The Kidney Drama (notes)

7/17/2019 The Kidney Drama (notes)

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The Kidney Drama: Acute Kidney Injury and Chronic KidneyDisease

Defnition o AKI:A Sudden impairment of kidney function which results in retention ofnitrogenous and other waste products normally cleared by the kidneys.

OR

Acute kidney injury is dened as an abrupt (within 48 hours) reduction inkidney function based on an eleation in serum creatinine leel! areduction in urine output! the need for renal replacement therapy(dialysis)! or a combination of these factors

Comparision& Defnition o AKI / CKD / AKD(Acute Kidney Disease / !KD (!o "no#n "idneydisease



$pidemio%oy• A"# complicates about $% & ' of acute care hospital admissions and

' of admissions to the #*+

• #t is a major medical complication

$tio%oy and 'resentation*auses of A"# hae been classically diided into three broad categories

• ,re%renal

• -enal

• ,ost -enal (usually obstruction)

'R$R$!A)*auses of ,re%-enal A"#

% /ypoolemia

% 0ecreased *ardiac 1utput% 0ecreased e2ectie circulating olumeo **3o ier 3ailure

% #mpaired -enal Autoregulationo 5SA#0s

o A*6i7A-o *yclosporin

Pre-Renal Explanation% -emember that about 9' of our *ardiac 1utput comes out to the

"idneys% #s the most common form of A"#% :he ,athophysiology is that there is a rise of *r 7 +5 concentration

due to inade;uate renal plasma <ow and intra%glomerular hydrostaticpressure to support normal glomerular ltration.

% y denition it S/1+0 not lead to parenchymal changes and is rapidlyreersible once intraglomerular hemodynamics are restored.

% /oweer prolonged periods of this pre%renal a=otemia may lead toischemic injury termed >acute tubular necrosis? (A:5)

•5ormal @3- is maintained by relatie resistance from the a2erentand e2erent (eiting) arterioles which would determine

o @lomerular ,lasma 3lowo :ranscapillaryhydraulic pressure gradient

• Bild degree of hypoolemia and reductions in in cardiac output elicit

compensatory renal physiological changes.

• @3- can be maintained despite reduced renal <ow by A:## mediatedrenal e2erent asoconstriction and also autoregulation mechanisms.(insert action of A:## here from B-*, book)

o /oweer there is a limit to these mechanisms and it will

eentually decompensate



• :here are a number of factors which determine the robustness ofthe auto%regulatory response and thereby the risk of pre%renal injury

o ArtherosclerosisC longstanding /:5

/ylanosis and myointimal hyperplasia causing structural

narrowing of the intrarenal arterioles and impairedcapacity for renal a2erent asodilatation.

o #n *"0 renal a2erent asodilatation will be operating at

maimal capacity to maimi=e @3- in response to reducedfunctional renal mass.o 0rugs can a2ect the compensatory changes needed to

maintain @3- 5SA#0 inhibit ,@ production (,@69! ,rostacycline)

• limit a2. Dasodilat

A*6i and A- limit e2erent asoconstriction (inhibit

A:##)

• 6ample for those with -AS E because renale2erent asoconstriction is needed to maintain@3- due to low renal profusion.



R$!A)/I!TRI!*IC

Intrinsic Causes :

• @lomerular E Acute @lomerular 5ephritis

• :ubuleso #schemia (A:5)o Sepsis 7 infectiono 5ephrotoins

6ogenous #odinated contrast! Aminoglycosides! *isplatin!

Amphothericin

6ndogenous /emolysis! -habdomyolysis! Byeloma!#ntratubular *rystals! B:F! +ric Acid (:umor ysis)

o Dascular

Dasculitis

Balignant /ypertension

::, 7 /+S

-enal artery embolus! -enal Dein thrombosis

• #nterstitiumo Allergic (,*5! -ifampicin)o #nfection (seere pyelonephritis! egionella! Sepsis)

o #nltration (ymphoma! eukemia)o #n<ammatory (Sjogren! :ubointerstitial nephritis! Sepsis)

Intrinsic Explanation

• :he most common causes are sepsis! ischemia! nephrotoins(endogenous and eogenous)

• ,re%renal can adance to tubular injury

Peculiar Situations:

• Sepsis associated A"#

o 0ecrease in @3- can occur een without hypotensiono Some of the reasons why

in<ammation and interstitial oedema

/emodynamic e2ects of sepsis itself! arising from general

arterial asodilation mediated by cytokines that upregulateepression of 51 Synthase in the asculature (causingdilatation) reduces @3-

• #schemia associated A"#o /ealthy kidneys receied up to 9' of *1 and account for G'

of resting oygen consumption 0espite only constituting lessthen .$' of the :otal body mass

o 1ne of the most hypoic prone areas.



o :he outer medulla is ulnerable to ischemic damage because ofthe architecture of the blood essels that supply oygen andnutrients to the tubules.

'O*T Rena%

,ost -enal *auses

• ladder outlet

obstruction• ilateral peloureteral

obstruction

• asically any obstruction



Dianostic $+a%uation O AKI• Acute "idney #njury is asymptomatic until etreme loss of function is

reached and there are 51 characteristic clinical ndings.

• 0iagnosis usually occurs within the contet of another acute illness.

• ,resence of A"# is inferred by an eleation of Sr*r concentration.

