Acute Renal Failure

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Transcript Acute Renal Failure

Renal Diseases
Kidney Functions
Nephron
The Functional unit of the kidney is called
 Ureters

• Where the final urine product travels through
to reach the bladder

Bladder
• Place where urine is temporarily stored
Kidney Functions
Kidneys have a remarkable role in :
 Regulate extracellular fluid volume and
osmolarity

Regulate electrolyte concentrations

Regulate acid-base balance

Excrete metabolic waste products like
urea and creatinine and a number of
drugs and toxins

Help to regulate blood pressure by
secreting the enzyme renin

Produce the hormone erythropoietin,
which stimulates the production of red
blood cells in the bone marrow

Convert vitamin D to its active form
thereby plays a primary role in calcium
regulation and bone formation
Acute Renal Failure
Acute Renal Failure
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in acute renal failure the kidney function
deteriorates rapidly over hours or days.
The loss of kidney function reduces urine
output and allows nitrogenous wastes to
build up in blood
The degree of kidney dysfunction may be
mild to severe
With treatment acute renal failure is often
reversible although the mortality rate are
high ranging from 36-86 %
Causes of Acute Renal Failure
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Acute Renal Failure is a consequence
of :
• Severe illness
• Injury
• Surgery
To aid in diagnosis and treatment, its cauces
are commenly classified as:
prerenal- intrinsic- postrenal
Causes
• Prerenal factors : cause a sudden reduction in
blood flow to the kidneys; often involve a severe
stress – heart failure, shock, or blood loss
• Intrinsic causes : infections, toxins, drugs, or
direct trauma
• Postrenal factors : those that prevent excretion of
urine due to urinary tract obstructions
Consequences of acute renal failure
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A decline in renal function alters the
composition of blood and urine.
The kidney may become unable to
regulate the levels of electrolytes , acid,
and nitrogenous wastes in the blood.
Urine may be diminished in quantity or
absent, leading to fluid retention
Fluid and electrolyte imbalances
• Edema ( is an early symptom )appear as
puffiness in face and hands and swelling of
the feet and ankles
• Edema may be related to absence of urine or
oliguria
Oliguria: an abnormally low amount of urine
often less than 400 mL/day
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The reduced excretion of electrolytes
Consequences
results in :
1- Sodium retention which contributes to edema
2- Hyperkalemia ( elevated serum potassium
levels) can alter heart rate and lead to heart
failure
3- Hyperphosphatemia ( elevated serum
phosphate levels ) can increase secretion of
parathyroid hormones and reduce blood
calcium levels
Consequences

