This document provides an overview of a lecture on the renal system. It discusses renal anatomy and physiology, assessment of renal health, interpretation of kidney function labs, acute and chronic kidney disease, dialysis options, and kidney transplantation. The objectives are to understand renal structures and functions, diseases of the kidney like pyelonephritis and glomerulonephritis, compare acute and chronic kidney disease, interpret kidney labs, explain nursing care of renal patients, and discuss dialysis and transplantation. Fun facts, diseases statistics, and the functions of kidney structures like the nephron are also reviewed.

1. Susan Schlueter, BSN-RN, CPN

2. Overview of lecture
 Renal anatomy and physiologic functions
 Assessment of healthy renal system
 Lab interpretation in regards to renal health and kidney function
 Diseases of the kidney
 Acute vs Chronic Kidney Failure
 Dialysis: hemodialysis and peritoneal dialysis
 Kidney transplant

3. Objectives
 Identify and define the anatomic
structures and physiological functions
of the kidney.
 Understand specific diseases of the
kidney including pyelonephritis,
glomerulonephritis, and polycystic
kidney disease.
 Compare and contrast acute and
chronic kidney disease, including
causes, classification, treatment,
management, and prognosis.
 Interpret lab values in regards to renal
health: electrolytes, kidney function,
BUN, creatinine, creatinine clearance,
urine osmolarity.
 Explain nursing care of the renal
system, especially assessment of renal
health, prevention of renal
complications, and management of
patients with kidney disease.
 Compare and contrast hemodialysis
and peritoneal dialysis, the mechanism
and rationale of each.
 Discuss kidney transplant: rationale,
process, maintenance, prognosis, and
ethics surrounding transplantation.

4. Some “fun” facts
 What percentage of your kidney function can you lose before you might
need dialysis?
 Chronic kidney disease is more common in men or women?
 Your entire volume of blood and fluids will circulate how many times
in an hour? (approximately)
 How much of that blood and circulated fluids becomes urine?
 ____% of your blood supply is in your kidneys at any given time.

5. Some “not so fun” facts
 African Americans are 4x more likely to develop chronic kidney disease
(CKD) than Caucasian Americans are. Hispanic Americans are 1.5x
more likely to develop CKD than non-Hispanic whites.
 Of all adults with hypertension, about 20% have CKD.
 Of all adults with diabetes, about 35% have CKD.
 Of all adults older than age 65, about 40% have CKD.

6. Functions of the Kidney
 Big picture function: maintain homeostasis in the body
 Major functions: filtration and collection
 Other functions: helps regulate blood pressure, osmolarity and
electrolyte concentrations in the blood, helps regulates pH, stimulates
red blood cell production, helps regulate calcium and vitamin D levels.

7. Kidney Anatomy
 Macrostrucure:
 Blood supply
 Cortex
 Medulla
 Calyxes
 Renal Pelvis

8. Diseases impacted by parts of the Nephron

9. Micro-structure
 The Nephron
 Afferent arteriole
 Glomerulus
 Efferent arteriole
 Bowman’s Capsule
 Proximal convoluted tubule
 Loop of Henle
 Distal convoluted tubule
 Collecting tubule or duct

10. A musical number to help remember!
https://www.youtube.com/watch?v=kVF65d1X8SU

11. Follow the blood and
filtrate/urine through
the kidney:
Where does the blood enter the
kidney?
What happens when it enters the
glomerulus?
Where does the filtrate go?
PCT... What’s reabsorbed?
How DOES the Loop of Henle
work?
DCT… now what’s reabsorbed?
Collecting duct is fed by what?
Collecting duct empties where?
Ok, back to the vasculature, how
and where does blood exit the
kidney?

12. GFR
 The afferent and efferent
arterioles, renal artery
and renal vein, all need to
be the right size with no
obstructions to keep the
glomeruli filtering at a
steady rate.
 What happens if there is
obstruction or if the size
of the lumen is changed?

