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N2100 renal lecture spring 2014 voice over
1.
2.
Homeostasis: acidbase, BP
Excrete urea, toxins,
water
Produce
Erythropoetin
(hormone that
stimulates RBC
production)
Produce Renin (reninangiotensin system
regulates BP)
Convert Vitamin D
into useable form
Think about the
nursing implications
of each!
3. Two thirds of all chronic
kidney disease is
related to other
chronic illnesses.
Diabetes (43%)
Hypertension (23%)
1)
Why and how do each
of these conditions
damage the kidney?
2) What can be done to
prevent or manage
these underlying
conditions?
4.
Nephrotoxic Drugs:
-Aminoglycosides: Ex. gentamycin,
tobramycin, amikacin, neomycin
-Amphotericin B
-Vancomycin
Chronic use of NSAIDS (especially cardiac
patients and patients with cirrhosis)
Patients with Creat > 2.0 who receive
radiopaque contrast dye
5.
Glomerular filtration rate (GFR) is a test used to
check how well the kidneys are working.
Specifically, it estimates how much blood passes
through the tiny filters in the kidneys, called
glomeruli, each minute.
The GFR test measures how well your kidneys are
filtering a waste called creatinine, which is
produced by the muscles.
When the kidneys aren't working well, creatinine
builds up in the blood.
Normal results range from 90 - 120
mL/min/1.73 m2
6.
Lab values – Measuring kidney function
Serum Creatinine
◦ Creatinine is a product of creatine metabolism from
muscle dependent of muscle mass
◦ Creatinine is eliminated primarily by glomerular
filtration (GFR). As GFR , serum creatinine .
◦ Doubling of creatinine suggests a 50% drop in GFR
(estimated).
8.
Characteristic of glomerular injury from
diabetets, infections, renal toxins, immune
disorders.
Excretion of 3.5 g or more of protein in the
urine per day.
Loss of serum proteins and sodium retention
9.
Glomerular capillaries are damaged Leads
to increased permeability to proteins
Decreased osmotic pressure leads to
proteinuria, hypoalbuminemia, and edema.
MAY LEAD TO RENAL FAILURE…..PREVENTION
OF CAUSES IS CRITICAL!!!
10.
Progressive loss of renal function
Associated with systemic disease such as
hypertension, diabetes mellitus, intrinsic
kidney disease.
Diabetes (40%), Hypertension (25%), and
Glomerulonephritis (10%)
Kidney damage as GFR less than 60
ml/min/1.73m2 for 3 months or more.
12. Management and goals:
Restrict dietary protein
Intensive insulin therapy if needed
Optimize BP control (tight regulation)
◦ Goal for CKD – BP 130/85
◦ Goal for Proteinuria – BP 125/75
Manage hyperlipidemia
◦ Goal of LDL - <100
13. Stage 1: Kidney damage but normal GFR
(>90), “At risk”
Stage 2: Kidney damage with mild decrease in
GFR (60-89), “Chronic Renal Insufficiency” or
CRI
Stage 3: Moderate decrease in GFR (30-59),
CRI or CRF (“Chronic Renal Failure”)
Stage 4: Severe decrease in GFR (15-29), CHF
Stage 5: Kidney Failure, GFR < 15, more than
90% of nephrons have lost function, ESRD
“End Stage Renal Disease”, dialysis or
transplant required to survive.
14. Rapid loss of renal function, progressive azotemia
(accumulation of nitrogenous waste products such
as BUN) and increasing serum creatinine.
Uremia (literally “urine in the blood”) is a condition in which renal
function declines to the point that symptoms develop in multiple
body systems.
Often associated with Oliguria (output less than 400 ml/day)
In 30% of cases there is a normal or increased urinary output
Oliguric patients have a higher mortality rate
Develops over hours or days with progressive elevation of BUN,
creatinine, and K+.
ARF follows severe, prolonged hypotension or hypovolemia or
exposure to a nephrotoxic agent, also can be due to obstruction of
urine outflow.
THINK PREVENTION!!!
16. 1. INITIATING PHASE
Begins at time of insult until S&S seen (hours to
days)
2. OLIGURIC or ANURIC PHASE
Oliguria caused by GFR decrease
Begins 1-7 days after insult depending on cause
Usually lasts usually 10-14 days (may last up to
8 weeks)
Longer the phase, poorer prognosis of renal
recovery
Manifestations are changes in UOP, fluid &
electrolyte balances, & uremia
in serum levels of urea, creatinine, uric acid,
K+ & Mg
17. Acute Renal Failure Stages
3. DIURETIC PHASE
-Gradual increase of UOP can reach 1-2 (or more) L
per day. Nephrons are still not fully functional
-Caused by osmotic diuresis and inability of tubules
to concentrate.
