RENAL DISORDER
ACUTE RENAL
FAILURE
DEFINITION:
“Acute renal failure (ARF) is
manifested as an abrupt decline in glomerular filtration rate occurring over a
period of days or weeks. This results in accumulation of water, nitrogenous
wastes products and other toxins.”
The patient may be anuric
(<50mL urine/24hrs), oliguric (<400 mL urine/24hrs), pass normal volumes
of urine or may even be polyuric.
RIFLE classification
Stage
|
Serum Creatinine
|
|
Urine output
|
Risk renal failure
|
Cr. x 1.5 normal
|
or
|
UO < 0.5ml / kg / hour for
6 hours
|
Injury to kidney
|
Cr. x 2 normal
|
or
|
UO < 0.5ml / kg / hour
for 12 hours
|
Failure of kidney function
|
Cr. x 3 normal
|
or
|
Anuric for 12 hours
|
Loss kidney function
|
Need renal replacement
therapy x 4 weeks
|
||
End stage renal disease
|
Need renal replacement
therapy for > 13 weeks
|
1. Pre renal
(functional)
2. Intra renal
(renal or intrinsic)
3. Post renal
1. 1-Pre-RENAL
(FUNCTIONAL):
If renal tubular and glomerular function is intact but clearance
is limited by factors compromising renal perfusion, the failure is termed pre
renal failure. It results from hypo perfusion of the renal parenchyma, with or
without systemic arterial hypotension. Pre renal ARF is rapidly reversible if
the underlying cause is corrected. In prerenal acute kidney injury,
there is nothing wrong with the kidney itself.
CAUSES:
Ø Hypovolemia
o
Diarrhea, vomiting, dehydration
o
Inappropriate diuretic therapy
Ø Decreased cardiac output
o
Cardiac failure
o
Hypotension
Ø
Sepsis
Ø
Drugs;
o
NSAIDs, ciclosporin
o
ACE inhibitors
o
Angiotensin receptor blockers (ARBs)
Ø
preexisting medical conditions, such as
atherosclerosis
Ø
excessive use of diuretics (water pills)
is a major cause of prerenal ARF
2. INTRARENAL ARF:
“Any form of damage to the renal infrastructure (renal
parenchyma) usually involving some form of ischemic or nephrotoxic insult may
result in intra renal ARF”
CAUSES:
The
most common causes of intrinsic acute kidney injury are acute tubular necrosis
(ATN), acute glomerulonephritis (AGN), and acute interstitial nephritis
(AIN).
i.
Acute
Tubular Necrosis:
The most common cause that
result from ischemia or direct exposure to toxins, severe burns etc.
ii.
Tubulointerstitial
Nephritis:
Acute interstitial nephritis (AIN) is inflammation of the kidneys. It is usually
caused by a medicine, such as an antibiotic or a nonsteroidal anti-inflammatory drug like naproxen or ibuprofen. Be safe with medicines. Read and
follow all instructions on the label.AIN may also be caused by a streptococcal,
viral infection.
iii.
Glomerulonephritis:
Glomerulonephritis is a condition in
which the tiny blood vessels in the kidneys become inflamed and damaged.
Damaged glomeruli do not filter blood properly. Acute glomerulonephritis may be
caused by an abnormal immune system
response. Such as in
- Lupus (systemic lupus erythematosus).
- Bacterial or viral infections.
3. POST RENAL ARF:
Post renal ARF may develop as
the result of obstruction at any level within the urinary collection system
from the renal tubule to urethra. Postrenal ARF is caused by an acute obstruction that affects
the normal flow of urine out of both kidneys. The blockage causes pressure to
build in all of the renal nephrons (tubular filtering units that produce urine).
The excessive fluid pressure ultimately causes the nephrons to shut down. The
degree of renal failure corresponds directly with the degree of obstruction.
Postrenal ARF is seen most often in elderly men with enlarged prostate that obstructs the normal
flow of urine.
i.
