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CHATER 36: KIDNEY FAILURE  laboratory determinations of

serum K
 Renal Insufficiency – loss of kidney  sodium imbalance
function but not so sever o hyponatremia - because do not
 uremia (uremic syndrome) – high BUN
excrete a lot of fluid = fluid retention
and creatinine SYMPTOMATIC
= sodium dilution (amount of sodium
o alters protein-binding sites,
the same but water increases)
absorption, distribution, and  overhydration
metabolism of drugs  low/ no sodium IVF
 azotemia - high BUN and creatinine  hypervolemia – decreased Ht
ASYMPTOMATIC and Hb
 all electrolytes in blood will raise because it  SNS
cannot be discharged  warm, moist, flushed
Acute Kidney Failure (AKF) skin
 cerebral edema
 abrupt, reversible  mental status changes
 decrease GFR = increase BUN and Urea o hypernatremia
 urinary output < 40 ml/hr (oliguria); but  high sodium medications and
may be normal or increased diet
 one of the leading cause of inpatient death  metabolic acidosis - because bicarbonate
 infection – major cause and hydrogen are not excreted by kidneys
 kidneys receive ¼ of cardiac output since they are damaged
 hypoperfussion  renin release
 altered renin release = AKF
 acute tubular necrosis (ANT) – most
Oliguria in ATN
common intrarenal cause
 ischemia (post-op) of ANT is common  tubular obstruction – tubular necrosis =
 inflammation  ischemia cell swelling, cell sloughing or ischemic edema = tubular
injury, necrosis obstruction = GFR decrease
 nephrotoxicity limited at proximal tubules  back leak = normal GFR; filtrate resorption
 oliguria happens increase, ischemia is the underlying cause
 AKF with hypertension if pt is  decreased blood flow = ischemic blood
hypervolemic flow = changes in glomerular permeability
 kidney cannot resorb sodium and water = and decrease GFR. Arteriolar constriction
low urine specific gravity (dilute urine) due to renin release
 cannot excrete metabolic waste serum
BUN and creatinine high (Uremia) = Causes of AKF (1004)
platelets can’t clot blood  bleeding,  prerenal (55-70%) – anything decreases
angiodysplasia (GI vassodialtion  GI supply of blood to kidneys
bleeding), decreased cellular immunity  o hypovolemia
infection
o decreased cardiac output
 Pericarditis – due to waste accumulation
o systemic vasodilation
 less H and HCO3 production in tubules
o hypotension / hypoperfusion
 drowsiness, stupor, coma, increased RR
 intrarenal (25-40%) – damage to kidney
 Chronic Kidney Failure (CKF) – leading
o tubule / nephron damage
complication of AKF
 hyperkalemia – most sudden hazard in  acute tubular necrosis
oliguric AKF  glomerulonephritis
o normal people not conserve  rhabdomyolysis –muscle
destruction  myoglobin
potassium
o indicators of K toxicity: (protein) release  excreted
to kidneys = kidney damage
 changes in ECG
o vascular changes
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o nephrotoxins  Protein restriction until BUN and

