Presentation on Acute Renal Failure

8/3/2019 Presentation on Acute Renal Failure

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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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Presentation on Acute Renal Failure

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