CKD Flashcards
what is Chronic renal disease?
what are the clinical signs?
- Irreversible damage to the kidneys that impacts function
- Progressive
- Can be age-related degeneration
- Can have an underlying cause e.g.- Polycystic Kidney Disease, pyelonephritis, toxins, glomerulonephritis, neoplasia, amyloidosis, FIP
- Common in dogs, very common in cats!
Common presenting signs:
* PU/PD
* Anorexia
* Weight loss
* Vomiting and diarrhoea
* Dehydration
* Pallor
* Mucosal ulcers
* Uraemic breath
what are the breed, age and comorbidities that predispose to CKD?
gove examples of nephrotoxic drugs
Breed
Dogs- Westie, Boxer, Shar Pei, Bull Terrier, Cocker Spaniel, CKCS
Cats-Persian, Abyssinian, Siamese, Ragdoll, Burmese, Russian Blue, Maine Coon
Age
Older animals (age-related degeneration)
Can be juvenile if underlying familial issue (e.g. polycystic kidneys)
Comorbidities: conditions causing renal insult; previous acute kidney injury; nephrotoxic drugs
Conditions causing renal insult e.g. Hyperthyroidism, hypercalcemia, heart disease, periodontal disease, cystitis, urolithiasis, diabetes etc
Nephrotoxic Drugs- NSAID, aminoglycosides, sulphonamides, polymyxins, chemotherapeutics
what is the pathophysiology fo CKD?
- Nephron damage is self-perpetuating = progressive! This is irreversible.
- Decreased GFR results in build-up of products normal excreted- e.g. urea
- Reduced Erythropoietin (EPO) production = non-regenerative anaemia
- Altered Ca/P homeostasis = renal hyperparathyroidism
what is a uraemic crisis?
what are the clinical signs?
how do you treat a uraemic crisis?
Build-up of urea and other toxins usually excreted in kidneys to intolerable levels.
Seen in end-stage CKD and AKI
Clinical signs:
Vomiting/nausea, anorexia, lethargy, oral ulcers, melena (GI ulcers), anaemia, hypothermia, weakness, muscle tremors, seizures
treatment:
Work out if AKI, CKD, or acute on chronic and treat as needed but also…
* IVFT- Hartmann’s
* Replace dehydration + ongoing losses
* Care if AKI not to over perfuse- measure urine
* If can measure blood gases- assess for acidosis
* Bicarb if pH <7.2 or serum bicarb < 12
* Treat nausea/GI ulceration
* Omeprazole +/- H2 Blockers +/- sucralfate
* Antiemetics e.g. maropitant
* Pain relief – opioid
* nutritional support
* Appetite stimulants- Mirtazapine
* Feeding tubes (Nasogastric)
* Beware food aversion-DO NOT introduce renal diet in hospital!
How is CKD diagnosed?
Common history
* Weeks/ months of weight loss, reduced appetite
* PU/PD. Possible historic of renal insult
Exam
* BCS and coat quality reduced. Kidneys small and hard (enlarged possible dependant on cause e.g. PKD)
Biochemistry/ haematology
* K+ normal / v
* Relatively well for severity of azotaemia
* Non regenerative anaemia
Urine
USG < 1.035 (inappropriately dilute)
Sediment usually not active though possible if UTI.
Possible proteinuria.
CKD is staged - based on creatinine and SDMA in the hydrated patient (IRIS staging)
Early stage 2 is within reference range for many machines/labs!!
Substage based on proteinuria/systolic BP
When and why is CKD normally diagnosed?
Early stage (I or early II) - rarely picked up this soon
Abnormal renal imaging/ known insult OR
Persistent elevation/ increasing Creatinine/ SDMA OR
Persistent renal proteinuria
Later stages (Late II- IV)
Consistent clinical signs
Azotaemia/ persistently elevated creatinine/ SDMA
AND
USG <1.035 (cats) or <1.030 (dogs)
Waht are the markers for GFR?
