Module 7: Acute Kidney Injury and Chronic Kidney Disease Flashcards
Kidney (Renal) Failure
Partial or complete impairment of kidney function
that results in inability to excrete metabolic waste
products and water
Acute Kidney Injury
Ranges from slight deterioration to severe
impairment
Rapid loss of kidney function with:
Rise in serum creatinine and/or reduction in urine
output
Elevated BUN and K+
Azotemia—accumulation of nitrogenous waste
products
High mortality rate; other life-threatening conditions
Etiology and Pathophysiology of AKI - Prerenal
Prerenal
Causes: factors that reduce systemic circulation
causing reduction in renal blood flow which leads to
oliguria
* Severe dehydration, heart failure, decreased CO
Autoregulatory mechanisms attempt to preserve
blood flow
Prerenal azotemia results in Na+ excretion, increased
Na+ and H2O retention and decreased urine output
Etiology and Pathophysiology of AKI - Intrarenal
Intrarenal
Causes: problems that cause direct damage to kidney
tissue
* Prolonged ischemia
* Nephrotoxins
* Hemoglobin released from hemolyzed RBCs
* Myoglobin released from necrotic muscle cells
* Kidney diseases—acute glomerulonephritis and SLE
Intrarenal
Acute tubular necrosis (ATN)
* Results from ischemia, nephrotoxins, or sepsis
* Severe ischemia causes disruption in basement
membrane and patchy destruction of tubular epithelium
* Nephrotoxic agents cause necrosis of tubular epithelial cells—clog tubules
* Potentially reversible
Etiology and Pathophysiology of AKI - Postrenal
Postrenal
Causes: mechanical obstruction of outflow which
results reflux into renal pelvis, impairing kidney
function
* Benign prostatic hyperplasia, prostate cancer, calculi,
trauma, and extrarenal tumors
Bilateral ureteral obstruction—hydronephrosis; relieve obstruction in 48 hours increased chance of recovery
Acute Kidney Injury
Clinical Manifestations: Oliguric phase
Three phases: oliguric, diuretic, and recovery
RIFLE classification (Table 51.3 in the textbook)
Risk (R)
Injury (I)
Failure (F)
Loss (L)
End-stage renal disease (E)
Oliguric phase
Urinary changes—*oliguria
* Urinary output less than 400 mL/day
* Occurs within 1 to 7 days after injury
* Lasts 10 to 14 days (longer is poor prognosis)
* Urinalysis—casts, RBCs, WBCs, protein
* Specific gravity 1.010
* Osmolality 300 mOsm/kg
50% patients nonoliguric; greater than 400 mL
urine/day
Oliguric phase
Fluid volume
* Hypovolemia may exacerbate AKI
* Decreased urine output leads to fluid retention
Neck veins distended
Bounding pulse
Edema
Hypertension
* Fluid overload can lead to heart failure, pulmonary
edema, and pericardial and pleural effusions
Oliguric phase
Metabolic acidosis
* Impaired kidney cannot excrete hydrogen ions or acid
products of metabolism
* Serum bicarbonate production is decreased
Reabsorption and regeneration defective
* Severe acidosis develops
Kussmaul respirations—increasing exhaled CO2
Oliguric phase
Sodium balance
* Increased excretion of sodium—damaged tubules
* Hyponatremia can lead to cerebral edema
Potassium excess
* Impaired ability of kidneys to excrete K+
* Increased risk with massive tissue trauma
* Usually asymptomatic
* ECG changes—peaked T waves, widened QRS, ST
depression
Oliguric phase
Hematologic disorders
* Leukocytosis—infection may be fatal
Urinary and respiratory infections
Waste product accumulation