13. Nursing Assessment
 Many of the same questions as urinary assessment
 Medications
 Recent infections
 Edema
 Blood pressure
 Changes in weight
 Palpation of kidney/pain with percussion at CVA
 Interpretation of electrolytes, kidney function labs, and UA

14. Kidney Labs
 Electrolytes
 Sodium (Na)
 Potassium (K+)
 Calcium (Ca-total)
 Phosphorus (Phos)
 Bicarbonate (HCO₃‾)
 pH of blood

15. Kidney Labs
 Other blood tests
 Blood Urea Nitrogen (BUN)
 Serum Creatinine (Cr)
 BUN:Cr ratio

16. Kidney Labs
 Urine Studies
 Components of UA
 RBCs
 WBCs
 Protein
 Casts
 Nitrate
 Leukocyte Esterase
 Osmolarity
 Creatinine Clearance calculated
after 24 hour urine collection
 Glomerular Filtration Rate (GFR)
 Calculate by Urine Creatinine x Urine Volume then divide by Serum Creatinine
https://quizizz.com/admin/quiz/59eb8017ac6ed61000e50b24

17. Pharmacology: Antihypertensives
 ACE inhibitors
 Angiotensin I cannot convert to
angiotensin II. Less angio II means
more vasodilation, and less
constriction of the efferent
arteriole in the kidney
 Generally well tolerated and
inexpensive
 Captopril is recommended
specifically for nephropathy, but
any ACE will work
 Nursing considerations: BP
assessment, ensuring daily doses
 ARBs
 Blocks Angiotensin II receptors on
the blood vessel walls
 Lower risk of cough and
hyperkalemia
 Newer, more expensive
 Preferred for patients who cannot
tolerate ACE inhibitors
 Cozaar (losartan) and Avapro
(irbesartan) are preferred ARBs for
nephropathy, but again, any ARB
will work
 Nursing considerations: same as
ACE inhibitors

19. Pharmacology: Diuretics
Basic mechanism of diuretics: prevent sodium and chloride from being
reabsorbed, thereby preventing the passive reabsorption of water.
 Loop Diuretics (Lasix [Furosemide])
 Act on the ascending Loop of Henle
where a substantial amount of all NaCl
is reabsorbed (about 20%) producing
profound diuresis
 IV or oral
 Serious side effects:
 Hyponatremia, hypochloremia,
dehydration, hypotension, hypokalemia
 Nursing considerations: you tell me-
critical thinking time!
 Potassium Sparing Diuretics
(Spironolactone or triamterene)
 Acts on the distal nephron, most
reabsorption has already occurred
 Blocks the action of aldosterone, thus
retaining potassium and excreting sodium
 Scant diuresis, takes 1-2 days to start
taking effect
 Side effects: hyperkalemia, endocrine
effects
 Nursing considerations: avoid salt
substitutes which often contain potassium

21. Disorders of the Kidney

22. Vascular/Obstructive Problems
 Lumen size, obstructions?
 Renal Artery Stenosis
 Renal Vein Thrombosis
 Renal Calculi
 Polycystic Kidney Disease

23. Polycystic Kidney Disease
 Most common life-threatening inherited disease in the world
 Autosomal dominant, if 1 parent has disease, 50% chance of passing it to
child
 Accounts for 10-15% of CKD patients in the US
 Presents either in childhood or is latent until age 30s-40s
 Fluid-filled cysts form in the cortex and medulla, compressing the nearby
tissues. Most are several mm to several cm in size
 Asymptomatic in early stages, presents with HTN or hematuria
 Sometimes diagnosed incidentally because of UTI or kidney stone
 No treatment other than symptomatic- managing pain and infections, kidney
diet, fluid restriction, antihypertensive drugs, etc. Eventually may progress
ESRD and need dialysis or a transplant