Bladder
Outlet Obstruction:
due to an enlarged
prostate gland or bladder stones
ii.
Ureteral:
It includes the obstruction from
calculi, clot, carcinoma, surgery.
iii.
Renal
Pelvis or Tubules:
End channels of the renal
nephrons. It is induced by Uric acid, Sulfonamides, Acyclovir &
Oxalates.
Stages of Acute
Renal Failure:
Course of ARF may be divided into the three phases;
1. Initiating
phase or oligouric phase.
2. Maintenance
or diuretic phase.
3. Recovery
phase
1. Initiating phase or oligouric phase:
It is usually of 7-14 days but may last for 6
weeks. It starts from renal insult and ends at the point at which external
factors no longer reverse the damage caused by the obstruction or other causes
of ARF.
Urine Output; It may drop to 400mL/day or
even less (oligouric).
Nitrogen Waste Products;
Serum
creatinine, urea, sulphate, phosphate and organic acid level rise rapidly.
Hyponatremia
Hypocalcemia
Hyperkalemia;
may lead to neuromuscular depression, impaired cardiac conduction, arrhythmia,
respiratory depression, cardiac arrest and ultimately death.
2.
MAINTENANCE OR DIURETIC PHASE:
If
patient survives in the 1st phase then it enters the 2nd
phase i.e. diuretic phase. It involves the marked increase in urine output (>
500mL/day) to several liters. It lasts for 7days and corresponds to recommencement of tubular function. This
phase carries risk of GI bleeding and fluid and electrolyte imbalance.
3.
Recovery
Phase:
Patient who survives in diuretic
phase has a good prognosis and pass to recovery phase. It involves the recovery
of renal function where the regeneration of tubule cells take place slowly over
the period of months to years.
SIGNS AND SYMPTOMS
OF ARF:
- decreased urine
output (although occasionally, urine output remains normal)
- chest pain or
pressure
- jugular vein
distention
- fluid retention,
causing edematous legs, ankles, or feet
- shortness of
breath
- confusion
- nausea
- seizures or coma
in severe cases
9. ARF with Volume Depletion:
It includes dry mucosa, postural hypotension, tachycardia,
and cold extremities. Other signs & symptoms associated with uremia as a result of
accumulation of wastes include nausea, vomiting, headache, muscle cramps,
fatigue and decline level of consciousness.
10. ARF with Volume Overload:
It includes odema, weight gain, orthopnea and pulmonary
crackles.
Acute
Kidney Failure Diagnosis
Kidney failure is often detected from blood or urine tests.
Ø Levels of urea (blood urea nitrogen [BUN]) and creatinine
are high in kidney failure. This is called azotemia.
Ø
Electrolyte levels in the blood may be abnormally high or
low because of improper filtering.
Ø
When the duration and severity of kidney failure is severe, the red blood cell count may be low. This is called anemia.
Ø The amount of urine produced over a period of hours may also
be measured for quantity and quality or the amount of wastes being excreted.
When kidney tissue is injured, protein and desirable substances may be
inappropriately excreted in the urine. In some cases, the amount of urine
remaining in the bladder after urination will be measured by an ultrasound
device called a bladder scanner.
Ø In some cases, tissue samples of the kidneys are taken
(biopsy) to find the cause of the renal failure.
MANAGEMENT
OF ACUTE RENAL FAILURE:
EARLY PREVENTIVE AND SUPPORTIVE THERAPY:
Ø
Improving the renal blood flow
Ø
Reducing renal vasoconstriction
Ø
And removing Nephrotoxins from kidney
1.
Identification of Patient at
Risk:
Patient with pre-existing chronic renal failure, diabetes,
jaundice and elderly are at a high risk. Their condition will deteriorate more
quickly than the other.
2.
Withdrawal and Avoidance of
Nephrotoxic Drugs
3.