* Increased BUN and *serum creatinine levels
Neurologic disorders
* Fatigue and difficulty concentrating
* Seizures, stupor, coma
AKI Diagnostic Studies
Diagnostic studies
Thorough history
Serum creatinine, BUN, electrolytes
Urinalysis
Renal ultrasound
Renal scan
CT scan
Renal biopsy
Diagnostic studies
Contraindications for contrast medium
* MRI or MRA with gadolinium contrast medium—may be fatal
* Contrast-induced nephropathy (CIN)
* Diabetics taking metformin: hold 48 hours before and
after use of contrast medium; risk of lactic acidosis
* If contrast is needed for high-risk patients—use low-
dose and optimal hydration
AKI Care
Ensure adequate intravascular volume and cardiac
output
Loop diuretics (e.g., furosemide [Lasix])
Osmotic diuretics (e.g., mannitol)
Closely monitor fluid intake during oliguric phase
Fluid restriction calculation: All fluid losses for
previous 24 hours + 600 mL
Hyperkalemia therapies
Temporary—move K+ into cells
* Insulin and sodium bicarbonate
dysrhythmias—stabilizes myocardium
* Calcium gluconate
Remove K+ from body
* Sodium polystyrene sulfonate (Kayexalate) or
Patiromer (Veltassa)
* Dialysis
Dietary restriction
Indications for renal replacement therapy (RRT)
Volume overload
Elevated serum potassium level
Metabolic acidosis
BUN level > 120 mg/dL (43 mmol/L)
Significant change in mental status
Pericarditis, pericardial effusion, or cardiac
tamponade
Clinical status of patient
Renal replacement therapy (RRT)
Peritoneal dialysis (PD)
* Not frequently used
Intermittent hemodialysis (HD)
* Emergent therapy
Continuous renal replacement therapy (CRRT)
* Cannulation of artery and vein
* Continuously 24 hours
Nutrition therapy
Maintain adequate caloric intake
* Primarily carbohydrates and fat
* Adequate protein to prevent breakdown
Restrict sodium, K+, phosphate
Calcium supplements or phosphate-binding agents
Enteral/parenteral nutrition
Gerontologic Considerations
Acute Kidney Injury
Decreased GFR with aging
More susceptible to AKI
Dehydration
* Polypharmacy- diuretics, laxatives
* Illness and immobility
Hypotension, diuretic therapy, aminoglycoside
therapy, obstructive disorders, surgery, infection, and
contrast medium
decreased reduced ability to recover
RRT still an option
Chronic Kidney Disease
Progressive, irreversible loss of kidney function
Greater than 26 million American adults have
CKD; more common than AKI
Increased prevalence related to aging population,
increased obesity, increased diabetes and HTN
Over half a million Americans are receiving
treatment for ESRD; high mortality rate
Kidney disease improving global outcomes (KDIGO)
defines CKD as
Kidney damage
* Pathologic abnormalities
* Markers of damage
Blood, urine, imaging tests
Low glomerular filtration rate (GFR)
* <60 mL/min/1.73m2 for longer than 3 months
Leading causes
Diabetes—50%
Hypertension—25%
Other: glomerulonephritis, cystic diseases, urologic
diseases
Persons with CKD are often asymptomatic; ~ 70%
aware
Underdiagnosed and untreated
Course and prognosis are variable
Medicare covers ~80% of the costs
Considered a disability
See Promoting Health Equity Box
Increased incidence with Blacks, Native Americans,
and Hispanics
CKD Clinical Manifestations
Result of retained substances
Urea
Creatinine
Phenols
Hormones
Electrolytes
Water
Uremia
Early stages
No change in urine output
Polyuria may be present related to diabetes.
