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AKI and CKD

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Renal Notes
Exam #3
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Func ons of the Kidneys – “A WET BED”
o A – acid base balance
o W – water removal and regula on
o E – erythropoiesis
o T – toxin removal
o B – BP control
o E – electrolyte balance
o D – Vitamin D metabolism
Diagnos c Tests
o BUN (10-20 mg/dL)
o Serum Crea nine level (0.5- 1.2 mg/dL)
o
▪
Biggest indicator of kidney disfunc on
▪
There is no other pathological reason for the crea nine to be elevated other
than kidney dysfunc on
Urinalysis
▪
If the pt is having kidney issues they will have protein and glucose in their urine
●
●
▪
o
o
o
Closer look at the renal pelvis
CT and MRI
▪
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Xray of the kidneys, ureters, bladder
Intravenous Pyelography
▪
o
Specific gravity is checked as well
● This will be higher in renal failure pts
Urine Culture and Sensi vity
Crea nine Clearance Test (24 hour urine)
KUB
▪
o
Protein are large molecules and if the kidneys are dumping protein it
indicates that there is damage
A lot of pts who are in renal failure are diabe c – renal threshold is 220
o But there are some pts who are not diabe c and their kidneys
are not working properly so the renal threshold is lower – 100
Make sure that they are not ge ng IV contrast with either of these
o Renal Angiography
Diabe c Nephropathy
o Long-term complica on of diabetes mellitus
o
Most common cause of renal failure
▪
o
o
Atherosclero c changes decrease blood to kidney
Need smaller doses of insulin as progresses
▪
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most pa ents on dialysis are diabe c
r/t kidneys unable to breakdown insulin and excrete it
o Chronic renal failure develops
Acute Kidney Injury
o Old name: Acute renal failure
o Sudden loss of kidney func on
▪
o
Waste products accumulate
▪
o
which leads to azotemia
Oliguria
▪
o
o
rapid onset of hours to days
w/output less than 20 ml/hr (norm 30ml/hr) or 400 ml/day
May recover-usually reversible
Pathophysiology
▪
Reduced blood flow to the kidney from hypovolemia, hypotension, reduced
cardiac output & heart failure, obstruc on of the kidney or lower urinary tract
from a tumor or bilateral obstruc on of the renal arteries or veins
▪
o
Leads to decreased GFR, increased BUN & Crea nine and oliguria
Causes
▪
3 categories lead to acute renal failure
●
Prerenal Failure (before the kidneys) MAP<60
o **Remember – this is a problem that is occurring BEFORE it
even gets to the kidneys
▪
A low MAP (decreased blood supply)
Nephrons in the kidneys are not ge ng good
perfusion and this causes the GFR to drop
Decreased blood supply to kidneys-low BP in renal artery
●
o
▪
when nephrons receive inadequate blood supply they
are unable to make urine and waste is not adequately
removed
o
Causes
▪
Hypovolemia
▪
Decreased cardiac output (Shock & Heart failure)
●
▪
Decreased peripheral resistance - vasodila on
▪
Renal vascular obstruc on
Intra-renal Failure (w/in the kidneys)
o Damage to nephrons from prolonged renal ischemia
▪
Myoglobinuria
●
▪
o
Transfusion reac ons
Nephrotoxic Injury (more common cause of intra-renal failure)
▪
An bio cs
●
●
o
o
o
Vancomycin
Gentamicin
▪
NSAIDS
▪
Contrast dye
Infec ous Processes
▪
Acute pyelonephri s
▪
Acute glomerulonephri s
Autoimmune disorders
▪
●
Can lead to rhabdomyolysis
Lupus
Post Renal Failure (a er the kidneys)
o Obstruc on of urinary collec ng system