24. Pyelonephritis, Etiology
 Almost always an ascending bacterial infection- a UTI gone really bad!
 Occasionally a descending bacterial infection, endocarditis or sepsis
 Rarely caused by a virus, fungus, or protozoa
 Inflammation starts in the cortex then spreads to the medulla
 Prompt treatment is required, 15% of cases of urosepsis will lead to
death via septic shock if untreated
 Can cause abscesses
 Pregnancy, pre-existing vesicoureteral reflux or obstruction are risk
factors

25. Pyelonephritis, Clinical Manifestations
 Range of symptoms, from mild fatigue to chills/fever, vomiting, flank
pain, malaise, and urinary complaints such as dysuria, frequency, and
sudden urge to urinate
 CVA tenderness usually present
 Fever may be present, with related tachycardia and tachypnea
 U/A shows pyuria, bacteriuria, and hematuria, possibly casts
 CBC shows leukocytosis
 Ultrasound may identify anatomic abnormalities, abscess, or calculi

26. Pyelonephritis, Nursing Interventions
 History and assessment
 Vital signs
 Obtain urine culture and sensitivities
 Goals
 Normal renal function
 Normal body temperature
 No complications
 Relief of pain
 No recurrence of symptoms

27. Pyelonephritis, Nursing Interventions
 Teaching
 Encourage adequate fluid intake
 Encourage rest
 UTI prevention/recurrence prevention
 Rationale of therapy
 Medications
 Antibiotics
 Pain/antipyretics
 Follow up care and repeat UA/UC

28. Chronic Pyelonephritis
 Kidneys become atrophic and lose function due to fibrosis/scar tissue
formations, an inflammatory response, usually in response to multiple
infections of the upper urinary system
 Presents as decreasing kidney function, elevated Cr
 Diagnosed by imaging- ultrasound or CT
 Biopsy done to determine extent of damage, how deep inflammation has
intruded, and which structures are affected
 Treatment starts with eradicating the underlying cause, but the damage is
usually permanent
 Prognosis: one or both kidneys affected? Extent of damage? Most patients
with chronic pyelonephritis will progress to End Stage Kidney/Renal Disease.
(ESKD, ESRD)

29. Case Study 1
 See Handout 1
 Any questions about s/s or abbreviations?
 Discuss which clinical manifestations cause you to suspect
pyelonephritis. Where there any other conditions that you considered?
 What risk factors does she have for UTI? Pyelonephritis?
 Acute or Chronic?
 What’s the appropriate treatment?
 Specific teaching?
 Follow up needed?

30. Glomerulonephritis, Etiology
 3rd leading cause of ESRD in US
 Acute (also known as Rapidly Progressive GN, or RPGN) or Chronic
 Immunologic process that can either swiftly or slowly cause progressive
damage to the glomeruli
 Most commonly seen form of acute GN is Acute Poststreptococcal
Glomerulonephritis (APSGN). Exact etiology is unknown
 Chronic GN has a more insidious onset, can be caused by many types of
immune or vascular conditions, or co-morbidities that can cause scarring of
the glomeruli: lupus, vasculitis, diabetic neuropathy, HTN…
 Often diagnosed incidentally, can be confirmed by CT, ultrasound, or biopsy

31. Glomerulonephritis, Clinical Manifestations
 Generalized edema
 Tends to start in “leakier” vessels like capillaries around the eyes-
periorbital edema often seen first, but eventually progresses to whole body
edema, including ascites
 Hypertension
 Oliguria, or hematuria with a smoky/rusty appearance, proteinuria
 Abdominal or flank pain

32. Glomerulonephritis, Nursing Assessment
 Renal assessment
 Health history
 How is urination?
 Smoky urine is a sign of bleeding in the upper urinary system
 Edema/weight gain
 CVA tenderness
 Recent infections
 Vital signs- BP and temp… why?
 Labs- what should be ordered?
 Large numbers of erythrocytes and erythrocyte casts in urine are a
hallmark of glomerulonephritis