-Recovered ability to excrete wastes, but not
concentrate.
-Monitor for hypokalemia, hyponatremia &
dehydration
-Hypovolemia and hypotension can occur
Lasts 1-3 weeks
-Acid-base, electrolyte and waste product levels
begin to normalize.
18. 4. RECOVERY PHASE
Begins when GFR increases allowing
BUN and creatinine to reach a
plateau and decrease
May still have glycosuria and
decreased ability to concentrate
urine
Major improvements first 1-2
weeks but may take 12 months to
stabilize.
19. May excrete as much as 2L/day
Urine dilute and iso-osmolar
Hypertension and tachypnea and
symptoms of fluid overload are usually
seen
Can see orthostatic hypotension and
dry mucous membranes
Associated with less morbidity and
mortality
20.
Urinalysis
hemoglobin + in
pylonephritis, protein + in
diabetic nephropathy,
glomerulonephritis, WBC
(pyuria) + in infection
•Specific gravity of urine
1.001-1.035
•Sodium levels
-serum: 135-145 mmol/L
-urine (usually 24 hour
collection): 27-287mmol/d
Hematocrit
•Serum Creatinine
.6-1.2 mg/dL
•BUN
8-21, 10-31 if older than 90
•Urine Creatinine & Creatinine
Clearance: Determines extent of
nephron damage (decreased when
50% of nephrons lost)
21. -Treat cause
-Maintain fluid and electrolyte balance
-Prevent infection
-Monitor for arrhythmias (related to K+and
other electrolyte imbalances)
-Maintain nutritional status
Adequate protein (or restriction) depending on
catabolism
Restriction of K+, phosphate, magnesium, and/or
sodium
Dietary fat 30-40% total calories
If necessary, use TPN and/or Ca supplements,
phosphate-binders
22.
Protein: limit protein pre-dialysis (this slows
progression of renal failure). During dialysis,
protein is lost so patient will require more
protein. Concentrate on high value protein
(dairy and meat).
Potassium: limit due to hyperkalemia, especially
if on dialysis.
Salt: restrict use of salt due to renal damage
from ongoing hypertension. (canned goods,
processed foods, “fast foods,”, table salt). Make
sure salt substitute does not contain potassium.
Phosphorus: elevated in patients with renal
disease. (dairy products, yogurt, eggs)
Fluid restriction: carefully follow restrictions
23. ◦
◦
◦
◦
◦
◦
◦
◦
Fluid and electrolyte imbalance
Susceptibility to secondary infections
Anemia
Platelet dysfunction
Gastrointestinal (GI) complications
Uremic encephalopathy
Impaired wound healing
Alteration in urine output
Consider the role of the nurse in the prevention
and management of each of these!
24.
Fluid volume deficit r/t
(name cause or causes)
Fluid volume excess r/t
inability of kidneys to
produce urine
Risk for infection
Disturbed thought
processes
Fatigue
Anxiety
25. Monitor intake & output
Assess vital signs
Daily weights
Evaluate skin turgor,
mucous membranes
◦ Monitor dialysis site
◦ Monitor lab values (UA,
◦
◦
◦
◦
Specific gravity, Sodium
levels, BUN, & Serum
creatinine*)
(*best indicator of renal
function, not altered by other
temporary factors)
◦ Monitor urine (amount,
color, specific gravity,
glucose, protein,
sediment, blood)
◦ Monitor for pain,
bleeding, and neuro
status/seizures
◦ Monitor for murmurs &
dysrhythmias
◦ Prevent infection
◦ Frequent oral care
◦ Monitor lung sounds,
pulmonary toilet
◦ Restrict fluids
◦ Education!
26. • The last stage of kidney failure where GFR is <15. Dialysis or
transplantation required to survive.
•80% of GFR may be lost with few overt changes in body.
•Can survive without dialysis until almost 90% of nephrons are
lost
•Remaining nephrons hypertrophy and compensate.
•When creatinine clearance <15 ml/min (normal 85-135) need
transplant or dialysis to survive.
•ESRD patients are eligible for Medicare Disability.