CKD progression—increasing fluid retention; need
diuretic
After a period on dialysis, patients may become
anuric
Waste product accumulation
As GFR decreases, BUN and serum creatinine levels
increase
BUN level increase
* From kidney failure and protein intake, fever,
corticosteroids, and catabolism
* N/V, lethargy, fatigue, impaired thought processes, and headaches occur
*Serum creatinine clearance—most accurate indicator
Uremia
Uremia
Syndrome in which kidney function declines to the
point that symptoms occur in multiple body systems
Often occurs when GFR is less than or equal to
15 mL/min
Manifestations vary depending on cause, co-
morbidities, age, and adherence to medical regimen
Defective Carb Metabolism
Altered carbohydrate metabolism
Caused by impaired glucose metabolism
* From cellular insensitivity to normal action of insulin
* Mild-moderate hyperglycemia and hyperinsulinemia
Defective carbohydrate metabolism
Patients with diabetes who develop uremia may
require less insulin than before the onset of CKD
Excretion of insulin dependent on kidneys
Insulin dosing must be individualized
May improve after starting dialysis
Elevated Triglycerides
Elevated triglycerides
Hyperinsulinemia stimulates hepatic production of
triglycerides
Altered lipid metabolism
* Decreased levels of enzyme lipoprotein lipase
– Important in breakdown of lipoproteins
Increased VLDLs and LDLs, decreased HDLs
Most patients with CKD die from CV disease
Electrolyte Imbalances
Potassium (K+)
Hyperkalemia
* Most serious electrolyte disorder in kidney disease
* Fatal dysrhythmias
When serum potassium level reaches 7 to 8 mEq/L (7 to 8 mmol/L)
* Decreased excretion, breakdown of cellular protein,
bleeding, and metabolic acidosis leads to increased K+
Other sources: food, dietary supplements, drugs, and IV infusions
Sodium (Na+)
May be high, normal, or low
Impaired excretion causes sodium and water
retention
Dilutional hyponatremia may occur
* Edema
* Hypertension
* HF
Calcium and phosphate
See section on Musculoskeletal System (CKD mineral
and bone disorder)
Magnesium
Hypermagnesemia
* Related to ingestion of magnesium (e.g., milk of
magnesia, magnesium citrate, antacids)
* Can result in absence of reflexes, decreased mental
status, cardiac dysrhythmias, hypotension, respiratory
failure
Metabolic Acidosis
Metabolic acidosis
Results from
* Impaired ability of kidneys to excrete excess acid
* Defective reabsorption and regeneration of bicarbonate
Plasma bicarbonate level usually falls to
approximately 16 to 20 mEq/L (16 to 20 mmol/L)
Anemia
Anemia
Due to decreased production of erythropoietin
* Hormone stimulates bone marrow to make RBCs
Other factors: nutritional deficiencies, decreased RBC
life span, increased hemolysis, blood sampling, GI
bleeding, HD, increased PTH
Also decreased iron stores
Folic acid lost in dialysis
Bleeding tendencies
Defect in platelet function
Infection
Changes in WBC function
Altered immune response and function
Hyperglycemia and external trauma
Cardiovascular Disease closely linked
CV disease and CKD closely linked
Death often related to MI, ischemic heart disease,
PAD, HF, cardiomyopathy, and stroke
Traditional CV risk factors
* Hypertension and elevated lipids
Nontraditional CV risk factors
* Vascular calcification and arterial stiffness
Calcium deposits associated with stiffness of blood
vessels
Vascular smooth muscle cells change
* Chondrocytes or osteoblast-like cells
High calcium and phosphate totals
Impaired renal excretion
Drug therapies to treat bone disease
HTN
Hypertension
Both a cause and a consequence of CKD
* Aggravated by sodium and water retention
* Increased renin production may contribute
HTN, ECF volume overload, and anemia may
develop into left ventricular hypertrophy, which may
lead to cardiomyopathy and HF
* HTN can cause retinopathy, encephalopathy,
nephropathy
*BP control—one of most important goals
Dysrhythmias
Hyperkalemia and decreased coronary artery
perfusion
Uremic pericarditis can progress to effusion and
tamponade
Friction rub, chest pain, and fever
Respiratory
Kussmaul respirations related to acidosis
Dyspnea may occur with
Fluid overload
Pulmonary edema
Uremic pleuritis
Pleural effusions
Respiratory infections
GI
Every part of GI system is affected
Cause: excessive urea
* Stomatitis with exudates and ulcerations