33. Glomerulonephritis, Management
 Antibiotics only if acute infection (i.e. strep throat) is still present
 About 95% of APSGN patient recover or improve with conservative
management. About 5-15% of patient will develop chronic GN and about 1%
will progress to full renal failure
 Supportive treatments
 Rest is indicated until kidney is recovered (in acute GN)
 Pain management
 Hypertension is managed with ACEIs or ARBs
 Edema is managed with fluid and sodium restriction and diuretics
 Low protein diet may be recommended if BUN is high or if there is high
proteinuria
 Support for CKD management if needed

34. Glomerulonephritis, Nursing Interventions
 Frequent vitals, especially blood pressure as this will be indicative of
kidney function
 I/Os
 Daily weights
 Repositioning/preventing injury to edematous skin
 Teaching
 Diet: low sodium, low protein, fluid restriction
 Worsening of symptoms

35. A Note About Nephrosis (aka Nephrotic Syndrome)
 Similar s/s and outcomes to glomerulonephritis, but not caused by
inflammation of the glomeruli. Exact etiology unknown, but there appears to
be either idiopathic or acquired injury to the basement cells and/or podo cells
that make up the junction of the glomerulus and Bowman’s capsule, allowing
proteins to enter the capsule and be excreted.
 Key differences: no blood in urine, usually very high proteinuria.
 Eventually, the loss of the proteins leads to hyperalbuminemia, increased
triglycerides, anorexia/malnourishment, hypercoagulability, decreased immune
response, and decreased calcium absorption leading to skeletal deformities and
hypoparathyroidism.
 Treatment is essential the same as GN, management of underlying disease,
management of symptoms, balancing fluid, sodium, and proteins. However, also
should consider risk of infection and thrombus formation.

36. AKI vs CKD
 Acute kidney injury is a catch-all term for loss of kidney function (from
slight deterioration to severe) that happens in a rapid period of time
(hours to days)
 Chronic kidney disease is another catch-all term for loss of kidney
function that happens over a longer period of time, usually years
 AKI has the potential for recovery, CKD is progressive and irreversible
 AKI is usually seen in patients who have other life-threatening
conditions, and affects about 5% of hospitalized patients. CKD is
usually seen in patients who have other chronic illnesses/diseases that
are not immediately life threatening. 1 in every 9 Americans has CKD

37. AKI Etiology
 Can be caused by numerous conditions, classified by where the problem
originates:
 Pre-renal causes are independent of the actual kidney, caused by things further
upstream i.e. hypovolemia, decreased cardiac output, and decreased renal blood
flow. Essentially, they all lead to low perfusion/ischemia of the renal organ
 Intrarenal (or intrinsic) causes are etiologies that cause harm to the renal tissue,
affecting the nephron function. Common causes are nephrotoxic injury, interstitial
nephritis, prolonged ischemia, and other renal disorders such as
glomerulonephritis. The tissue most likely to be damaged is the epithelium of the
tubules, causing Acute Tubular Necrosis
 Post-renal causes are related to obstruction of urine out of the kidney, or urinary
reflux. Examples are BPH, bladder cancer, calculi, strictures, or trauma

38. RIFLE classification for
staging Acute Kidney Injury

39. Location
S/S ----
Pre-Renal Intrarenal Post-Renal
BUN:Cr >20 10<>20 >10
Urine
osmolarity
>500 <350 Almost all the
same as
Urine NA <10 >20 Intrarenal
Potassium May be decreased
due to vomiting, or
WNL
Elevated Injury- so
Urine Sp.
Gravity
>1.020 1.010-1.020 To differentiate
Look for
Creatinine Mildly elevated,
much slower rate
of elevation
Elevated,
usually at a rate
of
>0.3mg/dL/day
Signs of
obstruction
with
ultrasound
BUN Elevated Elevated Or CT.
UA
microscopy
Hyaline casts
(sometimes) or no
findings
Granular casts
Renal epithelial
cells

