Acute Renal Failure/Kidney Injury Flashcards
Define ARF
- clinical syndrome of sudden onset of haemodynamic, filtration and excretory failure of kidneys
- subsequent accumulation of metabolic (uraemia) toxins and dysregulation of fluid, electrolyte and acidness balance
Define ARF
- clinical syndrome of sudden onset of haemodynamic, filtration and excretory failure of kidneys
- subsequent accumulation of metabolic (uraemia) toxins and dysregulation of fluid, electrolyte and acidness balance
Define AKI
- acute kidney injury
- abrupt decline in kidney function
- acute ^ in creatinine concentration and/or acute decline in urine output (even if patient has not become azotaemic)
Is ARF reversible?
Potentially if dx early and animal supported while renal injury repaired
- irreversible renal damage may occur -> death
Define oliguria. How does its cause affect tx?
typically
How does ARF present? How can it be diagnosed?
- many cases no hx or CS
- potentially known toxin ingestion
- anuric/polyuric
- more often, lethargy, unwell, V+ or azotemia detected on bloods
- ureic signs (smell, ulcers etc.)
- dehydration
- brady/tachycardia
- painful kidneys
Define AKI
- acute kidney injury
- abrupt decline in kidney function
- acute ^ in creatinine concentration and/or acute decline in urine output (even if patient has not become azotaemic)
Is ARF reversible?
Potentially if dx early and animal supported while renal injury repaired
- irreversible renal damage may occur -> death
Clinical signs of ARF?
- anuria and oliguria characterise severe forms
- does NOT occur in all cases
- some will be PU
- NB: GFR does NOT = urine output
> GFR can v as urine output ^ if reabsorption is becoming less effective
How can pre-renal and renal azotemia be differentaited?
- need urine and bloods obtained simultaneously (before starting IVFT)
> USG >1.035 [cat] or >1.030 [dog] for pre-renal, 1.007-1.025 typically for a 1* renal
> urine sediment inflam/casts with 1* renal sometimes
> dipstick may show glycosuria in 1* renal sometimes - no biochem results can be used to make a distinction BUT hyperkalaemia more common in ARF or post-renal causes (though can occur in terminal phases of CKD
- respnse to fluid tx dramatic with pre-renal, minimal if renal cases
How does ARF present? How can it be diagnosed?
- many cases no
Can pre-renal azotemia ever be present when USG
Yes : diuretics or drugs affecting concentrating ability (functional impediment to urine concentration)
- fluids, diuretics, glucocorticoids, Addiosons, hypercalcaemia
> can be better prognosis if functional renal failure present rather than structural intrinsic renal disease (where nephrons have physically been lost)
Causes of post-renal azotemia?
- urethral obstruction
- bladder rupture
Causes of pre-renal azotemia?
- severe dehydration
- shock
- any condition -> poor renal perfusion
How can pre-renal and renal azotemia be differentaited?
- need urine and bloods obtained simultaneously (before starting IVFT)
> USG >1.035 [cat] or >1.030 [dog] for pre-renal, 1.007-1.025 typically for a 1* renal
> urine sediment inflam/casts with 1* renal sometimes
> dipstick may show glycosuria in 1* renal sometimes - no biochem results can be used to make a distinction BUT hyperkalaemia more common in ARF or post-renal causes (though can occur in terminal phases of CKD
- respnse to fluid tx dramatic with pre-renal, minimal if renal cases §
DO failing kidneys produce dilute urine?
NO! Canot dilute so hyposthenuria does NOT occur in kidney failure
Can pre-renal azotemia ever be present when USG
Yes : diuretics or drugs affecting concentrating ability (functional impediment to urine concentration)
- fluids, diuretics, glucocorticoids, Addiosons, hypercalcaemia
> can be better prognosis if functional renal failure present rather than structural intrinsic renal disease (where nephrons have physically been lost)
How can ARF and CKD be differentiated?
- NO LAB TESTS! Hyperphosphatemia seen with both acute and chronic
> Except renal BIOPSY (but this is invasive and results take a long time) - PE: poor BCS, poor quality haircoat
- Hx: wt loss, v apetite, PUPD v hx of access to nephrotoxic drugs or toxins
- non-regenerative anaemia typically with CKD but can occour with ARF (eg. d/t haemorrhagic shock) or overhydration
- renal size (generally v with CKD, ^ with ARF but some chronic dz -> normal/^ kidney size)
- presence of CKD mineral bone disorder (renal 2* hyperparathyroidism) : resorption of bone esp. around the teeth
> NB: rubber jaw may be a presenting sign but very rare and only seen in young growing animals
3 main causes of acute renal failure?
> pre-renal
intrinsic renal
- tubular necrosis (v. common) d/t ichaemia or toxins or both
- interstitial nephritis (common)
- acute glomerulonephritis (uncommon, next lect)
post-renal
What is hospital acquired ARF/AKI?
- ischaemia and toxin effects on kidney working synergistically -> tubular necrosis
- eg. CV dz pre-existing, age, fever, dehydration, drugs
Cause and clinical signs of pyelonephritis? How is it diagnosed?
