Acute renal failure Flashcards
1
Q
Define ARF
A
- sudden onset haemodynamic, filtration and excretory failure of kidneys
- subsequent accumulation of metabolic/uraemic toxins
- dysregulation of fluid, electrolyte and acid-base balance
2
Q
Defome AKI
A
= 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
3
Q
Is ARF reversible?
A
- yes potentially if diagnosed early after onset and animal is supported
- delay –> irreversible renal damage and death
4
Q
CS - ARF
A
- oliguria and anuria characterise severe ARF (not always though)
- polyuric (sometimes)
5
Q
Is urine output the same as GFR?
A
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
6
Q
Define loiguria
A
- variable definitions
- typically
7
Q
What is physiologica oliguria?
A
- 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
8
Q
Dx - ARF
A
- 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
9
Q
What 2 quesitons should always be asked with newly documented azotaemia?
A
- acute/chronic?
- pre-renal, renal or post-renal?
10
Q
How do you differentiate acute and chronic azotaemia?
A
- hx
- PE incl. renal size
- non-regenerative anaemia
- renal ultrasound
- CKD-Mineral Bone Disorder (secondary hyperparathyroidism). Care - hyperphosphataemia occurs with acute and chronic disease
11
Q
Causes - azotaemia
A
- High production of nitrogenous waste (pre-renal, urea only)
- Low GR (pre-renal with reduced renal perfusion, renal with intrinsic or functional renal disease or post-renal with urinary obstructin)
- Reabsorption urine escaped from urinary tract (Post-renal)
12
Q
When is UA indicated?
A
whenever blood tests are performed, especially when evaluating renal function
13
Q
Differentiate pre-renal and renal azotaemia by USG?
A
PRE-RENAL: Dog = >1.030 Cat = >1.035 RENAL: Dog =
14
Q
UA findings - Renal azotaemia
A
- glucosuria
- casts
- Ca oxalate
15
Q
What is the response to IVFT with pre-renal and renal azotaemia?
A
- Good response with pre-renal. May or may not have a response with renal azotaemia
16
Q
Describe pyelonephritis
A
- cause: ascending infection most common
- may be PU/PD
- not always azotaemic
- consider breaches of UT defences
- treat aggressively
17
Q
Breaches of UT defences that may –> pyelonephritis
A
- ANATOMICAL: ectopic ureters, perineal urethrostomy
- MEDICAL: diabetes, renal dz, nephroliths
- IATROGENIC: catheters, steroid therapy
18
Q
Tx - pyelonephritis
A
- AGGRESSIVE:
- culture urine, empiric AB initially
- re-culture on tx, continue 4-6wks
- reculture 1-2 wks post-tx
19
Q
Commonest leptospira serovars
A
- L.grippotyphosa
- L.pomona
- L.autumnalis
20
Q
CS - leptospirosis
A
- hepatic necrosis
- thrombocytopaenia
- vasculitis
21
Q
Dx - leptospirosis
A
- rising titre to non-vaccinal serovar
- PCR available, lack sensitivity - perhaps since many have received ABs by time this test is run.
22
Q
Tx - leptospirosis
A
ACUTE tx: - penicillins (usually amoxicillin) - penicillin G or ampicillin TO CLEAR INFECTION/ carrier status: doxycycline, 2 weeks
23
Q
3 main types of intrinsic renal failure
A
- TUBULAR NECROSIS (v common)
- INTERSTITAL NEPHRITIS (V common)
- ACUTE GLOMERULONEPHRITIS (uncommon)
24
Q
What are the 2 types of tubular necrosis?
A
- ischaemia (common)
2. toxins (common)
25
List toxins causing renal injury
* EG
* raisins/ grapes
* plants (lillies in cats)
- heavy meatals
- pesticides/ herbicides
- snake venom
- myoglobin/ haemoglobin
- calciferol rodenticides
26
Which therapeutic agents can cause renal injury?
- ANTIMICROBIALS: aminoglycosides, TCs, amphotericin B
- CHEMOTHERAPEUTICS: doxorubicin (cats), cisplatin and carboplatin, methotrexate
- NSAIDs
- ACEIs
- IV CONTRAST AGENTS
- MANY MORE
27
Causes - ischaemic ARF/AKI
- reduced intravascular volume
- hypotension
- decreased effective intravascular volume (HF, cirrhosis)
- sepsis
- drugs (cyclosporine, NSAIDs, ACEI)
- vascular dz (thrombosis, vasculitis)
28
Why are PCT cells prone to ischaemic injury?
v high metabolic rate making them particularly vulnerable --> mitochondrial injury, cell swelling and tubular obstruction
29
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.
True
30
Causes - hospital acquired AKI
- advanced age
- fever
- dehydration
- cardiac dz
- pre-existing renal dz
- anaesthesia/sx
- nephrotoxic drugs
31
Pathogenesis - hospital acquired AKI
- decreased glomerular ultrafiltration coefficient
- intra-tubular obstruction
- back-leak fluid across disrupted epithelium
- intra-renal vasoconstriction
32
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
33
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
34
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)
35
What is the most consistent renal protective effect?
correction of fluid deficits and mild ECF volume expansion
36
Antidote - EG
4-methylpyrazole (but prohibitively expensive in UK)
37
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
38
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
39
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
40
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
41
Can you tx ARF directly?
- No
- 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
42
Describe enzymuria
- measure enzymes in urine
- early indicator of AKI (before azotaemia)
- e.g. NAG, yGT, N-Gal
- monitor when tx with nephrotoxic drugs
43
Parameters to measure fluid balance with AKI patients
- 'ins and outs'
- CVP
- serial body weight
- serial PE
- serial PCV/TP
- OTHERS (electrolytes, ECG, renal function q48-72h)
44
2 methods of increasing urine output pharmacologically
- DIURETICS: furosemide, mannitol
| - VASOACTIVE AGENTS: dopamine, fenoldopam, diltiazem