 postrenal (5%) – obstruction between creatinine decrease
kidney and urethral meatus (any  prevent catabolism = muscle breakdown
abnormality in ureter, bladder, urethra, for protein  increased BUN
prostate)  CKF: protein 0.75 g/kg/day or 20% of
o ureteral and bladder neck caloric intake
obstruction  Protein restriction: 1 to 1.5 g/ kg ideal
body weight
Phases of AKF  AKF: protein depends on catabolism
 carbohydrate: 100g/day
 onset – initial, reversal, prevention
 sodium and potassium: restricted
 oliguric – 1 day after onset; problems:
 dietary supplements
inability to excrete fluids, regulate
 fat emulsions
electrolytes, excrete waste; most
 Primary prevention: avoid nephrotoxic
dangerous; the patient doesn’t excrete lot
drugs, label drugs, cleaners and solvents
of urine produce further damage to the
should be used in well-ventilated areas
kidney
 Secondary prevention:
 diuretic – large fluids (4-5 L/day) and
o supervise with sore throat, upper
electrolytes are lost; kidneys are not yet
healed; BUN and creatinine still raise with respiratory infection
volume raise; might think that pt is o treat bacteriuria and renal
recovering; problem is massive loss of fluid obstructive disease
 recovery (1 year) – some pt left with some o monitor urinary output of persons
renal dysfunction with major trauma, extensive burns,
massive blood loss, severe MI
Management:
Diagnosis: Deficient fluid volume / Excess
 BUN, creatinine, electrolyte levels fluid volume
 dialysis – specific gravity, osmolality, urine
sodium content  acute in ICU
 CBC, arterial blood gas, urine protein  constant monitoring of BP, ECG,
 Radio exam – determine cause of AKF pulmonary, and mental status
(postrenal failure)  mechanical ventilation
 ultrasound, CT scan, IVP, MRI, cystoscopy  hemodynamic monitoring (Swan-Ganz
– determine obstructive cause of AKF, size catheter)
of kidneys  hemodialysis or CRRT
 enlarged kidneys = hydronephrosis  emotional support
 X-ray abdomen or KUB – to determine  edema
stones  daily weigh
 renal biopsy – if cause of AKF is unknown  monitor pulmonary edema and CHF
 hypotonic solutions – for hypovolemia  central venous / arterial monitoring
 isotonic solutions + packed RBCs – for  avoid fluid overload
hypovolemia due to blood plasma loss  phosphate-binding medications prn
 loop diuretics (320 mg/day furosemide)
Diagnosis: Imbalanced nutrition: Less than
 mannitol and loop diuretics – for kidney
body requirements
failure due to nephrotoxins or ischemia
 low-dose dopamine – for hospital acquired  decrease potassium and protein intake
AKF  increase carbohydrates and fat intake
 glucocorticoids – for inflammation
 NSAIDs and ACE inhibitors – Diagnosis: Risk of Infection
contraindicated in AKF  maintain aseptic technique
 Diuretic phase  relieve pruritus
o fluid and electrolyte balance  maintain lung expansion

Diagnosis: Risk of Injury

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 walking and aerobic exercises when pt  phosphate: increased; calcium: low or

energy level increases normal
 skin care o due to simultaneous decrease in
 prevent bleeding phosphate excretion and reduce
ionized serum calcium
Gerontologic Considerations
o PTH increase serum calcium
 early signs are vague, mistaken with other  hypertension in ESRD due to increased
diseases total body water, kidney vasopressor
 acute infection may be absent release, low vasodepressor release
 do not easily tolerate treatment strategies  glucose intolerance (may occur, not
 fluid overload difficult to treat due to severe)
increased risk of CHF  high glucose – due to altered biochemical
environment by kidney failure; NOT mean
Chronic Kidney Failure (CKF) DM
 skin pigmentation (sallow / brownish)
 damage is irreversible
 uremic frost – crystals in skin due to
 some people have irreversible loss of
kidney failure and uremia
kidney function acutely
 muscular twitching, numbness in feet and
 affects all body systems
legs, pericarditis, pleuritic – disappear with
 end-stage renal disease (ESRD) - when
medications or dialysis
only 10% of kidney is functional
 pruritus
o causes:
 changes in menstrual cycle
 DM (44%)
 uremic women – low pregnancy
 hypertension (28%)
 ESRD not birth control
 glomerulonephritis (8%)
 erectile dysfunction
 others
 hypertriglyceridemia
 happens in all ages; most in 20-64 y/o
 atherosclerosis
 intact nephron hypothesis – only small
o low HDL, decrease lipolytic activity
nephrons are intact
due to uremia
 urinary output decrease through the
 Catabolism and proteinuria = negative
progress
nitrogen balance
Stages of CKF (1013)  decrease muscle mass