Optimization of Renal
Perfusion:
It includes rapid correction of body fluid
and electrolyte balance in order to maximize renal perfusion. Sodium
chloride 0.9% is an appropriate choice for it. Where needed inotropes
should be used to provide cardiac output.
4.
Establishing and Monitoring an
Adequate Diuresis:
If kidney does not show response to renal perfusion with
fluid replacement therapy then measures include;
ü Loop
diuretics
ü Mannitol
LOOP DIURETICS (Furosemide, Bumetanide ):
Loop diuretics reduce the renal
tubular cell metabolic demand and improve renal blood flow by stimulating
release of prostaglandins. It should be initiated after circulatory volume is
restored otherwise its use produce a negative fluid balance and precipitate pre
renal ARF.
Drug
|
Dosage Regimen
|
Furosemide
|
1-2g in 24hr in I.V infusion at a rate not more than
4mg/min
|
Bumetanide
|
0.5-1mg/day or maximum upto 20mg/day I.V or I.M
|
Mannitol:
It can wash intrarenal obstruction caused by tubular debris.
A dose of 0.5-1g/kg as a 10-20% infusion was previously recommended. But
it is associated with renal medullary hypoxia & potential damage in heart
failure patients.
ACE
inhibitors and angiotensin receptor blocker in ARF:
ACE inhibitor is completely contraindicated in a patient
with aortic or bilateral artery stenosis. Renin angiotensin system is
stimulated by low perfusion resulting from stenosis. Then angiotensin II is
produced which causes renal vasoconstriction which increases efferent
arteriolar tone which creates back pressure which maintain glomerular pressure
in poorly perfuse kidney. If angiotensin II production is inhibited then
efferent arteriolar dilatation results. Since increased efferent vascular
constriction maintains filtration in such patients then overall result of such
therapy will reduce the filtration at glomerulus leading to ARF.
NON
DIALYSIS TREATMENT OF ESTABLISHED ACUTE RENAL FAILURE:
1. Treatment
of Uremia:
Symptoms of uremia may be reduced by restricting protein
intake. Fat and carbohydrate should be taken to maintain a high energy intake
to prevent protein catabolism and promote anabolism. In severely ill patients
use of parenteral or enteral nutrition should be considered at an early stage.
2. Treatment
of Hyperkalemia:
Extracellular potassium level
rises as a result of tissue damage in sepsis, burns and acidosis. Dietary
potassium should be restricted. Avoid potassium supplements and potassium
sparing diuretics removed from treatment. Emergency treatment is necessary when
there are progressive changes in electrocardiogram associated with
hyperkalemia.
Emergency Treatment of Hyperkalemia:
ü
10-30 ml of calcium gluconate 10% intravenously over 5-10
minutes. This effect is short lived and dose can be repeated.
3.
Treatment
of acidosis:
ü
Sodium bicarbonate 1-6g/day in divided doses intravenously
may be used.
4.
Treatment
of Hypocalcaemia:
ü
Oral calcium supplementation with calcium gluconate or
lactate and vitamin D may be used to treat the hypocalcaemia of ARF if needed.
ü
Calcium gluconate is given IV in a dose of 1-2g over a
period of 10min followed by slow infusion (6-8hours) of an additional 1g.
5.
Treatment
of Hyperphosphatemia:
ü
Phosphate binding agent may be used such as calcium carbonate
or aluminium hydroxide in the mixture or capsules.
6.
Treatment
of Hyponatremia:
ü 3-5% sodium chloride may be administered by slow IV
infusion.
7.
Treatment
of Underlying Infection:
ü
Treat with appropriate antibiotic.
Renal Replacement Therapy:
Renal replacement
therapy is indicated in a patient with ARF when kidney function is poor and
life is at risk. It is used;
ü To remove toxins with severe symptoms (impaired
consciousness, pericarditis, and seizures).
ü To remove fluid resistant to diuretics (pulmonary edema) to
facilitate parenteral nutrition.