* Uremic fetor (urinous odor of breath)
* Anorexia, nausea, and vomiting
* Diabetic gastroparesis
* GI bleeding
* Constipation
CNS Depression
CNS depression
Lethargy, apathy
Decreased ability to concentrate
Fatigue, irritability
Altered mental ability (late)
Seizures
Coma
Hypertensive encephalopathy
Peripheral neuropathy
Restless legs syndrome
Paresthesias
Motor involvement
Footdrop
Muscle weakness and atrophy
Loss of deep tendon reflexes
Muscle twitching, jerking, asterixis, and nocturnal leg
cramps
Bones/Minerals
CKD mineral and bone disorder (CKD-MBD)
Systemic disorder of mineral and bone metabolism
Results in
* Skeletal complications (osteomalacia, osteitis fibrosa)
* Soft tissue complications (vascular calcifications)
Other
Pruritus
Calcium-phosphate deposits and sensory neuropathy
Itching may be intense
Leads to bleeding or infection
Uremic frost
Urea crystalizes on skin
BUN > 200 mg/dL
Infertility and decreased libido
Experienced by both sexes: low sperm counts;
amenorrhea
Sexual dysfunction
Physical, psychological, and medication side effects
Pregnancy during dialysis poses significant risk to
mother and infant
Personality and behavioral changes
Emotional lability
Withdrawal
Anxiety, depression, and grief
Fatigue, lethargy
Changes to: body image, lifestyle, occupation,
finances, and family roles and responsibilities
CKD Diagnostic Studies
History and physical assessment
Dipstick evaluation of protein
Albuminuria
Urinalysis
Renal ultrasound, scan, CT scan, biopsy
Albumin-to-creatinine ratio (1st am void)
Serum BUN, creatinine, creatinine clearance,
electrolytes, lipids, hemoglobin, hematocrit
GFR
CKD Care
Management
Stages 1 to 4
Control HTN, hyperparathyroid disease, CKD-MBD,
anemia, and dyslipidemia
Correct of ECF volume overload or deficit
RRT
Treat CV disease
Nutritional therapy
Drug therapy
Hyperkalemia
Restriction of high-potassium foods and drugs
Acute
* IV glucose and insulin
* IV 10% calcium gluconate
Sodium polystyrene sulfonate (Kayexalate)
* Cation-exchange resin; bowel exchanges Na+ for K+ ions
* Osmotic laxative action (diarrhea)
Patiromer (Veltessa)—binds K+ in GI tract
* May bind other oral meds; take 6 hours before or 6 hours after ; delayed onset
Dialysis—most effective
Hypertension
Weight loss (if indicated)
Therapeutic lifestyle changes
Diet recommendations (DASH Diet)
Antihypertensive drugs; often need 2 or more
* If diabetic—give ACE inhibitors and ARBs
CKD-mineral and bone disease (MBD)
Phosphate not restricted until patient requires renal
replacement therapy
* Phosphate intake then restricted to
< 1 g/day
CKD-MBD
Phosphate binders
* Calcium acetate (PhosLo)
* Calcium carbonate (Caltrate)
Bind phosphate in bowel and then excreted
* Sevelamer hydrochloride (Renagel)
Lowers cholesterol and LDL levels
Phosphate binders
* Should be administered with each meal
* Side effect: constipation
CKD-MBD
Avoid aluminum and magnesium preparations
Supplementing vitamin D
* Cholecalciferol
* Serum phosphate level must be lowered before calcium or vitamin D is administered
CKD Care Continued
Control secondary hyperparathyroidism
* Calcimimetic agents
Cinacalcet (Sensipar)
– Increase the sensitivity of calcium receptors in
parathyroid glands
* Subtotal or total parathyroidectomy
Anemia
Erythropoietin (EPO)
* Epoetin alfa (Epogen, Procrit)
* Darbepoeitin alfa (Aranesp)
* Given IV or subcutaneously
* Increased hemoglobin and hematocrit in 2 to 3 weeks
* Side effects: thromboembolism, hypertension
* Use lowest possible dose; contraindicated in
uncontrolled HTN
Anemia
Iron supplements
* If plasma ferritin level is <100 ng/mL
* Side effects: gastric irritation,
constipation
* May make stool dark in color
Anemia
Folic acid supplements
* Needed for RBC formation
* Removed by dialysis
Avoid blood transfusions
* Increase the development of antibodies
* May lead to iron overload
Dyslipidemia
Statins (HMG-CoA reductase inhibitors)
* Most effective for lowering LDL level
* Atorvastatin (Lipitor)
Fibrates (fibric acid derivatives)
* Used to lower triglyceride levels and increase HDLs
* Gemfibrozil (Lopid)
CKD Nutriton Therapy
Nutrition therapy
Designed to maintain good nutrition
Dietician referral
Calorie-protein malnutrition
* Monitor laboratory parameters
Protein intake
Normal for Stages 1 to 4 and HD patient
