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Flashcards in Acute renal failure Deck (44):
1

Define ARF

- sudden onset haemodynamic, filtration and excretory failure of kidneys
- subsequent accumulation of metabolic/uraemic toxins
- dysregulation of fluid, electrolyte and acid-base balance

2

Defome AKI

= 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

Is ARF reversible?

- yes potentially if diagnosed early after onset and animal is supported
- delay --> irreversible renal damage and death

4

CS - ARF

- oliguria and anuria characterise severe ARF (not always though)
- polyuric (sometimes)

5

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

6

Define loiguria

- variable definitions
- typically

7

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

8

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

9

What 2 quesitons should always be asked with newly documented azotaemia?

- acute/chronic?
- pre-renal, renal or post-renal?

10

How do you differentiate acute and chronic azotaemia?

- 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

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)

12

When is UA indicated?

whenever blood tests are performed, especially when evaluating renal function

13

Differentiate pre-renal and renal azotaemia by USG?

PRE-RENAL:
Dog = >1.030
Cat = >1.035
RENAL:
Dog =

14

UA findings - Renal azotaemia

- glucosuria
- casts
- Ca oxalate

15

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

16

Describe pyelonephritis

- cause: ascending infection most common
- may be PU/PD
- not always azotaemic
- consider breaches of UT defences
- treat aggressively

17

Breaches of UT defences that may --> pyelonephritis

- ANATOMICAL: ectopic ureters, perineal urethrostomy
- MEDICAL: diabetes, renal dz, nephroliths
- IATROGENIC: catheters, steroid therapy

18

Tx - pyelonephritis

- AGGRESSIVE:
- culture urine, empiric AB initially
- re-culture on tx, continue 4-6wks
- reculture 1-2 wks post-tx

19

Commonest leptospira serovars

- L.grippotyphosa
- L.pomona
- L.autumnalis

20

CS - leptospirosis

- hepatic necrosis
- thrombocytopaenia
- vasculitis

21

Dx - leptospirosis

- rising titre to non-vaccinal serovar
- PCR available, lack sensitivity - perhaps since many have received ABs by time this test is run.

22

Tx - leptospirosis

ACUTE tx:
- penicillins (usually amoxicillin)
- penicillin G or ampicillin
TO CLEAR INFECTION/ carrier status:
doxycycline, 2 weeks

23

3 main types of intrinsic renal failure

- TUBULAR NECROSIS (v common)
- INTERSTITAL NEPHRITIS (V common)
- ACUTE GLOMERULONEPHRITIS (uncommon)

24

What are the 2 types of tubular necrosis?

1. 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