41. Oliguric Phase
 Oliguric phase begins within 1-7 days of injury, if due to ischemia it starts within 24
hours. Nephrotoxic drug response, though, may be delayed up to a week
 About 50% of AKI patients will not be oliguric, delaying diagnosis. Generally,
patients are anuric if post-renal, oliguric if pre-renal, and non-oliguric if intrarenal
 If AKI is mild, and especially in pre-renal hypovolemia, fluids can correct AKI
 In more severe injuries, patients will have fluid retention, requiring careful
regulation of sodium and fluids. Edema, pulmonary edema, and pleural and cardiac
effusions become a concern
 Hyperkalemia, especially in trauma/burn patients and those already in metabolic
acidosis. Can cause cardiac dysrhythmias.
 Heme/Infectious disorders: at higher risk for eosinophilia, leukocytosis, often seen in
multi-system organ failure, low protection against urinary/lung infections
 Waste product accumulation: creatinine and BUN will rise, neurological
disturbances such as fatigue, seizures, and coma are possible

42. Diuretic Phase
 Kidneys recover the ability to excrete urine, but not to concentrate it.
Patients pass between 1-5 liters of urine per day
 At risk for hypovolemia, hypotension, hyponatremia, and hypokalemia
 Lasts 1-3 weeks, labs should begin normalizing toward the end of this
phase

43. Recovery Phase
 Kidneys resuming their usual functions, GFR increases, creatinine and
BUN are decreasing toward normal values
 Greatest improvements are seen in the first 1-2 weeks, but may take up
to 12 months for full recovery
 Outcome is determined by patient’s overall health, severity of the
kidney failure, and complications. Older adults do not recover as much
function as younger adults. Some patients never recover function and
progress to ESKD. However, most patients recover to the point of being
clinically asymptomatic, although there is scar tissue and an
insignificant loss of kidney function.

44. AKI Management
 Fluid volume management: make sure there is enough volume to have
adequate cardiac output to perfuse the kidneys (and rest of the body).
Administer diuretics in low doses. Fluid restriction- can have
600mL+all losses in previous 24 hours
 Hyperkalemia: lower potassium by administering IV insulin to move
potassium into cells, sodium bicarb to correct acidosis and shift
potassium into cells, calcium gluconate to prevent cardiac
dysrhythmias, Kayexalate to exchange potassium for sodium in the
bowel and excrete the potassium, or hemodialysis to remove
potassium. When less critical, restrict dietary potassium to 40mEq/day
 Continuous Renal Replacement Therapy

45. AKI Nursing Assessment
 Monitor vitals
 I/O, measure, calculate daily total, fluid replace/restrict, examine urine
color, follow labs such as urine protein, blood, and sediment
 Assess oral mucosa for dryness, inflammation
 Good oral care to prevent stomatitis, caused by ammonia in saliva
 Auscultate lungs for crackles, rhonchi, or diminished breath sounds
 Auscultate heart for murmurs, pericardial friction rub, assess EKG
 Review lab data, especially CBC, BMP, Creatinine, BUN
 Daily weight, at same time with same scale

46. AKI Nursing Planning
 Diagnoses
 Excess fluid volume related to kidney failure and fluid retention
 Risk for infection related to invasive lines, uremic toxins, and altered immune
responses secondary to kidney failure
 Fatigue related to anemia, metabolic acidosis, and uremic toxins
 Anxiety related to disease processes, therapeutic interventions, and uncertainty of
prognosis
 Potential complication: dysrhythmias related to electrolyte imbalance
 Goals
 Completely recover without any loss of kidney function
 Maintain normal fluid and electrolyte balance
 Decrease anxiety
 Adhere to and understand the need for careful follow-up care

47. Case Study
 Handout 2
 What are you thinking for a diagnosis?
 Risk factors of kidney failure?
 Significance of poor skin turgor?
 Significance of S₃ heart sound?
 Looking at the labs, how would you classify the injury?
 Why not glomerular disease?
 Calculate the BUN: Cr ratio. Does this confirm suspicions about etiology?
 First intervention?
 Then what?
 Prognosis?

