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Acute kidney Injury

and
Chronic kidney disease

Presented by: Ablola Kimberly, Sanoy, Ray Ann & Seria, Sharia
OBJECTIVES
General:
• This study aims to share knowledge about acute kidney injury and
chronic kidney disease.

Specific:
• To be able to define acute kidney injury and chronic kidney disease
• To know the causes of kidney diseases
• To provide information about how acute kidney disease and chronic
kidney disease occur.
• To know the Stages and signs and symptoms of AKI and CKD
• To know the Nursing Interventions and treatments for AKI and CKD
• Kidney diseases, especially End Stage Renal Disease (ESRD),
are already the 7th leading cause of death among the Filipinos.

• One Filipino develops chronic renal failure every hour or


about 120 Filipinos per million population per year.

• -NKTI (National Kidney Transplant Institute)


Anatomy and Physiology of kidney
• Kidneys are important parts of the urinary system.
• They are found at each side of the spine, below the rib cage of the
human body.
• Each kidney is as big as a fist, weighs ¼ pound and looks like a kidney
bean.
• The kidneys perform vital life-maintaining functions as monitors and
regulators of body fluid.
• They excrete fluids when the body has an excess of them and retain
the substances necessary for the body’s continuing function.
• They produce and release a variety of chemicals to keep the body
healthy and filter the entire blood supply every 2 minutes, excreting
waste materials through the urine.
The kidneys receive fresh
blood from the heart and
filters the blood via the
nephrons (glomerulus), which
creates a filtrate/urine that
will progress through the rest
of the nephron (renal tubule).

The renal tubule will fine-


tune the filtrate by pulling
out water and ions. Then
the substances left over will
be excreted in the urine.
• Remember the glomerulus does NOT normally filter blood
cells or proteins (just water, urea, creatinine, ions).

• Creatinine is the only substance filtered by the glomerulus


that is solely filtered from the bloodstream that is NOT
reabsorbed within the renal tubule.
• Therefore, measuring creatinine levels in the urine/blood
help us to determine the functionality of the kidneys,
specifically the nephron.
Primary Causes
Diabetes
Age 60 +

High
blood Tobacco use
pressure

Family history
Heart problems or stroke Obesity
Acute kidney injury
• Acute kidney injury (AKI) is a sudden episode of kidney
failure or kidney damage that happens within a few
hours or a few days.

• Acute kidney (AKI) is the rapid loss of kidney function


from renal cell damage.

• Occurs abruptly and can be reversible.


Causes
1.PRE-RENAL
• outside the kidney; caused by intravascular volume depletion such as with
blood loss associated with trauma or surgery, dehydration, decreased cardiac
output (as with cardiogenic shock), decreased peripheral vascular resistance,
decreased renovascular blood flow and pre renal infection or obstruction.
2.INTRA-RENAL
• Within the parenchyma of the kidney, caused by tubular necrosis,
prolonged pre renal ischemia, intra renal infection or obstruction, and
nephrotoxicity.
3.POST-RENAL
• Between the kidney and urethral meatus, such as bladder neck
obstruction, bladder cancer, calculi and post renal infection.
CATEGORIES

ISCHEMIC
•Heart disease ( decreased in cardiac output)
•Hypovolemia -does not conserve sodium and H2o
•Hypervolemia –does not excrete sodium and H2o
•Medication (vasoconstriction) antibiotics, NSAIDS.
•Systemic vasodilation
NEPHROTOXIC
• A.EXOGENOUS
• Antifungals/ Antinefectives
• Liver/kidney disease
• Age
• Shock

• B. ENDOGENOUS
• formation of crystals
• Hemoglobinuria and Myoglobenuria
• Multiple myeloma
CELL HYPOPERFUSION

CELL DEATH

DECOMPENSATION OR IMPAIRED KIDNEY FUNCTION


PHASES OF AKI
STAGES FEATURES DURATION
>Common triggering events: HOURS TO DAYS
significant blood loss, burns, fluid
ONSET loss, diabetes insipidus.
>Renal blood flow 25% normal
>Tissue oxygenation 25% of normal

>urine output below 400ml/day 8 TO 15 DAYS OR LONGER


>increases in blood urea Depending on nature of
nitrogen(BUN) and creatinine levels AKI and Dialysis initiation
OLIGURIC >Electrolyte disturbances, acidosis,
and fluid overload (from kidney’s
inability to excrete water)
>decreased in GFR
>Occurs when cause of AKI is 7 TO 14 DAYS
corrected
>Renal tubule scarring and
edema
DIURETIC >Increased in GFR
>urine output is 4-5L/day
>Possible electrolyte
depletion from excretion of
more water and osmotic
effects of high BUN

>Decreased edema SEVERAL MONTHS TO 1


>Normalization of fluid and YEAR
RECOVERY electrolyte balance
>Return GFR to 70% or 80% of
normal
SIGNS AND SYMPTOMS

• Increased in BUN and CREA – waste products


• Anemia (mild)
• Metabolic acidosis
• Decreased Sodium, Calcium
• Increased Potassium, Magnesium, Phosphorus
Management
• Provide Rest
• Restrict Fluid intake
• Emotional Support
• Monitor vital signs, especially for signs of hypertension, tachycardia,
tachypnea and irregular rate.
• Monitor intake and output hourly and urine color and characteristics.
• Monitor daily weight: nothing that an increase of ½ to 1lb/day,
indicates fluid retention
• Monitor for altered LOC caused by uremia
• Monitor signs of infection
• Monitor the lungs and rhonchi and monitor for edema
• Limit Sodium, Potassium intake as prescribed
• Administer medications as prescribed
Chronic kidney disease
Chronic kidney disease
• Significant decline in kidney function that happens over
a long period of time that leads to the build up of
waste, water, and electrolyte imbalances in the body.
• CKD is a slow, progressive, irreversible loss of kidney
function.
• GFR less than or equal to 60ml/min for 3 months or
longer.
Causes of CKD