o Blocks flow or urine from body (Bet/kidney & Urethral meatus)
▪
Urethral obstruc on
▪
Prosta c hypertension
▪
Bladder Cancer
▪
Ureteral obstruc on
▪
Calculi
▪
Abdominal tumor
▪
Spinal Cord disease
S/S of AKI
▪
Sudden decrease in urine output (<400 ml in 24 hours)
▪
Anorexia, N/V
o
▪
Sudden weight gain
▪
Decrease in LOC
▪
Halitosis
▪
Low BP, Tachycardiac, tachypneic
Four Phases of AKI
▪ Ini a on (Onset) Phase
● Starts with ini al insult and ends with oliguria
● Spans several hours to 2 days
● Renal func on begins to deteriorate but renal damage not yet
established
● Poten ally reversible during this phase
▪ Oliguric/Anuric Phase
● Increase in serum concentra on of normally excreted products
o urea, crea nine, uric acid, K+, Mg
▪
o
These will be high in the blood b/c they are normally
excreted
● Urine volume lowest
● Lasts 1-3 weeks
● Longer remains in this phase, the greater amount of renal damage
● Uremia and hyperkalemia common during this phase
o Watch for dysrhythmias
▪ Diure c Phase
● Renal ssue recovers and repairs itself
● Gradual increase in urine output
o GFR is recovering
● May lose large amounts of fluid due to salt and water accumula on
leading to dehydra on
▪ Recovery Phase (Convalescent )
● May take up to 3-12 months
● Laboratory values return to pt’s normal level
Medical Management
▪
Objec ves
●
●
▪
Restore normal chemical balance
Prevent complica ons un l repair of renal ssue and restora on of renal
func on occurs
Treat cause
●
●
Prerenal
o op mizing renal perfusion
Postrenal
●
▪
o remove the obstruc on
Intrarenal
o remove the cause
o treat infec on
Treatment needs to be suppor ve
●
Maintenance of Fluid Balance
o Fluid excesses
▪
o
Adequate renal blood flow
▪
o
IV fluids or transfusions of blood products
o Dopamine (low doses)
Dietary Management
▪ Adequate energy, protein, and micronutrients to maintain homeostasis
▪
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Diure cs to promote diuresis
Caloric requirements met with high carbohydrate meals because carbohydrates
have a protein sparing effect
▪ Restrict food and fluids with sodium, potassium and phosphorus
Chronic Kidney Disease (CKD)
o Defini on
▪
o
o
o
o
more months
Untreated CKD can result in end stage renal disease
Stages based on GFR-normal is 125 ml/min
Also called end stage renal disease (ESRD)-Stage 5 CKD
Gradual decrease in kidney func on
▪
o
o
o
Umbrella term that describes kidney damage or a decrease in the GFR for 3 or
inability to eliminate wastes
Irreversible
E ology
▪ Diabe c nephropathy
▪
Nephrosclerosis and HTN
▪
Glomerulonephri s
▪
Autoimmune diseases
Pathophysiology
▪
Large propor on of nephrons damaged
▪
Progressive disease process
▪
Renal insufficiency: 75% nephrons lost
▪
End-stage: 90% nephrons lost
▪
Uremia: Urea in the blood
●
●
▪
o
Uremic frost: frosty appearance of skin caused by wastes coming to
skin surface
Terminal stage
Affects all body systems
Assessment and Diagnos c Findings
▪
Fluid accumula on
●
●
▪
Electrolyte imbalances
●
▪
Elevated BUN, crea nine
Anuria or oliguria or large vol of urine w/o waste products (rare)
Acid-base imbalances
●
●
▪
Mental changes
Waste products retained
●
●
▪
Edema
HTN
Metabolic acidosis
o Renal buffering system not working
Rapid, deep resp to rid lungs of CO2 to correct acidosis
Anemia
●
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Inadequate erythropoie n produc on
Dietary deficiencies
▪
Calcium and Phosphorus Imbalance
▪
High magnesium levels
▪
▪
▪
●
Avoid antacids
●
Anorexia, N/V