48. CKD Basics
 Defined as either the presence of kidney damage or a GFR
< 60mL/Min/1.73m² for longer than 3 months
 Classified by stages, Stages 1-5, normal GFR to ESRD
 Can be asymptomatic, underdiagnosed, and undertreated. May not be
treated until there has been a significant loss of nephron function
 Prognosis is variable, some people live long, normal, active lives, others
progress to ESRD rapidly
 Leading causes are diabetes (50% of CKD patients) and HTN (25%)
 As kidney function declines, every system in the body is affected

50. Select CKD Clinical Manifestations
 Psychologic/Neurologic
 Anxiety, depression
 Fatigue
 Headache
 Sleep disturbances
 Encephalopathy
 Cardiovascular
 Hypertension
 Heart failure
 Coronary artery disease
 Pericarditis
 Peripheral artery disease
 Generalized edema
 Pulmonary
 Pulmonary edema
 Uremic pleuritis
 Pneumonia
 FEN
 Anorexia
 Nausea/vomiting
 Hyperkalemia
 Gastrointestinal
 Gastritis
 Gastrointestinal bleeding
 Musculoskeletal
 Vascular and soft tissue
calcifications
 Osteomalacia
 Osteitis fibrosa
 Paresthesias
 Restless leg syndrome
 Integumentary
 Pruritis
 Ecchymosis
 Dry scaly skin
• Metabolic
• Carbohydrate intolerance
• Hyperlipidemia
• Metabolic acidosis
• Waste product accumulation
• Endocrine/Reproductive
• Hyperparathyroidism
• Thyroid abnormalities
• Amenorrhea
• Erectile dysfunction
• Infertility
• Hematologic/Infectious disease
• Anemia
• Bleeding
• Infection
• Ocular- hypertensive retinopathy

51. CKD Management
 Similar to the other kidney diseases we’ve discussed: treat underlying
cause if possible, manage symptoms, and prevent worsening of
condition when possible
 What are some treatments/drugs you might expect to see in a patient with
CKD? (Refer to previous slide for ideas.)

52. CKD Nursing Assessment
 Obtain thorough health history, including any existing kidney disease or family
history of kidney disease
 Ask about the use of medications, including OTC and herbal supplements, to
determine if any nephrotoxic agents are present, or if anything might be contributing
to hypertension (exacerbating CKD)
 Decongestants such as Sudafed cause vasoconstriction
 Antacids can contain high levels of salt contributing to HTN, and also can interfere with
the absorption of some medications
 NSAIDs are known to contribute to AKI and the progression of CKD, especially when
taken frequently at high doses
 Assess dietary habits, weight trends, are there any problems with intake or
fluctuating weight?
 Remember that CKD is a chronic illness that has no cure, only progression toward
ESRD, and it affects every part of the patient’s life. Questions about coping,
adherence to treatment, support, etc. are all appropriate

53. CKD Nursing Diagnosis and Goals
 Excess fluid volume related to impaired kidney function
 Risk for electrolyte imbalance related to impaired kidney function resulting in
hyperkalemia, hypocalcemia, hyperphosphatemia, and altered vitamin D
absorption
 Imbalanced nutrition: less than body requirements related to restricted intake
of nutrients (especially protein), nausea, vomiting, anorexia, and stomatitis
 Many additional depending on current complications and presentation
 Goals:
 That a patient with CKD will:
 Demonstrate knowledge of and ability to comply with therapeutic regimen
 Participate in decision making for plan of care and future treatment modality
 Demonstrate effective coping strategies
 Continue with activities of daily living within physiologic functions

54. CKD Nursing Implementation
 Health promotion
 Encourage on-time check ups, appropriate follow up care, frequent labs. Make a
plan with the patient for medication management. Encourage patient to meet
with dietitian
 Teach patient to take daily BP and weight, identify signs of electrolyte
imbalance, fluid overload
 Give practical tips about diet and fluids - simple charts with examples of
approved or discouraged foods. Measurement systems for fluid restrictions.
Use of gum or hard candy to moisten mouth
 Encourage patient to find and use support. Talk about concerns regarding
lifestyle changes, living with a chronic illness, or big decisions such as
transplant

