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AKI
continuum from inapparent nephron injury or loss to _______________
prevalence
estimated to affect _______________% of _______________ horses
acute renal failure; 3-23; hospitalized
AKI - Risk factors
decreased _______________ and _______________
_______________
_______________
other causes
renal blood flow; hypoxia; SIRS; nephrotoxicity
AKI - Risk factors
decreased renal blood flow and hypoxia
kidney, esp the _______________, is susceptible to ischemic injury due to:
_______________
_______________
_______________
_______________
medulla; hypotension; dehydration; hypovolemia; anemia
AKI - Risk factors
SIRS
systemic inflammation from sepsis or endotoxemia
can cause _______________ injury, renal _______________ dysfunction and renal _______________
hypotensive; microcirculatory; cortical necrosis
AKI - Risk factors
Nephrotoxicity
Drugs
_______________
_______________
_______________
_______________
_______________
Others
_______________
_______________
aminoglycosides; oxytetracycline; bisphosphonates; NSAIDs; polymixin B; myoglobin; hemoglobin
AKI - Risk factors
nephrotoxicity
higher risk in _______________, _______________ horses and with the use of _______________ drugs
foals; older; nephrotoxic
AKI - Risk factors
other causes
_______________ injury
e.g. _______________
_______________ reactions
infections
_______________
_______________
immune-mediated glomerular; Purpura hemorrhagica; hypersensitivity; Actinobacillus; Lepto
What should you ALWAYS do before admin of aminoglycosides, oxytetracycline, NSAID, biphosphonates or polymixin B?
check CREATININE
T/F: Aminoglycosides are nephrotoxic due to admin of them at high doses
False (toxic due to MULTIPLE ADMIN, NOT high doses)
NSAIDs**
mechanism of nephrotoxicity
inhibition of COX blocks renal autoregulatory response to _______________
causes _______________ and _______________
hypoperfusion; medullary crest necrosis; interstitial nephritis
T/F: Selective COX2 inhibitors spare the GIT
True (BUT have similar renal effects as non-selective NSAIDs)
T/F: Selective COX2 inhibitors have less renal effects than non-selective NSAIDs
False (they have SIMILAR renal effects)
AKI
CS
_______________
_______________ lethargy
_______________
_______________ signs
inappetence; persistent (longer than excepted); oliguria; neuro
AKI
CS
oliguria
< _______________
neuro signs
_______________
0.5 ml/kg/hr; uremic encephalopathy
AKI - Dx
bloodwork
_______________ and _______________
urine output
challenging to measure in adult horses
_______________ and _______________ are key indicators
inc creatinine; BUN; oliguria; anuria
What are the way you can Dx AKI?
bloodwork (creatinine, BUN), urine output, U/A, imaging
AKI - Dx
U/A
microscopic _______________
_______________
_______________
_______________ USG despite _______________
hematuria; casts; glucosuria; low; hypovolemia
AKI - Dx
imaging
renal _______________ is often unremarkable
renal _______________ is NOT recommended
US; biopsy
Decreased urine production is a hallmark of what?
AKI
AKI - Bloodwork
Creatinine: _______________
BUN: _______________
USG: _______________
FENa (fractional excretion of Sodium): _______________
inc; inc; low (<1.020); inc
AKI - Bloodwork
Urine output: _______________
Na: _______________
K: _______________
Cl: _______________
U/A: _______________
oliguria/anuria; dec; inc; dec; proteinurina, hematuria, casts
What does FENa do?
normal = pre-renal
inc = renal
(differentiates pre-renal and renal causes )
AKI - Initial treatment
correct _______________
_______________
give _______________ and _______________ after above
primary disorder; IVF; inotropes; vasopressors
AKI - Initial Tx
IVF
to normalize intravascular volume, BP, _______________ and _______________
inotropes and vasopressors for _______________ AFTER _______________
renal blood flow; GFR; persistent hypotension; fluid replacement
Treating ARF (acute renal failure)
treat _______________
Abx, Sx, etc
_______________
give _______________ → diuresis
oliguria or anuria → _______________
predisposing disease; IV volume expansion; crystalloids; single dose of furosemide
AKI - Monitoring and support
_______________ by _______________% within _______________ indicates REVERSIBLE AKI
dec creatinine (serum); 30-50; 24-72hr
AKI - Monitoring and support
aim to induce _______________ and _______________ in oliguria/anuria cases
_______________ test for predicting _______________ and outcome of AKI
diuresis; polyuria; furosemide challenge; severity
AKI - Tx
_______________ can be done in SELECT cases with persistent _______________ and high _______________ levels
peritoneal dialysis; oliguria; nephrotoxic drug
AKI - Prognostic indicators
early detection and management improve outcomes
better prognostic indicator
_______________ > _______________
IVFT response; severity of initial INC creatinine
AKI - Prognostic indicators
_______________ with _______________ = guarded to poor prognosis
_______________ = GRAVE prognosis
persistent azotemia; oliguria/anuria; uremic encephalopathy
AKI - Prognostic indicators
persistent azotemia with oliguria/anuria = _______________ prognosis
uremic encephalopathy = _______________ prognosis
guarded to poor; grave
AKI - prognosis (long-term outlook)
sCr (serum creatinine) may normalize within _______________ post-injury
horses with _______________ sCr
likely have sufficient real function for a _______________ lifespan
but may have residual _______________ predisposing them to future renal issues
2-6m; near-normal; normal; damage
AKI
Prevention
close monitoring of _______________ in at-risk patients
management