Uremia
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Abnormal
accumulation
of
the
body’s
nitrogencontaining waste products especially
blood urea nitrogen (BUN), creatinine, and uric
acid in the blood.
Moreover, the tissue catabolism that accompanies
illness produces additional nitrogenous wastes
than usual.
• Symptoms of uremia:
fatigue, lethargy, confusion, headache,
anorexia, a metallic taste in the mouth,
nausea and vomiting, and diarrhea
In more serious cases:
rapid pulse, elevated blood pressure,
seizures, and delirium or coma
MNT for acute renal failure
Primary goal :
Treat the underlying illness in order to
prevent further damage to the kidneys.
Protein and energy
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Due to catabolic condition associated with
hypermetabolism and muscle wasting ,
sufficient protein and energy needed to
preserve body’s protein content and muscle
mass.
Initially , the patient may be provided with 35
kcalories/kilogram body weight/day and body
weight is monitored to ensure that energy
intake is adequate.
• protein
increases the kidney workload, but
intake should be sufficient to prevent
negative nitrogen balance and additional
weasting.
• Protein usually restricted to about 0.6 – 0.8
g/kg body weight/day
• With dialysis or kidney function
improvements – protein allowed up to 2 g/kg
body weight/day.
Fluids
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Fluid status can be assessed by:
1.
2.
3.
4.
Monitoring weight fluctuations,
Blood pressure,
Pulse rates,
Appearance of skin and mucous membranes
Measure serum sodium concentrations:
Low sodium level indicates excessive fluid intake
High sodium level suggests inadequate intake
• Daily
fluid needs determined by
measuring urine output and
adding 500 mL to replace the
water lost through skin, lungs and
perspiration
• Individuals with fever, vomiting, or
diarrhea require additional fluid
• Patients undergoing dialysis can
ingest fluids more freely.
Electrolytes
• Hyperphosphatemia : limit phosphorus
• Potassium limited to 2000–3000 mg/day
Serum electrolyte levels monitored closely
• With oliguria : sodium intakes limited to 1100 - 3300
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mg daily.
Sodium intake can be adjusted to match urinary
sodium losses unless edema is present.
If on dialysis: generally can consume electrolytes
more freely
• In oliguric patients (those with reduced urine
production), recovery from renal failure
sometimes begins with a period of diuresis,
in which large amounts of fluid are
excreted may need electrolyte replacement
to compensate for urinary losses
Enteral and parenteral nutrition
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Some patients need enteral or parenteral nutrition
support to obtain adequate energy
Renal formulas: more kcalorically dense and
have lower concentrations of protein and
electrolytes than slandered formulas
Enteral support (tube feeding) is generally
preferred over parenteral nutrition because it is
less likely to cause infection
Total parenteral nutrition used only if patients are
severely malnourished or cannot consume food
for more than 14 days
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Dialysis:
Treatment that
removes wastes and
excess fluid from the
blood after the
kidneys have
stopped functioning
Dialysis
1- Hemodialysis :
• Blood is circulated through a dialyzer
(artificial kidney), where it is bathed by
dialysate, a solution that selectively
removes fluid and wastes
• It takes 3-4 hours and required for 2-3
times /week
2- Peritoneal dialysis :
Dialysate is infused into a person’s
peritoneal cavity, and blood is filtered
by the peritoneum (the membrane
that surrounds the abdominal cavity)
after several hours ( 4-6 hours), the
dialysate is drained, removing
unneeded fluid and wastes
Dialysis
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The basics of dialysis
• Removal of solutes
• Removal of fluid
• Evaluation of dialysis treatment
Chronic Kidney Disease
CKD
Chronic Kidney Disease
Generally progresses over many years
without causing symptoms
Typically diagnosed late in the course of
illness, after most kidney function has been
lost
Most common causes :
 Diabetes mellitus (45%)
 Hypertension (27%)
1- Altered electrolytes and
hormones
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Usually develop during the final stage of renal failure
Hormonal adaptations occur to help regulate
electrolyte levels but may cause complications too
Increased aldosterone secretion helps to maintain
serum potassium levels but contributes to the
development of hypertension
Increased secretion of parathyroid hormone keeps
serum phosphate levels normal, but contributes to
bone loss (renal osteodystrophy)
Electrolyte imbalances may develop when
GFR becomes extremely low:
< 5 mL/minute
2- Uremic syndrome
Develops during the final stages of CKD
• GFR < 15 mL/per minute
• BUN > 60 mg/dL
• Complications of uremic syndrome
1. Subtle ‫خفيف‬mental dysfunctions
2. Neuromuscular changes : muscle cramping,
twitching,
3. Impaired hormone synthesis : erythropoietin –
anemia
4. Bleeding abnormalities – defects in platelet function
and clotting factors
Uremic syndrome cont’d
• Chronic
kidney
disease
worsens
cardiovascular disease risk : hypertension,
increased insulin resistance, and abnormal
blood lipids in addition , elevated parathyroid
hormone levels lead to calcification of blood
vessels and heart tissue
• Reduced immunity : poor immune responses
– develop infections, a frequent cause of death
3- Protein-energy malnutrition
• Anorexia : believed to be a primary cause
of poor food intake secondary to nausea
and vomiting, restrictive diets, uremia and
medications
• Nutrient losses : consequence of
vomiting,
diarrhea,
gastrointestinal
bleeding, concurrent catabolic disease
and dialysis
MNT of CKD
The goal of CKD is to:
 Slow disease progression and prevent symptoms.
 Prevent PEM and weight loss
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The following table summarizes the dietary
guidelines apply to patients in stage 1 to 4.
By stage 5 either hemodialysis or peritoneal
dialysis
is
necessary.
Actual
nutrition
recommendation should be based on the results of
nutrition assessment.
1- Energy
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Energy intake should be high enough to allow
patients to maintain a healthy weight and to