55. Caution foods:
 High Sodium
 Most sauces and gravies, including meat
tenderizer and soy sauce
 Processed lunch meat
 Smoked meats/fish (BACON!)
 Pickled foods
 High Potassium
 Fruits such as apricots, avocado, bananas,
citrus, pears, nectarines…
 Veggies such as celery, dry beans,
potatoes, leafy greens, tomatoes, squash…
 Whole grains, especially those containing
bran
 Peanuts (including PEANUT BUTTER)
 Sardines and clams
 Milk (and ice cream, pudding and yogurt)
 High Phosphorus
 Milk, cheese, custard, pudding, ice cream
 Dried beans or peas
 Nuts
 CHOCOLATE!
 Dark cola
 Sausage and hot dogs.
 High Protein
 Meats and fish
 Dairy
 Eggs
 Nuts
 Soy/tofu

56. End Stage Renal Disease
 Kidney function is at 10% or less, GFR is less than 15mL/min
 Options are:
 Dialysis
 Hemodialysis
 Peritoneal dialysis
 Transplantation
 Live donor organ
 Deceased donor organ
 Transplantation may not be an option for all patients because of lack of a suitable
donor kidney, patients may be physically or mentally unsuitable for the
transplantation process, some patients may be opposed to transplantation for
religious or ethical reasons

57. Overview of Dialysis
https://www.youtube.com/watch?v=fKlY2SKi_dk

58. AV Fistula
https://www.youtube.com/watch?v=6EqXoLdWgfs&t=23s

59. Life with Peritoneal Dialysis
https://www.youtube.com/watch?v=q3SJ_5UAYkc

60. Closeup of Vascular Access
https://www.youtube.com/watch?v=hCMOTNeDBmE

61. Complications of Dialysis
 HD
 Hypotension during tx, from rapid loss
of vascular fluid
 Muscle cramps- unknown etiology,
usually seen/are worst in 1st month of
tx
 Loss of blood can occur from operator
error, accidental rupture of dialysis
membrane, accidental disconnection of
tubing during tx, post-needle removal
 Hepatitis B and C have outbreaks
among dialysis population, usually due
to breaks in infection control processes.
At this time, Hep C is more prevalent,
about 10% of HD patients are positive
 PD
 Exit site infection
 Peritonitis. Tx can be oral, IV or
peritoneal abx. Repeated infections cause
adhesions, requiring cessation of PD
 Hernias, from large volumes
 Low back pain from increased pressure
 Bleeding from catheter insertion
 Atelectasis or PNA from displacement of
diaphragm
 Protein loss during times of increased
peritoneal permeability

62. Critical Thinking Time
 Pros of HD?
 Cons of HD?
 Pros of PD?
 Cons of PD?

63. Nursing Considerations for Dialysis
 Daily weights to track fluid status. Pt should know his “dry” weight
 Be SURE patient had an AM weight on day of his run, and obtain a post weight
upon return
 Vital signs- hyper/hypotension, fever indicating infection
 Never take BP ______________!!
 Assess lungs for crackles, heart for dysrhythmias
 Assess access site. In PD, look for redness, swelling, and drainage. In HD,
look for redness, warmth, oozing. Listen to bruit, assess distal pulse, feel the
thrill. Patient should have no pain at access site
 If your HD pt has an arterial access catheter instead of AV graft, assess site for
redness, swelling, drainage, pain. Do not use for giving meds/fluids, do not flush
with saline (unless your facility has a protocol that allows you to)

64. Nursing Considerations for Dialysis
 Know pre-dialysis labs, anticipate which labs might be corrected by
dialysis and which won’t (i.e. dialysis will correct hyperK+ but not
anemia)
 Make sure labs are NOT drawn from the arm with the AV fistula!
 Scheduled medications: some may need to be held before HD
 Antihypertensive meds should be held, as drop in BP is expected
 Antiarrhythmics may be given
 Drugs likely to be “eaten” by the dialysis process such as water soluble
vitamins should be held
 Held drugs can be administered 2-4 hours after run is complete, if patient
is stable

65. Keep an Eye on Your Orders!
 Practitioners will add labs all the
time
 Then replacements
 Then more labs
 Then more replacements
 Then….