ü Hyperkalemia with marked ECG changes.
ü Increased acidosis (pH<7.1)
Forms of
Renal Replacement Therapy:
ü Hemodialysis
ü Haemofilteration
DEFINITION:
Chronic
renal failure (CRF) is the progressive loss of kidney function leading to
irreversible structural damage to existing nephron.
PATHOPHYSIOLOGY
There
are approximately 1 million nephrons per kidney, each maintaining its own
single nephron eGFR (estimated glomerular filtration rate). Progressive loss of
nephron function results in adaptive changes in remaining nephrons to increase
single nephron eGFR which in turn causes hypertrophy and irreversible nephron
loss leading to continuous cycle of nephron destruction.
Factors
involved in pathophysiology:
Susceptibility
factors
These factors increase the risk for kidney disease but do not directly
cause kidney damage.
·
Advanced age
·
Reduced kidney mass and low birth weight
·
Family history
·
Systemic inflammation
·
Dyslipidemia (abnormal amount of lipids)
Initiation
factors
These factors initiate kidney
damage and can be modified by drug therapy.
·
Diabetes mellitus
·
Hypertension
·
Autoimmune disease
·
Polycystic kidney disease
·
Drug toxicity
Progression
factors
These factors cause decline in kidney function after initiation of kidney
damage.
·
Glycemia in diabetics
·
Hypertension
·
Proteinuria
·
Smoking
CLASSIFICATION
OF CRF:
1: Pre-renal
2: Renal
3: Post-renal
PRE-RENAL:
Causes of pre-renal CRF are
·
Chronic liver failure
·
Poor cardiac function
·
Atherosclerosis (hardening of renal arteries)
RENAL:
Causes of
renal CFR are as under:
·
Diabetic
nephropathy: Kidney
disease associated with diabetes: the most common cause of kidney disease.
·
Hypertension nephron-sclerosis: the
second leading cause of CRF
POST-RENAL:
Interference with normal flow of
urine produce back pressure with kidney, damage nephron and lead to obstructive
neuropathy, a disease of urinary tract.
·
Bladder outlet
obstruction: It
is due to enlarged prostate gland or bladder stone.
·
Neurogenic bladder: An over distended bladder
caused by impaired communicator nerve fibers from bladder to the spinal cord.
·
Kidney stone: In both ureters, the tubes that
pass urine flow from each kidney to bladder.
Stages of CRF:
STAGE
|
GFR
|
Symptoms and Effects
|
Stage 1
|
Normal
>/=90ml/min
|
No
such symptoms
|
Stage 2
|
Mild
reduction
(GFR
60 – 89 ml/min)
GFR
of 60 may represent 50% loss in function.
|
•
Higher than normal levels of creatinine or urea in the
blood
•
Blood or protein in the urine
•
Evidence of kidney damage in an MRI, CT scan, ultrasound
or contrast X-ray
|
Stage 3
|
Moderate
reduction
(GFR
30 – 59 ml/min)
|
·
Calcium absorption decreases
·
Malnutrition onset
·
Anemia
|
Stage 4
|
Severe
reduction
(GFR
15 – 29 ml/min)
|
·
Serum triglycerides increase
·
Hyperphosphatemia
·
Metabolic acidosis
·
Hyperkalemia
|
Stage 5
|
(GFR less than 15
ml/min)
|
·
Marked decrease in:
Hemoglobin, Hematocrit,
Calcium
·
Fluid overload
·
Uremic syndrome develops affecting all body systems can be
diminished with early diagnosis & treatment.
·
Fatal if no treatment
|
Diagnosis:
·
Blood test
Blood test (BUN) may be ordered
to determine whether waste substances are being adequately filtered out. If
levels of urea and creatinine are persistently high, the doctor will most
likely diagnose end-stage kidney disease.
·
Urine test
Urine test helps find out whether
there is either blood or protein in the urine.
