CHRONIC KIDNEY DISEASE
a.k.a CHRONIC RENAL FAILURE
- CKD is an umbrella term that describes kidney
damage / ↓ in GFR for 3 or more mos.
o GFR: bld test that checks how well
kidneys are working
estimates how much bld passes thru
glomeruli each minute
kidneys have glomeruli
-
-
filters & helps remove
wastes and excess fluids
from bld
o obtain bld sample
 let client fast for 8 hrs
associated w/ ↓ quality of life, ↑ health care
expenditures, premature death
significant ↓ in renal fx; IRREVERSIBLE
o (AKD – reversible)
Untreated CKD = END-STAGE RENAL DSE (ESRD)
- necessitate kidney replacement therapy
o dialysis
o kidney transplantation (last resort)
- STAGE 1 to STAGE 5
PATHOPHYSIOLOGY
4 BASIC PROCESSES: FORMATION OF URINE
1. FILTRATION – mass movement of water and
solutes from plasma to the renal tubule that
occurs in the renal corpuscle.
o 180 liters of fluid are filtered by the
kidneys every day
o entire plasma volume (about 3 liters) is
filtered 60 times a day
o primarily driven by hydraulic pressure
(blood pressure) in the capillaries of the
glomerulus.
- kidneys filter much more fluid than the amount of
urine that is actually excreted (about 1.5 liters per
day). This is essential for the kidneys to rapidly remove
waste and toxins from the plasma efficiently.
2. REABSORPTION - movement of water and
solutes from the tubule back into the plasma
(70% is reabsorbed)
Reabsorption of water and specific solutes occurs
to varying degrees over the entire length of the
renal tubule.
o many important solutes (glucose, amino
acids, bicarbonate) are actively
transported out of the proximal tubule
such that their concentrations are
normally extremely low in the remaining
fluid.
REGULATED REABSORPTION: hormones
control the rate of transport of sodium and
water depending on systemic conditions,
takes place in the distal tubule and collecting
duct.
3. SECRETION - Even after filtration has occured,
the tubules continue to secrete additional
substances into the tubular fluid. This enhances
the kidney's ability to eliminate certain wastes
and toxins (urea & crea). It is also essential to
regulation of plasma potassium concentrations
and pH.
4. EXCRETION - end result of the above three
processes. last product is urine
NEPHRONS
kidneys have millions of nephrons
nephrons have glomerulus
- glomerulus: filters fluid & ions (electrolytes,
bicarbs), waste products (urea – BUN, crea)
o UREA – by product of protein breakdown
from liver
o CREATININE – waste product from
breakdown of muscles
o thus, we have your GFR
Stage 1: (+) proteinuria (seen in U/A)
Stage 2: mild loss of renal fx w/ proteinuria
Stage 3: mild to severe loss of renal fx
first 3 stages = asymptomatic
however, s/sx will become more
evident as dse progresses
Stage 4: severe loss of renal fx
Stage 5: ESRD
-
-
-
ASSESSMENT
Subjective cues
- Nausea
- Loss of
appetite
- fatigue &
weakness
- sleep problems
- anxiety
- anorexia
- paresthesia
Objective cues
- ↑ serum crea levels
Glomerulus not functioning well
= waste products (toxins, crea)
are not being filtered and stays
in the body
- edema
water is retained, hypervolemia,
fluid overload
- ↓ UO
Malfunction of glomeruli =
water is not excreted
Oliguria: <400 ml/day
Anuria: <100 mL/day
- High BP
Due to hypervolemia, pressure
↑
- abnormalities w/ Ca & P, & Mg
↓ Ca due to ↓ Vit. D
- Anemia
Kidney malfunctions = low
erythropoietin (EPO – stimulates
the production of RBC in bone
marrow)
- Metabolic acidosis
Commonly found in px w/ CKD
Causes: impaired ammonia
excretion, reduced tubular
bicarb reabsorption, insufficient
renal bicarb production in
relation to the amount of
acids synthesised by the body
and ingested with food.