66. Transplantation

67. Transplantation Basics
 It works! 90-95% of all transplants have > 1 year survival rate
 But, fewer than 4% of ESKD patients will receive a transplant. The wait for
a deceased donor (about 73% of all transplants) averages 2-5 years
 Must be approved to become a recipient, and then get on the list.
Criteria vary by transplant center
 Kidneys are matched by ABO group and HLA typing, age, length of
wait, number of antibodies, and location
 The donor kidney may be removed laparoscopically or open surgery
 Recipient will be opened from iliac crest to pubis symphysis. Usually,
old kidney is just left in place, with key vascularization transferred to
the new kidney

68. Post-op Care
 Donor may have significant pain, emotional response. Can be
discharged 2-5 days post-op
 Recipient may still need dialysis for a few days until new kidney
becomes functional
 Careful fluid and electrolyte management, making sure kidney has
adequate perfusion and fluids
 Foley catheter for accurate I/Os and to assess for clots in bladder. If
urine output drops suddenly, check Foley for a clot in tubing
 ATN (a potentially reversible form of intrinsic renal failure) may
develop, dialysis will be needed for possibly a period of weeks

69. Post-transplant Care
 Immunosuppressive therapy to decrease risk of rejection
 Frequent monitoring for long-term risks/complication
 Rejection
 Infection
 CV disease (Immunosuppressants can worsen HTN and dyslipidemia)
 Cancers are more prevalent in transplant patients, likely because of the effects of
the immunosuppressants. Common types are basal and squamous cell carcinoma
of the skin, Hodgkin’s and non-Hodgkin’s lymphoma, and Kaposi sarcoma
 Recurrence of original kidney disease
 Corticosteroid related complications: necrosis of hip and knee joints, peptic ulcer
disease, glucose intolerance, cataracts, infections, and malignancies

70. Ethical Concerns with Transplant
 Organ procurement
 Coercion or payment of a familiar live donor.
 Foreign travel to an unfamiliar live donor.
 Black Market
 Criteria for being on the list
 No smoking/alcohol/drug abuse
 Morbid obesity
 Previous non-compliance with treatment plan
 Principles of social justice and healthcare ethics:
 Community and the common good (stewardship), human dignity
 Autonomy, beneficence, justice, non-maleficence

71. Transplant Ethics Case Study
 Handout 3
 Discuss your initial reaction, did that change as you read the study?
 What information causes indecisiveness for you?
 Can an adolescent be held accountable for his own healthcare?
 In this case, what principles does autonomy conflict with?

72. What the Author of the Case Study Concluded:
 “It would be inappropriate to give a teenager a kidney if the odds of graft survival
were low. This would not only be a poor allocation of scarce resources, it would also
be dangerous for the teen, as noted above. It would be equally inappropriate to deny
a teenager access to a transplant simply because he was judged on the basis of age to
be at high risk for nonadherence.
 The best approach in this situation is to make an individualized assessment of the
barriers to adherence, the likelihood of nonadherence, and the potential benefits of
interventions that might improve adherence. In this case, since the patient is already
on dialysis, his ability to adhere to the demands of that regimen might be considered
a “trial of therapy” that will give information about the likelihood that he would
adhere to posttransplant treatment. He should be given clear instructions about what
is expected of him, feedback whether or not he adheres to the demands of dialysis,
and an endpoint to this “trial of therapy.” If he is able take medication, manage his
diet and fluids, and keep his appointments in clinic and in dialysis, then he should
be eligible for a second transplant.”
 Do you agree? Additional thoughts?

73. THANK YOU
I hope I’ve inspired this… And NOT this!