·
Kidney scans
Kidney scans may include MRI, CT
scan or an ultrasound scan. The aim is to determine whether there are any
blockages in the urine flow. These scans can also reveal the size and shape of
the kidneys. In advanced stages of kidney disease the kidneys are smaller and
have an uneven shape.
·
Kidney biopsy
·
Small sample of kidney
tissue is extracted and examined for cell damage. An analysis of kidney tissue
makes it easier to make a precise diagnosis of kidney disease.
·
Glomerular filtration rate (GFR)
GFR is a test that measures the
glomerular filtration rate - it compares the levels of waste products in the
patient's blood and urine. GFR measures how many milliliters of waste the
kidneys can filter per minute. The kidneys of healthy individuals can typically
filter over 90 ml per minute.
Causes and associated conditions:
In the majority of cases,
progressive kidney damage is the result of a chronic disease (a long-term
disease), such as:
Diabetes
Chronic kidney disease is linked
to diabetes types 1 and 2. If the patient's diabetes is not well controlled,
excess sugar (glucose) can accumulate in the blood. Kidney disease is not
common during the first 10 years of diabetes; it more commonly occurs 15-25
years after diagnosis of diabetes.
Hypertension (high blood pressure)
High blood pressure can damage the glomeruli -
parts of the kidney involved in filtering waste products.
Obstructed urine flow
If urine flow is blocked it can back up into
the kidney from the bladder (vesicoureteral reflux). Blocked urine flow
increases pressure on the kidneys and undermines their function. Possible
causes include an enlarged prostate, kidney stones, or a tumor.
Kidney diseases
Including:
·
Polycystic kidney disease (inherited kidney disorder, fluid filled
cysts are formed in kidneys)
·
Pyelonephritis (life threatening infection leading to renal
scarring)
·
Glomerulonephritis (group of diseases that injure the part of
kidney that filters blood, glomeruli)
Kidney artery stenosis
The renal artery narrows or is blocked before
it enters the kidney.
Certain toxins
Including fuels, solvents (such
as carbon tetrachloride), and lead (and lead-based paint, pipes, and soldering
materials).
Fetal developmental problem
If the kidneys do not develop properly in the
unborn baby while it is developing in the womb.
Systemic lupus erythematosis
It is an autoimmune disease. The
body's own immune system attacks the kidneys as though they were foreign
tissue.
Malaria and yellow fever
It is known to cause impaired
kidney function.
Some medications
Overuse of, for example, NSAIDs
(non-steroidal anti-inflammatory drugs) such as aspirin or ibuprofen.
Illegal substance abuse
Such as heroin or cocaine.
Injury
A sharp blow or physical injury to the
kidney(s) can result in kidney disease.
Chronic
kidney disease treatment
There is no current cure for
chronic kidney disease. However, some therapies can help control the signs and
symptoms, reduce the risk of complications, and slow the progression of the
disease. Patients with chronic kidney disease typically need to take a large
number of medications. Treatments include:
Anemia treatment
Hemoglobin is the substance in
red blood cells that carries vital oxygen around the body. If hemoglobin levels
are low, the patient has anemia. Some kidney disease patients with anemia will
require blood transfusions. A patient with kidney disease will usually have to
take iron supplements, either in the form of daily ferrous sulphate tablets, or
occasionally in the form of injections.
Phosphate balance
People with kidney disease may
not be able to eliminate phosphate from their body properly. Patients will be
advised to reduce their nutritional phosphate intake - this usually means
reducing consumption of dairy products, red meat, eggs, and fish.
Vitamin D
Patients with kidney disease
typically have low levels of vitamin D. Vitamin D is essential for healthy
bones. The vitamin D we obtain from the sun or from food has to be activated by
the kidneys before the body can use it. Patients may be given alfacalcidol, or
calcitriol.
High blood pressure
High blood pressure is a common
problem for patients with chronic kidney disease. It is important to bring the
blood pressure down to protect the kidneys, and subsequently slow down the
progression of the disease.