prevent wasting.
35 cal/ kg body weight˂ 60 years
30-35 ˃60 years
• Foods and beverages of high energy and
nutrient
density is recommended
• Malnourished patients may require oral formulas or
tube feedings to maintain weight
• Patients
•
undergoing peritoneal dialysis can
absorb a substantial amount of glucose from
the dialysate ( in order to draw fluid from blood to
peritoneal cavity by osmosis) that may contribute
as many as 800 kcalories daily .
These calories must be included in the
estimation of energy intake -weight gain is
sometimes a problem
2- Protein
• Predialysis :
0.6 to 0.75 grams/kg body weight/day
• Low-protein diets produce fewer nitrogenous
wastes so reduce risk of uremia
• Low-protein diets supply less phosphorus so
reducing risks associated with
hyperphosphatemia
• 50% of the protein should be from highquality sources
Protein
• Care taken to provide enough protein to meet needs and
prevent wasting
• Once dialysis begun:
protein restrictions relaxed
≥ 1.2 to 1.3 grams/kg body weight/day
• Dialysis removes nitrogenous wastes
• results in some amino acids losses during the
procedure
• 50% of the protein should be from high-quality
sources
3- Lipids
• Some renal patients at risk for coronary heart
•
disease and are therefore advised to restrict
saturated fat , trans fat and cholesterol
Amount taken as necessary to maintain a As
necessary to maintain healthy lipid profile
• Renal
diets include high-fat foods to
increase calories but patients should be
encouraged to select foods providing mostly
unsaturated fats such as nuts, seeds, salad
dressings,
mayonnaise,
avocados
and
soybean products
4- Fluids and sodium
•
As CKD progresses, the patient excrete less
urine and the kidneys can’t handle normal
sodium and fluid intake
• Recommendations depend on total urine
output, changes in body weight ,blood
pressure and serum sodium levels.
1. Decrease in body weight – low blood pressure
means fluid and sodium loss
2. Increase in body weight - high blood pressure
means fluid and sodium retention
• Fluids are not restricted until urine output
decreases
• Fluid intake should match the daily urine
output in patient who is neither dehydrated
or over-dehydrated
Once on dialysis – sodium and fluid
intakes controlled so that water weight
gain is 2 pounds(= 908 gm) between
dialysis treatments
5- Potassium
• Predialysis – can handle typical intakes of
•
potassium
Potassium restriction are usually necessary only
in patients with elevated potassium levels
• Supplementation may be needed for patients
using potassium-wasting diuretics
Potassium
• Dialysis patients should control potassium intakes
to prevent hyperkalemia and in some cases
hypokalemia
Hyperkalemia : abnormal elevation of serum
potassium levels
Hypokalemia: low serum potassium levels
• Patients are taught foods that
contain levels
of potassium acceptable for renal diets.
• They should avoid foods rich in potassium
such as banana, beet, dried fruits, orange,
milk and milk products, spinach and
tomato.
6- Calcium, phosphorus and vitamin D
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To prevent bone disease calcium and
phosphorus may need adjustment
• Foods high in phosphorus should be
avoided –
protein-restricted diets are low in phosphorus
•
Before dialysis calcium intake = 800-1000 mg/
day )
• After dialysis begun calcium and vitamin D
supplementation is required
Calcium: ≤ 2000 from diet and medications
7- Vitamins and minerals
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The restrictive renal diet interferes with
vitamin and mineral intakes .
Patients treated with dialysis lose water
soluble vitamin and some trace minerals
into the dialysate.
• Folate – 1 mg/day
• Vitamin B6 – 10 mg/day
• Vitamin C – < 100 mg/day because
excessive intake can contribute to kidney
stone formation in individuals at risk
• supplementation with vitamins A and E not
recommended because they may
accumulate in renal failure patients
• Intravenous administration of iron with
erythropoietin therapy is more effective than
oral intake of iron alone.
Kidney Stones
Kidney Stones
Kidney stone : crystalline mass that forms
within the urinary tract. Also called renal
calculi
Formation of Kidney Stones
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About 70% of kidney stones is made up
primarily of calcium oxalate
Less commonly , stones are composed
of uric acid, amino acid cystine,
calcium phosphate
Factors that predispose to
stone formation:
 Dehydration or low urine volume which
promotes the crystallization of minerals or
other compounds in the urine.
 Obstruction that prevent the flow of urine and
encourage salt precipitation
 Urine acidity which affect the dissolution of
urinary constituents
 Renal disease which is associated with
calcium or phosphate accumulation
1- Calcium oxalate stones
Commonly associated with:
1- Hypercalciuria ( elevated urinary calcium levels)
• Excessive calcium in urine may result from:
• Excessive calcium absorption
• Impaired reabsorption of calcium in kidney tubules
• Elevated serum levels of parathyroid hormone or vitamin D
• Hyperoxaluria (Excessive urinary oxalate ) also promotes
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the formation of calcium oxalate crystals
Hyperoxaluria may reflect an increase in the body
synthesis of oxalate or increase the absorption from
dietary sources
People who form calcium oxalate
stones are advised to reduce their dietary intake of oxalate
• Avoid supplementation with vitamin C which degrades to
oxalate in the body.
2- Uric acid stones
• Uric acid stones develop when urine is
abnormally acidic, contains excessive
uric acid or both
• Frequently associated with gout
Gout: a metabolic disorder characterized
by elevation uric acid levels in the blood
and urine
• Other
diseases that increase the uric acid
stones include leukemia and lymphoma
which are associated with overproduction of
purines
• Purines : products of nucleotide metabolism
that degrade to uric acid.
• Purine-rich diet contributes to high uric acid
levels( organ meats and sea foods)
3- Cystine stones
• It occurs as a consequence of cystinuria
• Cystinuria :inherited disorder of amino acid
metabolism cystine
• Renal tubules are unable to reabsorb cystine
normally
• Stones occur when cystine concentration is
excessive in the urine leading to subsequent
crystallization and stone formation.
Consequences of kidney stones