> ascending UTI -> renal pelvis and medulla causing an INTERSTITIAL NEPHRITIS
CS
- systemic illness (fever, renal pain, nephromegaly)
- BUT signs may be absent
- PUPD esp with E. Coli
- can cause acute/chronic renal azotemia
Dx presumptive based on cultures obtained from LUT, imaging and hx findings
- if pelvis dilated can aspirate for culture under u/s guidance
Tx pyelonephritis?
As for complicated UTIs (selection of ABx based on culture, 4-6w tx, cultures a week after starting and finishing tx)
What infectious organism also causes an interstitial nephritis?
> Leptiospriosis
- ZOONOTIC
- spirochete bacteria (each serovar typuically has 1+ host species that carry the organism asymptomatically and shed in the urine)
Clinical signs of leptospirosis in a non-host organism>
- ARF
- hepatocellular necoris
Most common route of infection of leptospirosis?
- contaminated water
> most commonly now non-vaccinal serovars that affect dogs (ie. not canicola or icterohaemorrhagica)
Do cats get lepto?
No resistant
How can lepto be dx?
- high Ab titre to non-vaccinal serovars
- rising titre over a few weeks
- PCR (not very sensitive, maybe d/t Ab use before testing?)
Tx leptospirosis?
- tx ARF
- penicillins (usually amoxicillin)
- if dx confirmed then 2w course doxycycline prescribed to eliminate infection and prevent dog become a chronic carrier
What must be remembered about lepto?
ZOONOTIC
- carefully manage patients, don’t come into contact with urine
2 causes of tubular necrosis?
> ischaemia
- outer medulla exists in a constant state of oxygen deprivation
- cells of PCT high metabolic rate
- mitochondrial injury, cell swelling, tubular obstruction
- d/t yhpovolaemia, v effective circulating volume (heart failure/cirrhosis), thrombosis, excessive renal vasoconstriction
- pre-renal azotemia can -> renal d/t ischameia if hypoperfusion not rectified
toxins
- may occour concurrently and synergistically with ishaemia
- often leaves some BM intact so if given the supportive tx kidneys can recover
Egs of nephrotoxic drugs and substances?
> drugs - Abx (aminoglycosides, tetracyclines, amphotericin B [fungal]) - chemotx (doxorubicin [cats], cis and carboplatin, methotrexate) - NSAIDs - ACEI - IV contrast agents > other - hypercalcaemua - rasins/grapes (dogs) - ethylene glycol (cats) - plants [lillies] (cats) -myoglobin/haemoglobin - heavy metals - pesticides/herbicides - snake venom
3 miscellaneous causes of ARF/AKI?
> lyme disease - borrelia burgdorferi - acute glomerular disease > Renal lymphoma > cutaneous/renal vascular glomerulopathy (New FOrest Syndomre/Alabama Rot) - thrombotic microangiopathy
How can ARF be prevented?
> some unavoidable (toxins etc.)
in the hospital ID patients at high risk
- pre-existing CKD
- dehydrationhypovolaemia/hypotension
- sepsis/fever/hyperthermia
- systemic dz/multiple organ failure
- prolonged anaesthesia
- drug tx (NSAIDs, aminoglycosides, cisplatin, amphotericin, ACEI)
more effectively prevented by correcting fluid deficits and mild ECF volume expansion
Tx ARF/AKI?
aim to maintain the animal while kidneys repair themselves
> prevent continued toxin exposure or give antidotes
- induce vomiting, NB: maintain euvolaemia
- 4-methylpyrazole for ethyleme glycol $$$
> Tx 1* underlying disease if possible
> correct fluid deficits
- monitor in and outs to prevent overhydration
- aim for mild 3-5% ECVF fluid expansion
> Recitfy potassium and acid/base balance
> attempt to ^ urine output if required
- NB: urine output does NOT = GFR
> other pharmacological tx
- controversial and infrequently used
> control V+
- address nutritional requirements
> renal replacement tx
- haemodialysis or peritoneal dialysis
Give examples of drugs that can be used to attempt to ^ urine output if necessary?
> mannitol
- slow IV bolus
- ^ renal blood flow, v cellular swelling, dispense tubular debris and scavenge free radiacal (Appaz)
- indicated early in course of ARF but animal MUST BE EUVOLAEMIC, not in hert failure or overhydrated
- only useful if already producing some urine
- rarely used
furosemide
- boluses or CRI
- +- other drugs
- promotes formation of urine, facilitates management of overhyration and hyperkalaemia
- may deplete circulating volume -> pre-renal insult
Which other pharmacological tx may be used 9controversially) with ARF?
> dopamine
- suggested to cuase renal vasodilation and ^ blood flow at low dodses
- not recommended unless ^ BP needed- high doses -> tachycardia, arrhythmias, vasoconstriction
- do not use in cats
Fenoldopam
- selective DA1 ag sometimes used in preference
Diltiazem
- pre-glomerular arteriolar dilation and improve renal blood flow
- v calcium influx into damaged tubular cells may also be beneficial
Can extensive tubular injury be repaired?
- even if potentially reversible usually not possible to keep patients alive for weeks/months like humans on dialysis to allow regeneration
What can be used as an earlier indicator of acute renal failure?
Enzymeuria (occurs before azotaemia begins)