Fluid retention
People with chronic kidney
disease need to be careful with their fluid intake. Most patients will be asked
to restrict their fluid intake. If the kidneys do not work properly, the
patient is much more susceptible to fluid build-up.
Skin itching
Antihistamines, such as
chlorphenamine, may help alleviate symptoms of itching.
Diet
Following a proper diet is vital
for effective kidney failure treatment. As mentioned above, restricting the
amount of protein in the diet may help slow down the progression of the
disease. Salt intake needs to be carefully regulated to control hypertension.
Potassium and phosphorus consumption, over time, may also need to be
restricted.
NSAIDs (non-steroidal anti-inflammatory
drugs)
NSAIDs, such as aspirin or
ibuprofen should be avoided and only taken if a doctor recommends them.
End-stage kidney
disease treatment
This is when the kidneys are
functioning at less than 10-15
percent of normal capacity. Measures used so far - diet, medications, and
treatments controlling underlying causes are no longer enough. The kidneys of
patients with end-stage kidney disease cannot keep up with the waste and fluid
elimination process on their own. The patient will need dialysis or a kidney
transplant in order to survive. Most doctors will try to delay the need for
dialysis or a kidney transplant for as long as possible because they carry the
risk of potentially serious complications.
Kidney dialysis
Peritoneal dialysis is a
treatment option for chronic kidney disease. This is the removal of waste
products and excessive fluids from blood when the kidneys cannot do the job
properly any more. Dialysis has some serious risks, including infection.
There are two main types of
kidney dialysis.
Hemodialysis
Blood is pumped out of the
patient's body and goes through a dialyzer (an artificial kidney). The patient
undergoes hemodialysis about three times per week. Each session lasts for at
least 3 hours.
Peritoneal dialysis
The blood is filtered in the
patient's own abdomen; in the peritoneal cavity which contains a vast network
of tiny blood vessels. A catheter is implanted into the abdomen, into which a
dialysis solution is infused and drained out for as long as is necessary to
remove waste and excess fluid.
Kidney transplant
A kidney transplant is a better
option than dialysis for patients who have no other conditions apart from
kidney failure. Even so, candidates for kidney transplant will have to undergo
dialysis until they receive a new kidney.
The kidney donor and recipient
should have the same blood type, cell-surface proteins and antibodies, in order
to minimize the risk of rejection of the new kidney. Siblings or very close
relatives are usually the best types of donors. If a living donor is not
possible, the search will begin for a cadaver donor (dead person).
•
1. Applied
Therapeutics: The Clinical Use Of Drugs, 9th Edition by Koda-Kimble, Mary Anne;
Young, Lloyd Yee; Alldredge, Brian K.; Corelli, Robin L.
•
2.
Pharmacotherapy Handbook Seventh Edition by Barbara G. Wells, PharmD, FASHP,
FCCP, BCPP & Joseph T. DiPiro, PharmD, FCCP
•
3.clinical
Pharmacy & therapeutics by Roger walker
•
4. U.S.
Department of Health and Human Services. Healthy People 2010. 2nd ed. With
Understanding and Improving Health and Objectives for Improving Health. 2 vols.
Washington, DC: U.S. Government Printing Office; November 2000.
•
5. Henrich WL et
al. Analgesics and the kidney: summary and recommendations to the Scientific
Advisory Board of the National Kidney Foundation from an Ad Hoc Committee of
the National Kidney Foundation. Am J Kidney Dis 1996;27:162.
•
6. Bennett WM et
al. The renal effects of nonsteroidal anti-inflammatory drugs: summary and
recommendations. Am J Kidney Dis 1996;28 (Suppl 1):S56.
•
7. Perneger TV
et al. Risk of kidney failure associated with the use of acetaminophen,
aspirin, and nonsteroidal antiinflammatory drugs. N Engl J Med 1994;331:675.
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