In most cases, small stones can readily pass
through the ureters and out of the body with
minimal treatment.
1- Renal colic:
• A stone passes through the ureter can produce
severe pain called renal colic
• The pain begins suddenly in the back and
intensifies as the stone follows the ureter’s
course down to the abdomen toward the
bladder
• Pain may be severe enough
to cause nausea and vomiting
2- Urinary tract complications
• Hematuria as a result of damaging the kidney
or ureter lining
Hematuria: blood in the urine
• May cause urinary tract obstruction or
infection
Treatment of kidney stones
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Drinking 12-16 cups of fluids/day
Additional fluids if in hot weather or if
individual is extremely active
Medication which reduce urinary calcium ,
reduces oxalate absorption , reduces uric
acid production in the body and reduce
cystine levels
MNT for Calcium oxalate stones
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Diet containing 800 – 1200 mg of calcium
per day is recommended because calcium
combines with oxalate in the intestines ,
reducing its absorption and in turn helping to
control hyperoxaluria
Moderate protein and sodium restriction is
advised because high protein and sodium
intakes increase urinary calcium excretion
• Foods high in oxalate should be restricted
because it increase urinary calcium
excretion
• Protein 0.8 – 1 gm / kg/ day
• Sodium no more than 3450mg/ day
• Vitamin C limited to DRI(75-90 mg/day)
MNT for Uric acid stones
• High fluid intakes
• restriction of Purine rich
l
foods
MNT for Cystine stones
• High fluid intakes