especially S. aureus and S. epidermidis. Both of
these bacteria are part of our skin’s normal flora, so an improper technique (poor
handwashing, lack of gloves) can lead to infection. Peritonitis results in abdominal pain, with
rebound pain, and cloudy effluent (drained fluid). The catheter exit site can also get
infected.
Sometimes the patient can’t get fluid in or out. Catheter and other obstructions can occur
due to clots or compression on the peritoneal catheter from abdominal organs. It’s important
to prevent constipation. The patient might have hyperglycemia due to high sugar content in
dialysate.
KIDNEY TRANSPLANT
Once on dialysis, the patient is on dialysis forever, unless they are able to get a transplant.
Anyone on dialysis is technically a candidate for transplant, though most dialysis patients will
not qualify. Whereas dialysis was once considered a bridge therapy to a transplant, for many
it is now a destination therapy.
Organ transplant is a major surgery and comes with all the risks. During surgery, the donated
kidney is removed from the donor and sutured into the recipient, and the old non-working
kidney is left in place. During surgery, a Foley catheter will be inserted and following
surgery, the surgeon will be looking for urine production. This often happens immediately.
Pain management, infection/sepsis monitoring, respiratory assessment and cardiac
monitoring are all part of the post-surgery are. In addition, the patient should be ambulated
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early and learn to manage their complex medication regimen right away. Patients should
also be monitored for signs of depression, which is commonly seen post-transplant.
The patient may receive a liver from a living donor (related or unrelated). A living donation is
usually a directed donation, and as long as the patient can withstand the stress of surgery and
has the resources to take care of the organ, the transplant can be done.
MANAGEMENT OF DONOR ORGANS
Most transplant recipients receive their new livers from
cadavers. In the United States, cadaver donated organs are
allocated by the Organ Procurement and Transplant
Network (OPTN, a government agency) in
conjunction with United Network for Organ
Sharing (UNOS, a non-profit organization).
To receive a transplant, a recipient must demonstrate that they:
• Will survive long enough to make the transplant cost-effective,
• Will take responsibility to ensure they take proper care of the organ (e.g. no drinking,
smoking, good medication adherence), and
• Are sick enough but not too sick. Most of this is determined using an algorithm that
considers all the different factors.
The criteria for kidney transplant are:
Be over 18 years of age
Receive an estimated post-transplant survival (EPTS) score (the algorithm)
Have a longer expected post-transplant survival time than others on the list
Be within distance to receive the organ before the organ “expires.” So, when an organ
becomes available it will go to the person with the best score and can have the organ
transplanted before the organ would go bad.
Because of this, living donations are becoming more prevalent. Blood relatives are more likely
to be a match and result in fewer rejections, but strangers can also come forward and offer to
donate. Still, a living donor must go through physical and psychological testing to make sure
they will not suffer any adverse side effects or trauma.
COMPLICATIONS OF KIDNEY TRANSPLANTS
The most significant complication is organ rejection. Even more than with blood, significant
typing and cross-matching is done, but without immunosuppressant medications, a recipient
will have an alloimmune response reject the new kidney. Consequently, adherence to drug
regimens is essential. The patient must consistently take anti-rejection/immunosuppressant
drugs as long as they have the kidney: prednisone, tacrolimus (Prograf), cyclosporine
(Gengraf), and myfortic (CellCept) are a few. Keep in mind, rejection can happen at any time:
immediately following implant (hyperacute), shortly after implant (acute), and much later
(chronic).
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Immediately prior to and following surgery, patients have their immune systems
suppressed; consequently, infections are a high risk. Immunosuppressants do not target just
the new organ, instead they suppress the entire immune system. This leaves the patient with a
life-long increased risk of infection. Transplant patients (and anyone on an
immunosuppressant) are often hospitalized for opportunistic infections.
Drugs such as prednisone (a corticosteroid) can also cause the release of sugar from the liver
turning the patient into a diabetic. Transplant recipients have an increased risk of
cardiovascular disease, and immunosuppressants can worsen existing hyperlipidemia and
hypertension. Immunosuppressants also increase the incidence of cancers.
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Appendix A. Renal Infections
Condition
Urinary Tract
Infection:
Umbrella term
Cause
Upper:
Kidney & ureters
Lower:
Bladder & urethra
Stasis
E. coli - #1 cause (80%)
Catheters (CAUTI)
Pyelonephritis
Infection of upper
urinary tract (i.e.
functional part of
kidney)
One sided
Begins as lower tract UTI
Urethritis
Bacteria
Inflammation of
Trichomonas (F)
the urethra
Chlamydia (M)
(upper)
Gonorrhea (M)
Glomerulonephritis UTI
Inflammation of
Systemic infection
the glomerulus
(post-Streptococcal
both kidneys
glomerulonephritis)
Manifestation
Painful urination
Abdominal/flank pain
Fever
Lower tract
Symptoms
Hesitancy/Intermittency
Dribbling, retention
Incomplete void
Dysuria, urgency, Nocturia,
incontinence, nocturnal
enuresis
Flank pain
Fever, chills, malaise
Emesis, dysuria, urgency,
frequency
Discharge from urethral
meatus
Dysuria, urgency, frequency
Challenging with women
Sudden onset with temporary
remission
Generalized edema
HTN
Oliguria, hematuria,
proteinuria, cloudy/rusty
color
Diagnosis
Urine dipstick
Clean-catch
urinalysis
Urine culture
Ultrasound
Treatment
Antibiotics
Phenazopyridine
(local
analgesic)
Complications
Pyelonephritis
Urethritis
Urosepsis
Urinalysis
Pyuria,
hematuria
WBC
Urine culture
CBC
Elevated WBC
Left shift
Ultrasound
Urinalysis
Urine culture
Antibiotics
Pain
management
Hospitalization
Urosepsis
Chronic pyelonephritis
Urinalysis
erythrocytes
Urine culture
Antistreptolysin-o
titers
Decreased
complement
Elevated BUN/Cr
Antibiotic
targeted to
infectious
agent
Antibiotics (if
Permanent kidney
bacterial)
damage
Steroids
Kidney failure
Antihypertensive
(if severe)
Rest
Fluid restriction
Protein
restriction
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