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●
Fluid overload
Hyperkalemia - Arrhythmias
GI
CV
Respiratory
●
▪
Pulmonary edema
Neuromuscular
●
Confusion and irritability
▪
Psychosocial
●
▪
Renal
●
●
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▪
Urine output varies from scant to normal
Specific Gravity
o varies by cause
BUN and serum crea nine levels increase
Increase in blood phosphate, decrease in calcium levels
●
●
o
Decreased concentra on
Phosphorus and calcium have a reciprocal rela onship – when one is
high the other is low
In CKD phosphorus is high, therefore calcium is normally low
Medical Management
▪
Emergency Medica ons
●
●
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IV dextrose and Insulin
o Will help bring down high K+ levels
10 % Calcium Gluconate
Sodium Polystyrene (Kayexalate)
o Binds to K+ and excretes it through BM
o Contraindicated in pts w/ a bowel obstruc on or ileus
Albuterol
o Works similar to insulin – pushes K+ back into the cells
o Contraindicated in pts who are tachycardic
Bicarbonate
o If pt acido c
▪
Maintenance Medica ons
●
Calcium & Phosphorus Binders
o Calcium
▪
o
Given daily to help raise calcium levels
Sevelamer (Renagel)
▪
Phosphorous is given when the pt eats b/c there is a lot
of phosphorus in foods
● This helps to not raise their phosphorous levels
and in turn helps to raise their calcium levels
▪
If the pt is not ea ng they do not need to take this b/c it
binds to the phosphorus in foods
▪
●
them
An hypertensives
o Pts are hypertensive b/c of the fluid reten on
o ACE inhibitors are common for renal pts
▪
●
●
Can cause K+ reten on (Monitor)
Erythropoie n-Epogen
o Pts w/ CKD lack erythropoie n so this helps replace it
o Given typically IV on dialysis days
o Specific parameters are set by the Dr
▪
●
Milk products and soup have a lot of phosphorus in
Make sure to check lab values before administering to
avoid clo ng issues!
An seizure Agents
o Prophylac c
o B/c of the toxic build up in the system from CKD pts are more
prone to seizures
Iron
o Indica on – anemia
o Don’t give on an empty stomach
o Don’t give w/ a phosphorus binder b/c they can prevent the
body from absorbing the iron
▪
If ordered together – give phosphorus binder when the
pt is ea ng and then give the iron about a half hour to
an hour a er they are done ea ng
▪
**Drug therapy always a challenge b/c 2/3 of all drugs or their metabolites are
▪
eliminated by the kidneys
Diet
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▪
o
High calorie
Low protein
o unless dialysis – then they can have high protein
Low sodium, potassium, phosphorus
Increased calcium
Vitamins
Fluid restric on
Nursing Management
▪
Monitor fluid and electrolyte balance
▪
Reduce metabolic rate
▪
Promote pulmonary func on
▪
Prevent infec on
▪
Provide skin care
▪
Provide psychosocial support
▪
Prevent complica ons
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●
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Hyperkalemia
Metabolic acidosis
Pericardi s
Pulmonary edema
●
High serum phosphate level
Renal Labs
Lab
Reference Range
BUN
10-20 mg/dL
Crea nine
M: 0.6 – 1.2 mg/dL
F: 0.5 – 1.1 mg/dL
GFR (glomerular filtra on)
>90 mL/min
Sodium
136 – 145 mEq/L
Calcium
9 – 10.5 mg/dL
Potassium
3.5 – 5.0 mEq/L
Phosphorous
3.0 – 4.5 mg/dL
Magnesium
1.3 – 2.1 mEq/L
Urinalysis
Specific Gravity
1.00 – 1.04
pH
4.6 – 8
Glucose
None
Ketones
None
Protein
0 – 0.8 mg/dL
RBC’s
0–2
WBC’s
0–4
Bacteria
<1000 colonies/mL
Leukocytes
None
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