Pruritus – Uremic pruritus
Aka KIDNEY-ASSOC. PRURITUS
Due to elevated BUN
Itching due to urea crystals on
the skin --- white frost (uremic
frost) in the skin
Also caused by Ca phosphate
crystals (accumulated in skin)
Uremic – excessive urea in bld
Occurs when both kidneys stop
working
Common problem to px w/ ESRD
check K & Phosphate & Mg (↑)
Ca is depleted
due to phosphate
bones become weak & brittle
(+) proteinuria ---- hematuria
(albumin – oncotic pressure)
EPO = helps created RBC & bone marrow
RENIN – increases BP
- since there is less water, renin is stimulated to
increase BP (HPN)
Vit. D malabsorption: Hypocalcemia
MEDICAL MANAGEMENT
SPECIAL NOTATION
1. The mgt of px w/ CKD includes tx of the
underlying causes
2. Nutritional therapy
3. Renal replacement therapy (dialysis, kidney
transplant)
4. Measures to treat hyperlipidemia
5. Measures to lower K
Laboratory/Diagnostic Examination
Hx & PE
- Identification of reversible kidney dse
- Renal UTZ
- Renal scan
- CT scan
- renal biopsy
- BUN, serum creatinine, creatinine clearance
levels – bld
often a blood sample may also be taken to
measure crea, serum protein levels, & BUN,
esp. when 24-hour urine has been ordered
-
-
Serum electrolytes
Lipid profile
Protein-to-creatinine ratio i1st morning
voided specimen
Urine is collected in a container
The collection process generally begins first
thing in the morning
For a 24-hour urine collection, the process
generally begins by discarding the first
morning void and then collecting all of the
urine for the remaining 24-hour period. --send to lab, refrigerated, no preservatives
in the container
Occasionally, a split 24-hour sample w/ a
night collection, 11-7, separated form the
collection of morning (7-11) may be used
Assoc. w/ 24-hour total protein excretion
Urinalysis (proteinuria)
Hematocrit & hemoglobin levels
Underlying causes:
- high BP
- DM
MEDICATIONS:
- Erythropoietin therapy
o so anemia would not occur
o expensive
o also used in cancer px esp. if hemoglobin
is ↓
- Ca supplementation, phosphate binders (Ca
carbonate)
o used for tx of hyperphosphatemia
o ex. Ca acetate
- Antihypertensive therapy
o ACE (-pril) or ARBs (-sartan)
o slows the process of renal dse in px. w/
diabetes by interfering w. reninangiotensin system;
o reduce intraglomerular pressure by
inhibiting angiotensin II ̶ mediated
efferent arteriolar vasoconstriction.
-
Adjustment of drug dosages to degree of renal
fx
IV FLUIDS:
- correction of extracellular fluid volume overload
/ deficit
During ESRD: px will experience
- hypovolemia
- anemia
- electrolyte imbalance
- waste product retention
- low UO
focus interventions on s/sx of hyperkalemia: muscle
weakness, palpitations, urine abnormalities,
dysrhythmias
1.
2.
3.
4.
5.
6.
7.
8.
NURSING INTERVENTIONS
Assess fluid status & identify potential sources
of imbalance
Nutritional intake: Implement a dietary program
to ensure proper nutritional intake w/in limits of
the tx regimen
Independence: Promote positive self feelings by
encouraging increased self-care & greater
independence
Protein: Promote intake of high-biologic-value
protein foods: eggs, dairy products, meats
a. minimize protein, needs some to prevent
muscle wasting but not as madami kasi
may sir ana sa kidney
Medication: Alter sched of meds so that they are
not given immediately before meals
Rest: Encourage alternating activity w/ rest
S/SX of electrolyte imbalance, esp. high K
a. N: 3.5 – 5 mEq/L
b. hyperkalemia: Tall, tinted T wave,
widened QRS, long PR interval
c. restrict K-rich foods: potatoes,
avocadoes, strawberries
d. KAYEXALATE as ordered (orally / rectally)
to decrease K
Alternative ways of reducing thirst, such that
sucking on ice cubes, lemon, hard candy
Report any of the following:
- Weight gain >4 lb (2kg)
- Increasing BP
- Shortness of breath (due to fluid accumulation in
lungs)
- Edema
- Increasing fatigue / weakness
- Confusion / lethargy
o
due to accumulation of toxic wastes
(ammonia, urea, crea)
o promote safety
Need changes, living w/ a chronic illness, and decisions
about type of dialysis or transplantation
CAUSES
-
DM
o
-
-
uncontrolled hyperlgycemia casues
glucose to stick to artery walls --damage to blood supply to kidneys
HPN
o
high pressure on artery walls to kidneys -- less blood supply to nephrons --- less
O2
others: Acute kidney injury, polycystic kidney
dse, infection, nephrotoxic drugs (NSAIDS –
paracetamol, acetaminophen, abx –
aminoglycosides, chemotherapeutic drugs,
contrast dyes)
TX
1. control BP and glucose
a. meds (ACE inhibitors, ARBs)
2. monitor GFR and BP regularly
3. Dialysis
4. Kidney transplant
NSG MGT:
Uremia – increased waste in bld (esp. BUN)
pH is usually less that 7.35 = metabolic acidosis
- kussmaul’s breathing (deep rapid breathing)
- check lung sounds: crackles – pulmonary edema
Anemia
- pale, tired, shortness of breath, confusion
- iron supplement
- EPO SC
- blood transfu
Low UO
- monitor I&O
- daily weight
Some doctors restrict fluid & low Na diet and CHON