Module 7: Acute Kidney Injury and Chronic Kidney Disease Flashcards

1
Q

Kidney (Renal) Failure

A

Partial or complete impairment of kidney function
that results in inability to excrete metabolic waste
products and water

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2
Q

Acute Kidney Injury

A

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

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3
Q

Etiology and Pathophysiology of AKI - Prerenal

A

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

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4
Q

Etiology and Pathophysiology of AKI - Intrarenal

A

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

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5
Q

Etiology and Pathophysiology of AKI - Postrenal

A

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

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6
Q

Acute Kidney Injury
Clinical Manifestations: Oliguric phase

A

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

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7
Q

AKI Diagnostic Studies

A

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

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8
Q

AKI Care

A

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

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9
Q

Gerontologic Considerations
Acute Kidney Injury

A

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

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10
Q

Chronic Kidney Disease

A

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

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11
Q

CKD Clinical Manifestations

A

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

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12
Q

Uremia

A

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

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13
Q

Defective Carb Metabolism

A

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

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14
Q

Elevated Triglycerides

A

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

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15
Q

Electrolyte Imbalances

A

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

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16
Q

Metabolic Acidosis

A

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)

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17
Q

Anemia

A

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

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18
Q

Cardiovascular Disease closely linked

A

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

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19
Q

HTN

A

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

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20
Q

Respiratory

A

Kussmaul respirations related to acidosis
 Dyspnea may occur with
 Fluid overload
 Pulmonary edema
 Uremic pleuritis
 Pleural effusions
 Respiratory infections

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21
Q

GI

A

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

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22
Q

CNS Depression

A

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

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23
Q

Bones/Minerals

A

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)

24
Q

Other

A

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

25
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
26
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
27
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)
28
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
29
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
30
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
31
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
32
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
33
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
34
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
35
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
36
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
37
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
38
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
39
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
40
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
41
Kidney Transplant Histocompatibility Studies
Purpose of testing is to identify HLA antigens for both donors and potential recipients
42
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
43
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
44
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
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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
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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)
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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
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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
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Kidney Transplant Immunosuppressive Therapy
Goals  Adequately suppress immune response to prevent rejection  Maintain sufficient immunity to prevent overwhelming infection
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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
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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)
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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
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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
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Transplant Complications - Recurrence of Kidney Disease
Recurrence of original kidney disease  Glomerulonephritis  IgA nephropathy  Diabetic nephropathy  Focal segmental sclerosis
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