Increased for PD patient
Fluid restriction with HD
Intake depends on daily urine output
Sodium restriction
Diets vary from 2 to 4 g/day
Avoid high-sodium foods
Salt substitutes should be avoided because they
contain potassium chloride
Potassium restriction
Limit: 2 to 3 grams
High-potassium foods should be avoided with HD
Nutrition therapy
Phosphate restriction in ESRD
Limit: 1 gram per day
Foods high in phosphate
* Meat and dairy products
Most foods high in phosphate are high in protein
* Phosphate binders essential with dialysis
Dialysis
Movement of fluid/molecules across a
semipermeable membrane from one
compartment to another
Used to correct fluid and electrolyte imbalances
and removes waste products in kidney failure
Can be used to treat drug overdoses
2 methods of dialysis available
Peritoneal dialysis (PD)
Hemodialysis (HD)
Started when patient’s uremia can no longer be
adequately treated conservatively; GFR < 15
mL/min/1.73 m2
Nephrologist determines when to start
Uremic complications require dialysis
ESRD treated with dialysis because
There is a lack of donated organs
Some patients are physically or mentally unsuitable
for transplantation
Some patients do not want transplants
Age is not a factor in determining candidacy
General Principles of Dialysis
Diffusion
Movement of solutes from an area of greater
concentration to an area of lesser concentration
Osmosis
Movement of fluid from an area of lesser
concentration of solutes to area of greater
concentration
* Glucose in dialysate creates osmotic gradient to pull
fluid from the blood
Ultrafiltration
Water and fluid removal
Results when there is an osmotic gradient or pressure
gradient across membrane
* PD—glucose in dialysate
* HD—pressure gradient
Excess fluid moves into dialysate
Peritoneal Dialysis
Peritoneal access is obtained by inserting a catheter
through anterior abdominal wall
Technique for catheter placement varies; usually
done via surgery
PD may start right away or bed delayed until site
healed
Aseptic technique important to avoid peritonitis
Three phases of PD cycle (manual):
Inflow (fill)—2 to 3 L over 10 minutes
Dwell (equilibration) 20 to 30 minutes—8 hours
Drain 15 to 30 minutes
Cycle is repeated
Called an exchange
Volume depends on size of peritoneal cavity
Dextrose—osmotic agent
Automated peritoneal dialysis (APD)
Cycler delivers the dialysate during sleep Times and
controls fill, dwell, and drain phases; alarms and
monitors for safety
Continuous Ambulatory peritoneal dialysis (CAPD)
Manual exchange four times during the day
Peritoneal Dialysis Complications
Exit site infection
Redness, tenderness, drainage
Treat with antibiotics
Peritonitis—Exit site or tunnel infection
Abdominal pain, rebound tenderness, or cloudy
effluent with increased WBCs or bacteria, may
have fever
GI: diarrhea, vomiting, distention, increased bowel sounds
Treat with antibiotics
Repeated infections may cause adhesions
Hernias
Increased intrabdominal pressure from dialysate
Treatment: hernia repair
Lower back problems
Intraperitoneal infusion increases pressure
Treatment: binders and exercise
Bleeding
Common with initial catheter placement
New—active intraperitoneal bleeding; check BP and
hematocrit
Pulmonary complications
Decreased lung expansion atelectasis, pneumonia, or bronchitis
Elevate HOB, repositioning and deep breathing
Protein loss—monitor nutrition
Hemodialysis
Settings and Schedules
Most treated in a community-based center
Dialyzed for 3 to 4 hours, 3 days/wk
Other schedule options
Short daily HD
Long nocturnal HD
Home HD
Hemodialysis
Complications
Hypotension
Hypovolemia, decreased CO and SVR
Light-headed, nausea, seizures, vision changes, and chest pain
Treatment: decreasing volume of fluid removal and IV NSS
Muscle cramps
Decreased BP, hypovolemia, increased ultrafiltration, and low-sodium dialysate
Treatment: decrease ultrafiltration and IV fluids
Loss of blood
Blood not rinsed from dialyzer, accidental separation of tubing, dialysis membrane rupture or bleeding after
needles removed; heparin
Treatment: rinse all blood back, avoid excess heparin, and hold pressure to access sites
Hepatitis—8% to 10% hepatitis C
Infection control precautions
Hepatitis B—low incidence; administer vaccine
Continual Renal Replacement
Therapy
Method for treating AKI (acute kidney infection)