• May follow AKI


• Diabetes mellitus and other metabolic disorders
• Hypertension
• Chronic urinary obstruction
• Recurrent infection
• Renal artery occlusions
• Autoimmune disorders
Stages of CKD

• Stage 1: kidney damage with normal renal function GFR >90


ml/min but with proteinuria (3 months or more)
• Stage 2 : kidney damage with mild loss of renal function GFR
60-89 ml/min with proteinuria (3 months or more)
• Stage 3: Mild to severe loss of renal function GFR 30-59
ml/min
• Stage 4: Severe loss of renal function GFR 15-29ml/min
• Stage 5: End stage renal disease GFR less 15ml/min
Diagnostic test for CKD
Serum creatinine tests
• measure the amount of a substance called creatinine in your
blood.
The normal ranges of SCr are:
• 0.5 to 1.1. milligrams (mg) per deciliter (dL) in women
• 0.6 to 1.2 mg/dL in men

Glomerular filtration rate (GFR)


• an estimation of how well your kidneys are functioning.
The GFR reference range is as follows:
• 90 to 120 milliliters (mL) per minute: Normal
• Below 60 mL/min: CKD
• Below 15 ml/min: Kidney failure, also known as end-stage renal disease
(ESRD)
Creatinine Clearance
• Estimating GFR is a test called creatinine clearance, which compares
your serum creatinine with the amount of creatinine excreted in urine
over 24 hours.

The normal range of CrCl values are:


• 88 to 128 mL/min for women
• 97 to 137 mL/min for men excreted in urine over 24 hours.
Urinary Albumin
• One such protein, called albumin, can be used by the lab to detect
proteinuria, the excessive accumulation of protein characteristic of
kidney disease.

The normal ranges of urinary albumin are:


• 0 to 8 mg/dL (for the 24-hour urine test)
Blood urea nitrogen (BUN)
• measures the amount of a waste product in your blood, called urea
nitrogen.

The normal range of BUN values


• 6 to 21 mg/dL for women
• 8 to 24 mg/dL for men
• Electrolyte Imbalances:

• Hyperkalemia (>5.1 mEq/L): (normal level 3.5 – 5.1 mEq/L) at risk for
significant cardiac event due to the nephrons decreased ability to excrete
potassium.

Nursing Role:
• restrict potassium-rich foods (potatoes, avocados, strawberries, tomatoes,
spinach, oranges, bananas), monitor EKG for changes (tall peaked T-waves,
Wide QRS and prolonged PR interval)
• monitor lab values
• may be ordered to give Kayexalate orally or rectally to remove extra
potassium out of the blood
• place on cardiac monitor to watch rhythm
• Hypocalcemia (<8.6 mg/dL): normal level 8.6-10 mg/dL

• Phosphate builds up in the blood because it cannot be excreted out of the


kidney due to a damaged nephron, which leads to the decrease of calcium
“hypocalcemia”.

Nursing Role:
• Administer phosphate binders, such as calcium carbonate or “PhosLo
(calcium acetate)” to decrease phosphate levels. These medications works by
excreting phosphate in the stool found in food. Give with meals or
immediately after eating.
• Diet low in phosphate: Restrict foods high is phosphate: poultry, fish, dairy,
nuts, sodas, oatmeal.
• Safety due to weak bones.
Hypermagnesemia (>2.6 mg/dL): normal 1.6-2.6 mg/dL
• Patient is at risk for EKG changes, tendon reflexes diminished or absent,
lethargy.
Nursing role:
• Avoid administering magnesium based antacids or laxatives
• Low magnesium foods
• MD may order IV calcium to help decrease level
• LOW UOP and Fluid Overload:
• Monitor intake and output (strict)
• Daily weights
• Assess swelling and lung sounds “crackles”
• Monitor blood pressure
• Low sodium diet
Treatment for Chronic Kidney Disease
Early stages with normal GFR:
• Controlling blood pressure and glucose level
• Medications for hypertension that help protect the kidneys,
such as ACE inhibitors “pril” or ARBs “sartan”
• Monitoring GFR and blood pressure regularly
Advanced stages where GFR is abnormal:
• Dialysis
• Kidney transplant
• Diet changes
Dialysis
• Hemodialysis is a medical procedure wherein the blood is
filtered by hooking the patient to a dialysis machine using a
fistula, graft or catheter. Most patients go to dialysis centers
two or three times a week to avail of this treatment.

• Peritoneal Dialysis the removal of wastes and toxins from the


blood happens inside the body using a special cleaning solution
circulated through a catheter attached to the abdomen.

• Kidney Transplant offers the best survival rate and quality of life
to a person with ESRD. A new kidney can come from a live
donor or a deceased donor.
Nursing Interventions for CKD
• Safety: patient may be confused, assess neuro status
• Itching: due to deposits of urea crystals on the skin via the sweat
glands. It looks like frost on the skin and is called “uremic frost”
• Low protein diet: urea is a waste product of protein breakdown
(patient doesn’t need any more urea). However, patient needs
some protein to prevent muscle wasting.
• Assess for kussmaul breathing was is deep/rapid breaths from the
acid building up in the blood (metabolic acidosis). This type of
breathing is a compensatory mechanism by the respiratory system
to increase the blood’s ph.

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