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