Current defnition is (,ased on KDI-O -uide%ines

o *rCr rise o . 012mcmo%/) o+er 34 hour period

o *rCr rise . 5126 7ase%ine #hich is "no#n #ithin 8 days

o Reduction in urine output to 912m%s/"/hour or %onerthan 0 hours OR 299cc/day

• imitationso S*r is not a good marker on the basis that the relationship @3-

and Sr*r is a non linear relationshipo 1ften the earliest clue is the reduction in urine output

o

• Some important iochemistry markerso :able to do pre%renal and renal causes



*taes o AKI

*ome 'rincip%es ;anaement o AKI

51 Determine i there rea%%y is AKI or is it CKDG. ,oints towards A"#G. normal kidney prior to this ! normal renal function within

& days9. +S "+ normal 7 no renal parenchymal disease. 0isproportionate +r7*reat (ratio H 9)

9. ,oints towards *"0G. *omorbidities E 0B 7 /,: 7 history of analgesic abuse etc

9. Small 7 shrunken kidneys +: 56D6- 31-@6: arge"idneys (A0,"0)

. *ertain *"0 may hae normal si=ed kidneys%Byeloma!

0B! Amyloidosis! ,olycystic "idneys (often huge by thetime deelop *"0)

4. /yper%phosphatemia 7 /yper or /ypo%calcemia$. Anemia

1 Remo+e a%% antecedents to AKIG. -emoe all nephrotoic drugs9. Adjust 0rug doses

<1 Determine the cause o AKIG. -enal 7 ,re%-enal 7 ,ost -enal9. Assess <uid status. ook for signs of leeding



4. +S "+ E :-1 1bstructie uropathy

31 ;anae a%% )iethreatenin a7norma%ities

G. /yperkalemia (" H $.$)G. ytic *ocktail E G cc of *alcium gluconate G' gien oer G

mins ! glucose $' $cc and i insulin G units9. -esonium 7 1ral "alimate G$%9g :0S%I#0. Salbutamol nebuli=er

9. Seere Betabolic Acidosis (p/ J &.G)G. #ntubation if seere metabolic acidosis with respiratory

distress9. #D sodium bicarbonate Gcc oer G hour

= /oweer be careful in those K#:/1+: urine outputas it can cause hypernatremia and hypercarbiaandolume oerload (in oligouric7anuric patients)

. 3luid 1erloadG. *D insertion if unsure to monitor *D,9. # frusemide 4 E 8mg stat. *0 7 monitor urine output

4. /ypotension 7 /ypoolemiaG. #D 3luid boluses

= Aoid /6S 7 *olloids as it can cause more renalimpairment by irtue of large molecules

9. Bonitor urine output

21 >ydrate / >ydrate / >ydrate i it is a prerena% / rena% causeG. Strict i7o charting9. *0. Bonitor urine output

L. Decide or ear%y RRT / >D if any of the following present (i.e.indications for urgent /0) howeer be aware that the most accuratetiming for --: in A"# patients are not determined yet as moststudies are done in 6S-0 7 *"0 patients.

51 ?rea . 09 OR *ymptomatic ?remia (i.e. uremic pericarditis!encephalopathy! neuropathy) 51: omiting 7 nausea

9. >yper"a%emia (K. 012 refractory to medical therapy 1-associated with arrhythmias 7 6*@ changes at lower alues

. @%uid O+er%oad not responding to diuretics 7 anuric4. *e+ere ;eta7o%ic Acidosis (p> 815$. Dru A7use

, ,ar7ituates) )ithiumA A%coho% (;ethono% / ethano%

* *a%icy%ateT Theophy%%ine



'ronosis :59B #i%% proress to $*RDRena% Rep%acement Therapy in AKIThere are a %are num7er o moda%ities a+ai%a7%e

Intermittent >emodia%ysis (I>D

'eritonea% Dia%ysis ('D

Continuous Rena% Rep%acement Therapy (CRRT

o C>D@ (Continuous eno+enous>emodiaf%tration

o CA>D@ (Continuous Arterio+enous >emodiaf%tration

*ustained )o# $ciency >emodia%ysis (*)$D

Ehat is CRRT F

A family of modalities that proide continuous support to seerely ill

patients with A"# :here are two types *DD/03 and *AD/03

o ,referred to hae *DD/03 because it proides higher solute

clearances and eliminates the aderse complicationsassociated with arterial cannulation

o Surial *hances are the same in both groups in studies done

Ideas :CRRT * I>D * 'D

• Surial is similar in both groups if comparing *--: DS #/0

• /oweer in A groups there is no particular superior model in data

currently.

Some Benefts o CRRT over IHD

• onger 0ialysis hence continuous remoal of >bad? substances

• etter on lood ,ressure as it is slower compared to #/0 and S60hence able to be used for those een with ery low blood pressures1- on #onotropic support.

*ome inormation on Chronic Kidney DiseaseDefnition (as a7o+e



C%assifcation o CKD & Action '%ansSome Barkers of "idney 0amage

• ,roteinuria (+36B6 1- 94 hour urine protein 1- Albumin *reat-atio)

• -eduction of urine output

• Small Si=ed "idneys on +SRenal ultrasonography helps establish the diagnosis and prognosis by documentingthe size of the kidneys. Normal size indicates kidney disease that may be amenableto medical treatment. Small kidneys suggest irreversible disease. Asymmetry inkidney size suggests renovascular disease.

)on Term Rena% Rep%acement Therapy

• :here are two options for ong term --: as a wholeo /0o ,eritoneal 0ialysis



In our hospita%

• Ke would generally start workup if te patient is at *"0 9 already 1- ifserum *r is H 9

• Korkup usually that would be doneo +S "+o 6*/1

o Diral Screeningo :race aseline +rea and *reatinineo ,roper social history (S1*S1 7 6,3 7 @ot serant 7 /ome)

• :here is a 5ephrology #nformation Sheet to be gien to patients as well

• 1nce the patient is about *"0 4 aboe we would epect them todecline faster in terms of function hence preparation such as AD3formation

The Kidney Drama (notes)

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