27. Initially, polyuria (mostly
at night) due to
inability to concentrate
urine
Later, anuria=<
40ml/day
BUN rises (causing nausea,
vomiting, lethargy, fatigue
impaired thought process,
headaches.) Serum
creatinine rises, less so for
older person
Altered carbohydrate
metabolism due to insulin
resistance. Insulin is also
dependent on kidneys for
excretion
Elevated triglycerides:
hyperinsulinemia stimulates
hepatic production of
triglycerides.
Atherosclerotic changes
may worsen
28.
Hyperkalemia can
cause fatal arrhythmias
if >7.0-8.0
Metabolic acidosis
Anemia
Worsening
hypertension
Anorexia, nausea,
vomiting
Uremic breath
Neurologic changes
Renal osteodystrophy
r/t inability to produce
vitamin D so calcium is
released from the
bones
Skin changes: yellow,
dry, pruritis, uremic
frost (rare)
Petechiae and bruising
29. Preserve renal function
Delay need for dialysis or transplant
Alleviate symptoms
Improve body chemistry values
Provide optimal quality of life
Discuss living will and advanced directives
30. Remove end products of protein
metabolism from blood
Maintain a safe concentration of serum
electrolytes
Correct acidosis and replenish bicarbonate
levels
Remove excess fluid from the blood
31.
32. DIALYSIS
CONCEPTS
ULTRAFILTRATION:
Removal of fluid
from blood using
either osmotic or
hydrostatic pressure
DIFFUSION:
Passage of particles
(ions) from an area
of high
concentration to
low concentration.
SEMIPERMEABLE
MEMBRANE has pores
33.
Semi-permeable membrane is the
membrane lining the abdominal cavity
15% of dialysis in the USA, more outside
US
CAPD (Continuous Ambulatory Dialysis)
doesn’t require electricity, drains in and
out with gravity
Advantages: may be done at home, fewer
dietary restrictions, less cardiac stress,
better for diabetic patients, good for
patients with poor vascular access
Disadvantages: peritonitis, requires
surgery to place Tenckhoff catheter,
protein loss, discomfort r/t fluids in
abdomen
34.
35.
Artificial membrane is inside a dialyzer
Best for emergencies (rapid removal of
fluids, urea and creatinine) and CRRT
(Continuous Renal Replacement Therapy)
Life schedule= 3-4 hours, 3x per week
Advantages: effective K+ and triglyceride
removal, less protein loss
Disadvantages: vascular access problems,
extensive equipment needed, hypotension,
dietary and fluid restrictions, decreased
independence
37. -Only skilled dialysis nurses can access a
graft or shunt.
-Although you NEVER USE a fistula or
graft, you must ALWAYS ASSESS them:
FEEL for a THRILL (vibration) LISTEN for a
BRUIT (whooshing sound) In general, do
not cover. Protect from infection.
-If a SQ or IJ catheter has a dressing, use
sterile technique when changing
dressing.
-No BPs, IVs, or labs in arm with access
-Teach family to observe for s/s of
infection
38.
Hypotension
Sepsis: R/T infected access
Disequilibrium Syndrome: due to rapid
changes in blood of urea, sodium, causing
high osmotic gradient in brain resulting in
shift of fluid into brain causing cerebral
edema. (Slow or stop dialysis, infuse saline,
albumin or mannitol to draw fluid from
brain cells back into systemic circulation.)
Blood Loss related to accidental dislocation
of needle or separation of external shunt.
39.
Monitor weight, peripheral edema, BP,
AP, heart sounds
Check access, bruit and thrill
Temperature (fever could indicate infection)
Skin condition
Hold BP meds & meds that can be dialyzed
off (example: water-soluble vitamin
supplements, etc.) Pharmacist can provide
guidance, some drug books have an
appendix listing dialysis safe medications, if
any questions, consult MD
40.
41.
54,000 are on a waiting list
14,000 transplants/year
Waiting time for cadaver transplant: 18
mos. to 4 yrs.
Need immunosuppressive therapy for
life. Common oral medications include:
Steroid (prednisone), Mycophenolate
(MMF, Cellcept), Cyclosporine (CSA),
tacrolimus (Prograf)
Monitor for rejection & infection
Monitor urine output closely. Minimum
post transplant should be 30ml/hr
(720ml/day)
42.
Nursing Alerts
Gerontological Considerations – throughout
chapter
Glomerulonephritis
Nephrotic Syndrome/Nephrosclerosis
Causes, Phases, & Prevention Acute Renal
Failure –Chronic Kidney Disease – clinical
manifestations –Dialysis
Nursing Consideration for the patient with a
kidney transplant