 decreased kidney reserve Body system manifestation in CRF (1014-

 kidney insufficiency 1015)
 kidney failure – severe symptoms occur
 ESRD – kidney atrophy
Complications:
Manifestations:
 fluid and electrolyte imbalance
 anemia – due to decrease kidney
 shock
secretion of erythropoietin, diet restrictions,
 sepsis
decreased GI iron absorption
 bleeding
 RBC lifespan shorten due to uremia
 anemia
 azotemia and acidosis
 hypertension
 impaired hydrogen and potassium
 hyperkalemia
excretion
 CHF
 fluid and sodium imbalance = abnormal
 pulmonary edema
retention and secretion of sodium and
 pericarditis
water = urine volume increased,
 atherosclerosis
decreased, normal
 peptic ulcer disease
 hyperuricemia in ESRD, uric acid no
 osteodystrophy
relationship with kidney function
 peripheral neuropathy
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 metabolic encephalopathy  increase of electrolyte (hyper-) – hydration

 peritonitis unless contraindicated (first thing to do)
 decreased salivary flow  hemodialysis – last action, if all
hyperkalemia control fail
Management:  calcium inversely proportional to
 serum creatinine level phosphate
o high creatinine only if lot of  phosphate-binding agents, calcimimetic
nephrons destroyed agent, calcium supplements, vitamin D
 urine creatinine level analogs – for calcium and phosphorus
 creatinine clearance (12-24 hrs) equal to balance
GFR  maintain normotensive, normovolemic
o < 10 ml/min = kidney impairment state
 hypocalcemia and hyerphosphatemia =
 weight and height
bone demineralization
 BUN/creatinine ratio (10:1)
o kidney failure  decrease ability of
o creatinine: changes in response to
phosphorus excretion
kidney dysfunction
o acidosis = dissolution of alkaline
o BUN: change in response to
salts in bone = calcium and
dehydration and protein breakdown
phosphorus to blood
 blood chemistry, CBC, urinalysis – not
o decrease GFR + decrease
effective in ESRD
 KUB film phosphate = increased serum
 ultrasound, CT – WITHOUT CONTRAST phosphate and decrease calcium
IN AKF for it is nephrotoxic o PTH inhibits tubular resorption of
 drugs metabolized by kidneys (insulin, phosphates
meperidine, antibiotics) are greatly reduced o Kidneys cannot activate vitamin D
in renal failure  restrict phosphorus intake (no dairy and
 monitor for drug overdose protein)
 antihypertensive drugs  phosphate binders (calcium carbonate,
 immunosuppressant – for with calcium acetate) taken with meals and
glomerulonephritis snacks – to bind phosphorus
 diuretics  sevelamer – phosphate binder NOT
 sodium bicarbonate – for metabolic elevate calcium
acidosis  phosphate binders with aluminum (used
o GFR decrease = metabolic acidosis before)  accumulation of aluminum in
– due to reduced secretion of kidney failure
ammonia or impaired bicarbonate  aluminum overload = dementia,
resorption myopathy, eosteomalacia, anemia
o pH still ok due to buffers (bone  aluminum hydroxide – aluminum bind
salts) with phosphate giving a product of
 diuretics or sodium polystyrene sulfate aluminum phosphate (antacid) – can
(potassium-binding resin) (Kayexalate) – easily be excreted  treat
for hyperkalemia hyperphosphatemia
o sorbitol – enhance potassium o treat hyperphosphatemia
excretion to bowel o antacid
o enema (30-60 mins) o treat pruritus
o hemodialysis – severe  calcium carbonate – with meals = less
 IV insulin – for severe hyperkalemia risk of hypercalcemia
(temporary decrease) o treat hypercalcemia
o glucose then insulin because o antacid
potassium goes inside the cell with  activated vitamin D – for inadequate
glucose, with the help of insulin control of serum phosphorus,
hypercalcemia, bone pain, myopathy,
rising serum PTH
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 thiazide diuretics – best for CKF because  dialysis – draining blood; for hypovolemia,
it doesn’t have effect in the calcium progressive azotemia, hyperkalemia,
 calcium and phosphorus influenced by metabolic acidosis
vitamin D o methods:
 AKD hypercalcemia  hemodialysis
 CKD hypocalcemia because kidney  peritoneal dialysis
cannot activate vitamin D = not help in GI  continuous renal replacement
calcium absorption = PTH stimulation = therapy (CRRT)
release calcium from bone = osteoporosis,
hypocalcemia Hemodialysis
 osteoporosis happens in CKD  principles
 calcium absorption in distal convoluted o diffusion
tubule is dependent on PTH; even if have
o osmosis
PTH, No calcium absorption because
o ultrafiltration – more effective than
kidney is damage
osmosis in removing excess fluid;
 hyperparathyroidism – excretion of PTH
used in hemodialysis
in response hypocalcemia
 dialyzer – area (machine) of which
Anemia – because of the decrease production of exchange of fluid, electrolytes and waste
erythropoietin in kidney products occur
 end of dialysis, high-dose heparin used at
 erythropoietin administration (SC, IV; 50 each catheter port to prevent lumina
unit/kg; 3x a week) – for anemia; thrombosis
administered during dialysis  complications: thrombosis, infection
 Darbepoetin alfa (weekly) – long-acting  before dialysis: weigh pt, vital signs,
EPO physical status, blood sample
 iron stores evaluated before EPO
 supplemental iron with EPO Means of gaining access to Patient’s
 folate (1 mg/day) and vitamin B12 (100- bloodstream
1000 mgc IV) – development of RBC DNA
Dialysis Access (1023)
 BP, hematocrit rise during EPO therapy
 blood transfusion (temporary treatment);  arteriovenous fistula (AVF)– access of
caution for fluid overload choice in hemodialysis; artery and vein are
o packed RBC (no plasma) – prevent connected = atrial blood distended in vein
fluid overload = vein wall thicken = vein matures (6-12
 destroyed blood cell increases potassium = weeks) = mature vein cannulated by
more hyperkalemia to pt dialysis needle
o transfuse during dialysis to prevent o needle inserted early = infiltration of
hyperkalemia needle
 blood set – have filter to strain the blood o Patient NOT for fistula but for
transfused to pt arteriovenous graft
 venous set – no filter  vascular disease
 diabetes
GI disturbance
 long-term hypertension
 Uremia = anorexia, nausea, vomiting  advanced age
 Urea breakdown to ammonia – mucosal o never get BP at arm with fistula, if
irritant both arms have, get BP at the arm
 vinegar mouthwash – neutralize with nonfunctioning fistula
ammonia  arteriovenous graft (AVG)– attaching
 Halitosis – ammonia smell in breath synthetic tube to artery  tunneling to soft
 antacids (q2-4 hrs) – decrease GI tissue  vein
irritation o 3 weeks ready for cannulation
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o vein outflow may thicken  Continuous renal replacement therapy (CRRT)