prompt correction of primary dz, _______________ and _______________
cautious use of _______________ and avoiding simultaneous use of multiple nephrotoxic agents
creatinine; hypovolemia; hypotension; nephrotoxic drugs
CKD
definition
_______________ disease of the kidneys lasting more than _______________
staging
based on _______________ levels
similar to _______________ staging system for small animals
irreversible, progressive; 3m; sCr; IRIS
CKD - causes
_______________ of development
chronic _______________
_______________
_______________ causes
_______________ kidney disease
anomalies; interstitial nephritis; glomerulonephritis; infiltrative; end-stage
CKD - causes
anomalies of development
renal _______________
renal _______________
renal _______________
_______________ disease
agensis; hypoplasia; dysplasia; polycystic kidney
CKD - causes
chronic interstitial nephritis (CIN)
often follows _______________ from ischemia or nephrotoxicity → interstitial _______________
can also result from _______________ → _______________
_______________ often found with CIN
acute tubular necrosis; fibrosis; ascending UTIs; pyelonephritis; nephrolithiasis
CKD - causes
glomerulonephritis
_______________ inflammation
often associated with _______________ infections or _______________ conditions
causes _______________ and _______________
immune-mediated; chronic; autoimmune; proteinuria; hematuria
CKD - causes
infiltrative causes
_______________
_______________
_______________
_______________
neoplasia (LSA, carcinoma); nephroblastoma; amyloidosis; Halicephalobus gingivalis
CKD - causes
end-stage kidney disease
final stage of CKD
characterized by _______________ kidneys with _______________ surface and _______________ capsule
pale, shrunken, firm; irregular; adherent
CKD
CS
general
loss of _______________
decreased performance
_______________
urinary
mild to moderate _______________
CV
_______________
body condition; ventral edema; PU/PD; HYPERtension
CKD
CS
oral cavity
_______________
_______________
oral _______________
GI
_______________
dental tartar; gingivitis; ulcers; ulcers
CKD - Dx
subclinical detection
often _______________
most horses show ______________ (_______________) when CS 1st recognized
incidental; moderate to severe azotemia; IRIS stage III and IV)
CKD - Dx
bloodwork:
creatinine: _______________
BUN: _______________
_______________
_______________
_______________
INC; INC; mild anemia; INC Ca; DEC P
CKD - Dx
U/A
_______________
_______________
_______________
isothenuria (1.008 - 1.014); proteinuria; hematuria
CKD - Dx
imaging
_______________ kidneys on US
_______________ with _______________
small, irregular; enlarged ureters; ureteroliths
CKD - general management
free access to _______________
dietary adjustments
_______________ pasture
increased _______________
add _______________
monitor _______________
fresh water; good quality; carbs; fats; protein
CKD - general management
avoid _______________ supplementation
management of hypercalcemia with LOW Ca feeds
_______________ instead of _______________
excessive salt; grass hay; alfalfa
CKD - general management
potential use of _______________ and _______________
supportive care
monitor _______________, appetite, hydration status and renal function
omega-3 fatty acids; vit E; body condition
CKD - medical Tx
_______________ for any acute component or dehydration
glomerulonephritis
give _______________
give _______________
_______________ if it is causing persistent sepsis, pain, or obstructing urine flow
IVFT; corticosteroids; ACEi (benazepril, ramipril); nephrolith removal
What do ACEi do to help with CKD?
control BP, dec proteinuria, slow fibrosis
Bladder rupture
causes
_______________
_______________ injuries
_______________
trauma; foaling; obstructive urolithiasis
Bladder rupture
CS
abdominal distention
_______________ signs
dysuria
Dx
abdominal US
will see _______________
urine output
_______________ or _______________
colic; free abdominal fluid; decreased; absent
Bladder rupture - Dx
abdominocentesis
_______________:
fluid > serum
ratio _______________
bloodwork
_______________
_______________
_______________
creatinine; >2; azotemia; hyperK; hypoNa
Bladder rupture
Tx
_______________
supportive
_______________
_______________
Sx; IVF; Abx
If you have a foal come in with uroperitoneum, hyperkalemia, hyponatremia and azotemia what is the FIRST thing you should do?
stabilize (NOT Sx emergency and need to stabilize FIRST)
Ureteral (urethra??) rupture → _______________ → _______________
SQ urine; PAIN
Urolithiasis
types
_______________ = most common
_______________ = less common
Ca carbonate; Ca oxalate
Urolithiasis
pathogenesis
dietary factors
_______________ intake
imbalanced _______________
_______________
_______________
_______________ predisposition
high Ca; Ca:P ratio; dehydration; UTI; genetic
Urolithiasis
CS
_______________
_______________
_______________
hematuria; dysuria; pollakiuria
Urolithiasis
CS
_______________ signs
_______________
decreased _______________
colic; urine scalding; performance
Urolithiasis - Dx
Hx and CS
PE
palpation of _______________ and _______________
U/A
presence of ______________ and _______________
_______________
bladder; urethra; crystals; blood; INCREASED pH
Urolithiasis - Dx
Imaging
_______________ to visualize stones (bladder, kidney, ureter)
_______________
US; cystoscopy
Urolithiasis - Tx
_______________
_______________
_______________
medical management; Sx removal; lithotripsy
Urolithiasis - Tx
medical management
dietary modifications
reduce _______________ intake
adjust _______________
increase _______________
pain management
_______________
Ca; Ca:P ratio; water intake; NSAID