Means by which uremic toxins and fluids are
removed
Acid-base status and electrolyte are adjusted slowly
and continuously in hemodynamically unstable
patients
Over 24 hours
Can used with HD
Contraindication
Patient has life-threatening manifestations of uremia
that require rapid treatment
Various types of CRRT
Continuous venovenous hemofiltration (CVVH)
Slow continuous ultrafiltration (SCUF)
Continuous venovenous hemodialysis (CVVHD)
Continuous venovenous hemodiafiltration (CVVHDF)
Infusion of replacement fluid determined by
degree of fluid and electrolyte imbalance
Anticoagulants are needed to prevent blood
clotting
Customized to patient’s needs
CVVHD and CVVHDF
Uses dialysate
Dialysis fluid is attached to distal end of hemofilter
Can be continued as long as 30 to 40 days
Hemofilter should be changed every 24 to 48 hours
Able to obtain specimens
Ultrafiltrate should be clear yellow
If bloody, need to terminate
CRRT versus HD
CRRT versus HD
Blood pump is slower than HD
Continuous rather than intermittent
Fluid volume can be removed over days versus hours
Solute removal by convection (no dialysate required)
in addition to osmosis and diffusion
Less hemodynamic instability
Does not require constant monitoring by HD nurse
(need ICU nurse)
Does not require complicated HD equipment
CRRT Nursing Interventions
Specific nursing interventions
Obtain weights
Monitor and document laboratory values daily for fluid and electrolyte balance
Assess hourly intake and output, VS, and
hemodynamic status
Care for site to prevent infection
Wearable Artificial Kidney (WAK)
Recently developed and approved for use
Miniaturized dialysis machine; ~10 pounds
Carrier resembles a tool belt
Connects to patient via catheter
Designed to filter blood in ESRD
Can run continuously on batteries
Kidney Transplant
More than 100,000 patients are currently awaiting kidney transplants
Average wait time for cadaver is 2 to 5 years
17,000 transplants take place every year
Advances include:
Organ procurement and preservation
Surgical techniques
Tissue typing and matching
Immunosuppressant therapy
Prevention and treatment of graft rejection
Best treatment for ESRD
Very successful
1-year graft survival rate
Deceased donor transplants: 90%
Live donor transplants: 95%
Reverses pathophysiology of ESRD
Eliminates dialysis and dietary and lifestyle restrictions
Less expensive than dialysis after 1st year
Kidney Transplant
Recipient Selection
Candidacy determined by a variety of medical and
psychosocial factors that vary among transplant centers
Possible exclusions: obesity, smoker
Preemptive transplant (before dialysis is required) is
possible if recipient has a living donor
Contraindications to transplant
Advanced cancer
Refractory/untreated heart disease
Chronic respiratory failure
Extensive vascular disease
Chronic infection
Unresolved psychosocial disorders
HIV+ or hepatitis B or C are not contraindications
Surgical procedures may be required before
transplant
Coronary artery bypass or coronary angioplasty
Cholecystectomy
Bilateral nephrectomy
Kidney Transplant
Histocompatibility Studies
Purpose of testing is to identify HLA antigens for
both donors and potential recipients
Kidney Transplant
Donor Sources
Deceased donors with compatible blood type
Blood relatives
Emotionally related living donors
Altruistic living donors
Paired organ donation
Live donor
Extensive interprofessional evaluation
Crossmatches—check antibodies
Advantages
* Better patient and graft survival rates
* Immediate organ availability
* Immediate function/minimal cold time
* Opportunity to have recipient in best possible medical
condition since elective surgery
Live donor sees nephrologist for H & P
Laboratory studies
* 24-hour urine—creatinine clearance and total protein
* Complete blood count, chemistry and electrolyte
profiles
* Hepatitis B and C, HIV, CMV testing
Donor Sources: Live Donor
Diagnostic studies
ECG, chest x-ray
Renal ultrasound, arteriogram, 3-D CT scan
Psychologist or social worker evaluation
Emotional stability
Risks and benefits
Cost covered by recipient’s insurance
No compensation for lost wages
Paired organ donation
ABO incompatibility between donor and recipient
Find another donor/recipient pair with whom to
exchange kidneys
Plasmapheresis—option to remove antibodies from
recipient