thrombosis – 8-24 hrs; blood filtering with no machine,
 catheterization of femoral, internal depends on the BP(mean atrial 60 mmHg) of pt;
jugular, subclavian vein, inferior vena allows same mechanism kidney resorption and
cava(rare) - TEMPORARY filtration
o internal jugular vein (3 weeks) –
o recommended for too
vessel of choice
hemodynamically unstable to
o for short term
tolerate hemodialysis and peritoneal
o indicated for AKF or 3-week post-op
dialysis (advanced cardiac disease,
after placement of AVG or AVF
metabolic acidosis, abdominal
o large (12 F), 2 lumina
wounds, cerebral edema, sepsis)
o femoral vein (1 week) o composed of
o tunneled, cuffed hemodialysis  outflow and return tubing
catheters (> 3 weeks)– for longer  hemofiltrate collection
use  ultrafiltrate collection
Peritoneal Dialysis o convection – depends on BP
o diffusion – depends on pressure
 not use dialyzer; peritoneum is the gradient
membrane that filters the blood
 does not use blood vessels; water to Variations of CRRT:
peritoneum collects waste and go back out
 continuous venovenous hemofiltration
 not very good dialysis because blood is not
(CVVH) – most favored, no access to
directly cleaned
arteries; there is a machine
 allow pt control; done at hospital or home;
continuous for 36 hrs
 continuous arteriovenous
 temporary – sterile catheter
hemofiltration (CAVH)– removes large
 permanent – Tenckhoff peritoneal catheter
amount of plasma water and solutes (400-
– only remove when malfunction or another
800 ml/hr); for mild to moderate azotemia,
treatment method (transplant)
electrolyte disturbances; less favorable
 void before catheter insertion
because it relies on the pt BP thus less
 physician cleans abdomen  anesthesia
flow rate; need arterial access; increase
to 5 cm above abdomen  insert catheter
risk of bleeding, distal atheroembolic or
 dressing around protruding catheter
artery occlusive complications
 Continuous Ambulatory peritoneal
Dialysis (CAPD) – self-care; inexpensive
 continuous venovenous hemodialysis
 Continuous Cyclic peritoneal Dialysis
(CVVHD) – most recent; NO access to
(CCPD) – self- care; with a cycler, 6-8 hrs
arteries; sterile dialysate flows opposite of
dialysis (while sleeping), with alarms
blood to facilitate diffusion of solutes form
Advantages blood to ultrafiltrate

