Flashcards in Acute renal failure Deck (44):
- sudden onset haemodynamic, filtration and excretory failure of kidneys
- subsequent accumulation of metabolic/uraemic toxins
- dysregulation of fluid, electrolyte and acid-base balance
= Acute Kidney Injury
- may be preferred over ARF term
- abrupt decline kidney function
- acute increase in [creatinine] and/or acute decline in urine output even if patient hasn't become azotaemic
Is ARF reversible?
- yes potentially if diagnosed early after onset and animal is supported
- delay --> irreversible renal damage and death
CS - ARF
- oliguria and anuria characterise severe ARF (not always though)
- polyuric (sometimes)
Is urine output the same as GFR?
No - 99% fluid filtered by glomerulus is reabsorbed by the tubules. If this process becomes less effective and less reabsorption occurs, urine output may increase, even though GFR is declining
- variable definitions
What is physiologica oliguria?
- when oliguria occurs as result of normal hysiology
- if patient is hypovolaemic it is apprpriate for kidneys to conserve fluid and v. small urine volume to be produce
- appropriate tx is volume resuscitation, not diuretics
Dx - ARF
- no hx or PE are specific (dehydration, oral ulcer/uraemic colour, hypothermia, bradycardia/tachycardia, swollen painful kidneys or normal)
- occasioanlly known toxin ingestion or noted animal is anuric or polyuric
- usually unwell, lethargic or vomiting, azotaemia
What 2 quesitons should always be asked with newly documented azotaemia?
- pre-renal, renal or post-renal?
How do you differentiate acute and chronic azotaemia?
- PE incl. renal size
- non-regenerative anaemia
- renal ultrasound
- CKD-Mineral Bone Disorder (secondary hyperparathyroidism). Care - hyperphosphataemia occurs with acute and chronic disease
Causes - azotaemia
1. High production of nitrogenous waste (pre-renal, urea only)
2. Low GR (pre-renal with reduced renal perfusion, renal with intrinsic or functional renal disease or post-renal with urinary obstructin)
3. Reabsorption urine escaped from urinary tract (Post-renal)
When is UA indicated?
whenever blood tests are performed, especially when evaluating renal function
Differentiate pre-renal and renal azotaemia by USG?
Dog = >1.030
Cat = >1.035
UA findings - Renal azotaemia
- Ca oxalate
What is the response to IVFT with pre-renal and renal azotaemia?
- Good response with pre-renal. May or may not have a response with renal azotaemia
- cause: ascending infection most common
- may be PU/PD
- not always azotaemic
- consider breaches of UT defences
- treat aggressively
Breaches of UT defences that may --> pyelonephritis
- ANATOMICAL: ectopic ureters, perineal urethrostomy
- MEDICAL: diabetes, renal dz, nephroliths
- IATROGENIC: catheters, steroid therapy
Tx - pyelonephritis
- culture urine, empiric AB initially
- re-culture on tx, continue 4-6wks
- reculture 1-2 wks post-tx
Commonest leptospira serovars
CS - leptospirosis
- hepatic necrosis
Dx - leptospirosis
- rising titre to non-vaccinal serovar
- PCR available, lack sensitivity - perhaps since many have received ABs by time this test is run.
Tx - leptospirosis
- penicillins (usually amoxicillin)
- penicillin G or ampicillin
TO CLEAR INFECTION/ carrier status:
doxycycline, 2 weeks
3 main types of intrinsic renal failure
- TUBULAR NECROSIS (v common)
- INTERSTITAL NEPHRITIS (V common)
- ACUTE GLOMERULONEPHRITIS (uncommon)
What are the 2 types of tubular necrosis?
1. ischaemia (common)
2. toxins (common)
List toxins causing renal injury
* raisins/ grapes
* plants (lillies in cats)
- heavy meatals
- pesticides/ herbicides
- snake venom
- myoglobin/ haemoglobin
- calciferol rodenticides
Which therapeutic agents can cause renal injury?
- ANTIMICROBIALS: aminoglycosides, TCs, amphotericin B
- CHEMOTHERAPEUTICS: doxorubicin (cats), cisplatin and carboplatin, methotrexate
- IV CONTRAST AGENTS
- MANY MORE
Causes - ischaemic ARF/AKI
- reduced intravascular volume
- decreased effective intravascular volume (HF, cirrhosis)
- drugs (cyclosporine, NSAIDs, ACEI)
- vascular dz (thrombosis, vasculitis)
Why are PCT cells prone to ischaemic injury?
v high metabolic rate making them particularly vulnerable --> mitochondrial injury, cell swelling and tubular obstruction
T/F: a patient initially presenting with pre-renal azotaemia may progress to intrinsic renal azotaemia d/t ischaemia if hypoperfusion of kidneys not quickly rectified.
Causes - hospital acquired AKI
- advanced age
- cardiac dz
- pre-existing renal dz
- nephrotoxic drugs
Pathogenesis - hospital acquired AKI
- decreased glomerular ultrafiltration coefficient
- intra-tubular obstruction
- back-leak fluid across disrupted epithelium
- intra-renal vasoconstriction
Management principles - AKI/ARF
- tx inciting cause
- improve renal haemodynamics (mild volume expansion)
- maintain homeostasis (K, acid-base)
- supportive care (nutrition, control V)
- allow renal repair time to occur
Other causes ARF/AKI
- Lyme disease (B. burgdorferi) --> acute glomerular dz
- Renal lymphoa
- cutaneous and renal vascular glomerulopathy ('New Forest Syndrome in UK, 'Alabama rot' in USA): caused by a thrombotic microangiopathy
Which animals are at particular risk of ARF?
- pre-exisiting CKD
- dehydration/ hypovolaemia/ hypotension
- sepsis/ fever / hyperthermia
- systemic dz/ multiple organ failure
- prolonged anaesthesia
- drugs (NSAIDs, aminoglycosides, cisplatin, amphotericin, ACEI)
What is the most consistent renal protective effect?
correction of fluid deficits and mild ECF volume expansion
Antidote - EG
4-methylpyrazole (but prohibitively expensive in UK)
How much should you aim to expand ECF volume?
mild (3-5%) increase. REquires v vareful monitoring including serial measurements of body weight, urine output, CVP, PCV/TP and repeated PE
Name 2 drugs that increase urine output
- MANNITOL: if early in ARF course if not hypovolaemic, already overhydrated or in CHF. Thus rarely used.
- FUROSEMIDE: to promote urine formation, manage overhydration and hyperkalaemia. Improper monitoring --> pre-renal insult on established renal injury
Outline use of Dopamine in ARF
- catecholamine suggested to cause renal vasodilation and improved BF at low dose
- CONTROVERSIAL: should only be used if required to maintain BP
- high dose --> vasoconstriction, tachycardia and arrhythmias
- NOT in cats
- acts on both DA-1 and DA-2 receptors
- Fenoldopam is a selective DA-1-R agonist sometimes used preferentially
- diltiazam suggested as alternative
Outline diltiazem as alternative to dopamine in ARF
- causes pre-glomerular arteriolar dilation and improves renal BF
- reduced Ca influx into damaged tubular cells may also be beneficial
Can you tx ARF directly?
- maintain the animal while the kidneys repair
- usually not possible to keep patient alive for weeks-months if extensive tubular injury has occurred for their repair
- measure enzymes in urine
- early indicator of AKI (before azotaemia)
- e.g. NAG, yGT, N-Gal
- monitor when tx with nephrotoxic drugs
Parameters to measure fluid balance with AKI patients
- 'ins and outs'
- serial body weight
- serial PE
- serial PCV/TP
- OTHERS (electrolytes, ECG, renal function q48-72h)