* After transplant, patient gets plasmapheresis
Donor Sources
Deceased Donors
Deceased (cadaver) kidney donors are relatively
healthy persons that have suffered an
irreversible brain injury and are brain dead
Must have effective CV functions and on
ventilator to preserve organs
Permission of next of kin requested even with
signed donor card
Kidneys removed and preserved up to 72 hours
* Preferred cold time less than 24 hours
Kidney Transplant
Surgical Procedure - Live Donor
Live donor
Donor nephrectomy performed by a transplant
surgeon
Begins 1 or 2 hours before the recipient’s surgery is
started
Recipient is surgically prepared in a nearby operating
room
Laparoscopic donor nephrectomy
* Most common approach for removing kidney in living
donor
* Minimally invasive
Fewer risks, shorter recovery time
Open (conventional) nephrectomy
* Lateral incision
* Rib may need to be removed
Kidney Transplant Recipient
Kidney transplant recipient
Transplanted kidney usually placed extraperitoneal in
the iliac fossa
Right iliac fossa is preferred for anastomosis of blood
vessels and ureter
Before incision
Urinary catheter placed into bladder
* Antibiotic solution instilled
Distends the bladder
Decreases risk of infection
Crescent-shaped incision
Rapid revascularization critical
Donor artery anastomosed to recipient internal or
external iliac artery
Donor vein anastomosed to recipient external iliac
vein
Kidney transplant recipient
When anastomoses are complete,
clamps are released and blood flow reestablished
Urine may begin to flow from ureter immediately
Donor ureter tunneled through bladder submucosa
(ureteroneocystotomy)
Pre Op Care
Preoperative care
Emotional and physical preparation
* Stress that dialysis may be required
* Review need for immunosuppressive drugs and
prevention of infection
ECG
Chest x-ray
Laboratory studies
Dialysis, if needed
Post Op Care
Live donor
* Care is similar to that for open or laparoscopic
nephrectomy
* Closely monitor renal function
* Closely monitor hematocrit
* Donors usually experience more pain than recipient
* Acknowledge their gift!
Kidney transplant recipient
* Maintenance of fluid and electrolyte balance is the
priority
* Large volumes of urine may be produced soon after
transplanted kidney placed due to
New kidney’s ability to filter BUN
Abundance of fluids during operation
Initial renal tubular dysfunction
* Dehydration must be avoided
* Assess for hyponatremia/hypokalemia
* Acute tubular necrosis can occur
* Monitor urine output; maintain catheter patency
* Patient education: signs and symptoms of rejection,
infection, and surgical complications; follow-up care
Kidney Transplant
Immunosuppressive Therapy
Goals
Adequately suppress immune response to prevent
rejection
Maintain sufficient immunity to prevent overwhelming
infection
Kidney Transplant
Complications - Rejection
Rejection
Hyperacute (antibody-mediated, humoral) rejection
* Occurs minutes to hours after transplant
Acute rejection
* Occurs days to months after transplant
Chronic rejection
* Process occurs over months or years and is irreversible
* May go back on transplant list
Transplant Complications - Infection
Risk related to: suppression of normal defense
mechanisms, immunosuppressive drugs, and effects
of ESRD; compounded by systemic illnesses
Most common infections observed in 1st month:
pneumonia , wound infections, IV line and drain
infections, and UTIs
Fungal infections
* Candida
* Cryptococcus
* Aspergillus
* Pneumocystis jiroveci
Viral infections
* CMV
One of most common
* Epstein-Barr virus
* Herpes simplex virus (HSV)
* Varicella-zoster virus
* Polyomavirus (e.g., BK virus)
Transplant Complications - CVD
Cardiovascular disease
Transplant recipients have increased incidence of
atherosclerotic vascular disease
Immunosuppressants can worsen hypertension and
hyperlipidemia
Patients need to adhere to antihypertensive regimen
Transplant Complications - Cancer
Cancers
Primary cause— immunosuppressive therapy
Most common
* Skin cancers
* Posttransplant lymphoproliferative disorder
Regular screening is important
Preventive care
* Protective clothing and sunscreen
Transplant Complications - Recurrence of Kidney Disease
Recurrence of original kidney disease
Glomerulonephritis
IgA nephropathy
Diabetic nephropathy
Focal segmental sclerosis