 provides a ready state of blood chemistry  continuous arteriovenous hemodialysis

values (CAVHD) – sort of combination of CAVH
 easily taught and CVVHD
 pt self-dialysis everywhere without
machine  slow continuous ultrafiltration (SCUF) –
 few dietary restrictions; high-protein diet slowly removing small plasma water and
 pt more control on daily life solutes (150-300 ml/hr); for severe CHF
 can be used by pt who are not responding to diuretics; NOT FOR
hemodynamically unstable azotemia and electrolyte abnormalities for
only small amounts are removed
Guidelines for safe peritoneal dialysis (1025)
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 to monitor ESRD pt received sufficient nausea and vomiting, cloudy out-flow of

amount of hemodialysis, delivered dose solutions
should be measured and monitored
routinely
 Kinetic modelling – tool used to measure Diagnosis: Risk of Injury
how much dialysis pt needs
 adequate protein intake (no much/less)  avoid extensive tissue damage =
 primary prevention: UTI and obstruction, potassium to blood of CKF person
and hypertension – asymptomatic causes  control blood loss
of kidney failure; general health promotion;  soft toothbrush
yearly PA; urinalysis; blood glucose control  report melena (black, tarry stool)
 Secondary prevention: health immediately
maintenance, adequately treat medical  avoid aspirin – naturally excreted by
condition kidney; rapidly build to toxins; increase
bleeding time
Drugs that are prescribed differently for  avoid NSAIDs – increase risk of GI
dialysis patients (1018) bleeding; increased bleeding time
Drugs requiring caution in patients with  osmotically active particles and fluid =
kidney impairment (1018) changes in brain cells
 fluid accumulation and hypertension =
Treatment Goals for patient with kidney failure visual changes
(1019)
Diagnosis: Ineffective Coping

 psychosocial care
Diagnosis: Excess fluid volume  encourage compliance to regimen
 provide further information
 monitor input and output
 help patient regain control over life
 adequate fluid and sodium intake
 include family
 avoid salt substitutes since these contain
 vocational counseling
large potassium
 assure patients and families that death
 hemodialysis (3-5 hrs)
associated with complications of kidney
Diagnosis: Imbalanced nutrition: Less than failure (hyperkalemia) is generally quiet,
body requirements peaceful, without pain and discomfort

 GI tract ulcerated, bland foods to increase Gerontologic Considerations:

ingestion
 GFR decrease 10% every 10 years after
 iron supplement side effect: nausea and
50 y/o
constipation
 kidney failure related to atherosclerosis
o take iron with full stomach
o add laxative Kidney Transplant
 avoid simultaneous intake of iron and
 oldest and most common type of transplant
phosphate binders = impede oral iron
 twin is the best donor
absorption
 parents and children
Diagnosis: Risk of Infection  siblings – not so best than parents and
children
 skin care  person with transplant will be lifetime
 avoid tissue breakdown, edema immunosuppression therapy = increased
 pt avoid people with infection risk for infection
 avoid contamination of dialysis tubing
 culture dialysate fluid Primary sources of organs
 signs of peritonitis: elevated
 Living donors
temperature, chills, abdominal pain,
o advantages
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 improve pt and graft survival

