presentation on acute renal failure
TRANSCRIPT
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ACUTE RENAL FAILURE
PRESENTER DR GEORGE KASONDA
FACILITATOR DR J NTOGWISANGU
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Topic layout
Definition
Categories of ARF
Etiology and pathophysiology of each:(prerenal, renal, post renal ARF)
References
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Definition
Syndrome characterized by:
Rapid loss of kidney function
Which will result in accumulation of metabolicwaste products.
Disturbance of body homeostasis,
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Categories
THREE CATEGORIES
1. PRERENAL ARF (55%)
2. RENAL ARF(40%) 3. POST RENAL ARF(5%)
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Prerenal ARF
This is due to the decrease in blood flow to
the kidney.
Most common among hospitalize patient Rapidly reversible upon restoration of Blood
Volume
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PRERENAL ARF
kidneys normally receive an abundant blood supplyof about 1100 ml/min, or about 20 to 25 % of cardiacoutput
So, decreased renal blood flow is usuallyaccompanied by decreased GFR and decreased urineoutput of water and solutes.
Hence conditions that acutely diminish blood flow to
the kidneys cause oliguria. If renal blood flow is markedly reduced, total
cessation of urine output can occur -anuria.
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Pre.
As long as renal blood flow does not fall below
about 20 to 25 per cent of normal, ARF can
usually be reversed if the cause of the
ischemia is corrected before damage to the
renal cells has occurred
Kidney can endure a relatively large reduction
in blood flow before actual damage to the
renal cells occurs.
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Pathophysiology and autoregulation Loss of autoregulation and increased renal vasoconstriction:
the role of increased cytosolic and mitochondrial calcium.
Acute ischemic injury has been shown in experimental
animals to be associated with a loss of renal autoregulation (.
Moreover, rather than the normal autoregulatory renal
vasodilation that occurs during a decrease in renal perfusion
pressure, there is evidence that renal vasoconstriction
actually occurs in the ischemic kidney. An increase in the
response to renal nerve stimulation has also been observed
in association with an acute ischemic insult . Moreover, thevasoconstrictor response to exogenous norepinephrine and
endothelin has been observed to be increased in the acutely
ischemic kidney may be related to the resultant increase in
cytosolic calcium observed in the afferent arterioles of the
glomerulus.
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Causes of Prerenal ARF:
-Extracellular fluid loss
-Burn injury,Diarrhea
-Diuresis
-Major upper gastrointestinal hemorrhage
Inadequate Cardiac output
Severe Congestive cardiac failure
Renal Vasoconstriction
NSADs inhibit cyclooxygenase Depletes renal vasodilatory eicosanoids
Exacerbates vasoconstriction afferent arterioles
ACE Inhibitor --lower renal perfusion
Result in dilated efferent arterioles
Decrease Glomerular Filtration Rate
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Intrarenal ARF
Diseases that directly involve renal parenchyma.
Intra renal ARF is divided into conditions that
damage:1.Renal tubular epithelium (ATN)- ischemic or
nephrotoxic
2.Glomerular capillaries (GN)3.Renal interstitium.
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: 1.renal tubular epithelial damage
Most common cause of intrarenal ARF is triggered by
ischemia (ischemic ARF) or nephrotoxins(nephrotoxic
ARF) causing ATN(acute tubular necrosis)
Ischemic ARF -renal hypoperfusion causes ischemic
injury to tubular epithelium-3 phases:
1.initiation (hrs-days) GFR Decline
2.maintenance phase(1-2wks)-GFR stabilises3.recovery phase-marked diuresis.
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ATN due to toxins or medication
(nephrotoxic ATN) Carbon tetrachloride
Heavy metals (such as mercury and lead),
ethylene glycol, various insecticides,
Medications such as tetracyclines,cis-
platinum, acyclovir, amphotericinB etc.
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Cont.. nephrotoxic ATN
Nephrotoxic ARF- damage to kidneys by nephrotoxicpharmacologic agents.
Incidence is increased in elderly and pts with prexistingchronic renal insufficiency, effective hypovolemia or exposure
to other toxins.
Egs:1.radiocontrast agents and cyclosporin-intrarenalvasoconstriction->decrease GFR
2. antibiotics and cancer drugs- direct toxicity to tubules
epithelial cells and or intratubularobstruction(aminoglycosides, acyclovir,amphotericin B)
3. endogenous nephrotoxins- calcium, urate oxalate,myeloma light chains.
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2.Glomerulonephritis
caused by an abnormal immune reaction thatdamages the glomeruli.
In about 95 %of the pts, damage to the glomeruli
occurs 1 to 3 weeks after an infection elsewhere inthe body, usually caused by group A betastreptococci.
antibodies develop against the streptococcal antigen
-> Ag-Ab immune complexes which get depositedonto glomerular basement membrane.
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Cont.. of GN
The acute inflammation of the glomeruli usually
subsides in abt 2 weeks, and in most patients,
kidneys return to almost normal function within the
next few weeks to few months. Sometimes, many of the glomeruli are destroyed
beyond repair, and in a small percentage of patients,
progressive renal deterioration continues -> chronic
renalfailure
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2. Acute TubularNecrosis(ischemic
ATN and nephrotoxic ATN)
Severe ischemia of the kidney can result from
circulatory shock or any other disturbance that
severely impairs blood supply to the kidney.
If the ischemia is severe enough to seriously impairthe delivery of nutrients and oxygen to the renal
tubular epithelial cells, + if the insult is prolonged,
damage or eventual destruction of the epithelial cells
can occur.
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Ischemic ATN
tubular cells slough off and plug many of
the nephrons, so that there is no urine output
from the blocked nephrons
Most common causes of ischemic damage to
the tubular epithelium are the prerenal causes
of acute renal failure associated with
circulatory shock.
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Postrenal ARF
Diseases associated with urinary tract
obstruction.
obstruction of the urinary collecting systemanywhere from the calyces to the outflow
from the bladder.
Most common causes of obstruction of the
urinary tract outside the kidney are kidney
stones.
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Postrenal ARF
abnormalities in the lower urinary tract can block orpartially block urine flow and therefore lead to ARFeven when the kidneys blood supply and other
functions are initially normal. If the urine output of only one kidney is diminished,
no major change in body fluid composition will occurbecause the contralateral kidney can increase itsurine output sufficiently to maintain relativelynormal levels of extracellular electrolytes and solutesas well as normal extracellular fluid volume.
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Postrenal ARF
But chronic obstruction of the urinary tract, lasting forseveral days or weeks, can lead to irreversible kidneydamage.
Causes of postrenal ARF include:
1. Ureteric (calculi,blood clot,cancer,external compression)
2. bladder neck obstruction(neurogenic bladder, prostatehypertrophy, calculi, cancer).
3. obstruction of the urethra(stricture, congenital valve).
During early stages, continued GFR leads to increasedintraluminal pressure upstream->distension of proximalureter, pelvis, calyces->fall in GFR eventually.
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References
Guytons TextBook of Medical Physiology
Harrisons Principles of Internal Medicine.
www.google(family medicine.com).
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1.clinical feature,compesantion,management.