rates
 immediate availability Manifestations of renal transplant rejection
 schedule surgery when donor  fever > 37.7 ; masked by steroid therapy
is in best possible medical  pain of grafted kidney
condition  sudden weight gain (2-3 lbs in 1 day)
 immediate functioning of  edema
organ because there is  hypertension
minimal preservation time  general malaise
 Non-heart beating donors  elevated serum creatinine and BUN
o cardiopulmonary dead BUT NOT  decreased creatinine clearance
brain dead  ultrasound or biopsy evidence of rejection
o procurement: after heart stops
beating
 deceased donors
Hypertension
o evaluated well
 complication of kidney failure that is rarely
Contraindications for transplant cured by kidney transplant
 disseminated malignancies  associated with antirejection drugs
 chronic infections (except Hepa B and C) (prednisone, cyclosporine, tracrolimus)
 ongoing psychosocial problems Infection
(noncompliance to regimens and chemical
dependency)  due to immunosuppression
 Organisms responsible for infections in
Complications transplant recipients (1034): bacterial,
Transplant failure viral, fungal, parasitic infections

 rejection – major cause of transplant Malignancies

failure  cancer high risk due to altered immune
Types of rejection system

 Hypercute – within 48 hours after Management

transplant  ABO compatibility
o accelerated rejection - special type  blood cross match
of hypercute rejection (3-5 days);  CBC
reversed if early detected  renal and liver panel
 PTT and PT
 Acute – 1 week to 3 months after  viral titers
transplant; macrophage- antigen  creatinine clearance
interaction; treatment: increase steroid,  HIV, CMV, Epstein-Barr virus –
monoclonal antibodies, polyclonal contraindicated in kidney transplant
antibodies (antithymocyte globulin,  immunosuppressive drugs
antilymphocyte globulin)  diet same with ESRD
 continue control of sodium and calorie
 Chronic – 3 months or longer; slow content after surgery to manage side
progressive loss of graft function; major effects of high-dose steroid administered
unresolved problem in transplantation; less for immunosuppression
responsive to immunosuppressive  continue dialysis up to time of transplant
therapies  deceased donor longer kidney function
after transplant, hence dialysis will be
 graft-versus-host disease – special type continued for short time
of rejection occurs in recipients of allogenic  transplant (3 hrs)
bone marrow transplant
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 transplanted kidney placed  medication teaching – first priority from

extraperitoneally, in iliac fossa hospital to home
 pt kidney is not removed,UNLESS infected
or causing hypertension, - to maintain Common Medications preventing organ
EPO, BP control, prostaglandin synthesis rejection (1036-1037)
and metabolism Patient family teaching (1038)
Preoperative

 emotional and physical preparations

 inform 20% chance kidney will not function
immediately, dialysis for few weeks
 rationale of immunosuppression
 ECG, chest x-ray, lab studies – to ensure
optimal status
 dialysis
 wrap extremity containing vascular access
in Kerlix and labels it “dialysis access”
 avoid using affected extremity for BP
measurement, phlebotomy, of IV insertion

Postoperative

Care of the Donor

 living donor, similar to nephrectomy

 analgesia
 promote ambulation
 prevent pulmonary complications
 discharge 3-5 days
 return to work in 1 month

Care of the Recipient

 maintain fluid and electrolyte balance –

priority
 diuresis after blood supply to kidney is
reestablished, due to kidneys ability to
filter BUN, IVF abundance during
transplant, renal tubular dysfunction
 initially high urine output (1L/hr)
 monitor urinary output hourly
 IVF for 1st 12-24 hrs
 avoid dehydration
 monitor hypokalemia
 initial dialysis, stop when urinary output
increase and normal BUN
 decrease urine volume due to dehydration,
rejection, vascular thrombosis, obstruction
 blood clot in Foley catheter – cause of
early obstruction
 allow bladder anastomosis to heal
 careful sterile catheter irrigation to dislodge
occluding clots
 ultrasound within 24 hours
 hydronephrosis = obstruction