SDMA
Produced by all nucleated cells at constant rate and cleared by kidneys
Not affected by muscle mass
Increases at 40% nephron loss
BUT more expensive, less available and possibly less sensitive?
Serum Creatinine
Product of muscle metabolism
Produced at constant rate and excreted via kidney
Muscle atrophy/cachexia can decrease
Can increase after feeding- starved sample
only increase when >75% of nephrons already lost!
use either/both when staging CKD
what is the general treatment of CKD?
- Treat underlying cause if possible/known
- Slow progression by managing risk factors
- Recommendations vary by stage/substage but focus around monitoring/ controlling proteinuria, hypertension, hyperphosphatemia
- Diet is very important for stage II onwards!!
- In later stages, there is more emphasis on maintaining hydration and adequate nutrition, and treating secondary anaemia/acidosis/nausea
hyperphosphatataemia occurs with CKD this is due to Phosphate being filtered by kidneys:
what is the aims of treatment of CKD in relation to phosphate?
How is phosphate managed and monitored in CKD?
- Aim to keep to low end of ref range via
- Dietary restriction (renal diet)
- +/- enteric phosphate binders (e.g. Aluminium hydroxide)
- Monitor serum Phos monthly until stable then 3 monthly.
FGF23- new biomarker
* Increases in cats who have phos within target range but are still at increased risk of hyperparathyroidism
* Once phos stable consider measuring FGF23 – if elevated further restrict phos
* (care interpreting if anaemia/inflammatory dx or preexisting hypercalcaemia)
What are the causes of hypertension?
how is hypertension diagnosed?
when should hyper tension be treated?
- Primary –> stress/environment, idiopathic (prevalence >12% in healthy cats >10 yrs)
- Secondary –> iatrogenic (e.g. glucocorticoids), systemic disease including CRF (CKD)
The concern is end-organ damage if sustained! (CKD)
Diagnosis based on repeated measurements of systolic blood pressure
Treat when:
Approx 20% of CKD patients have incereased BP at diagnosis
A further 10-20% will develop increased BP over time- monitor!
Treat if SBP reliably and consistently >160 mm Hg and evidence of EOD (CKD = evidence)
what are the treatment options for hypertension?
what are the aims and drug choices for both dogs and cats?
- ACE inhibitors (ACEi)
e.g. Benazepril, Enalapril - Angiotensin receptor blockers (ARB)
e.g. Telmisartan, Spironolactone - Calcium Channel Blocker (CCB)
e.g. Amlodipine
Aim to reduce to < 150mmhg over a few weeks – quicker (hours) if severe ocular / CNS signs
Dogs – aim to interfere with RAAS activation . Should reduce BP and proteinuria
* ACE inhibitors (ACEi)
* If needed can add in Calcium Channel Blocker
Cats- start with CCB as more effective at reducing BP unless also proteinuria
* Can add ARB or ACEi to CCB to increase effect if needed.
* If also proteinuria, then start with an ARB (Telmisartan)
How is hypertension monitored?
Some antihypertensives should reduce proteinuria if present
Aim for >50% reduction in UPCR
Once stable and BP < 150mmHg can check BP Q4 months
Check for:
Evidence of worsening EOD on exam
Marked increase in azotaemia
Evidence syncope/hypotension (SBP < 120mmHg)
Wait 3-4 weeks between changes of drug doses (unless emergency), but check in 1-2 weeks if CRF stable
How do you check for proteinuria?
what is the treatment for proteinuria?
- If urine dipstick positive assess via Urine Protein Creatinine Ratio (UPCR)
- UPCR >0.5 (dog) or >0.4 (cat) –Likely caused by glomerular leakage
- IF no inflammation/haematuria
- (UPCR >3.5 = more likely primary glomerular disease- see later slides)
- Treatment - RAAS inhibitor (ACEI or ARB) and feed a clinical renal diet
what are the renal and extra-renal causes of renal diasease?
Renal:
* Glomerular disease
* Fanconi’s syndrome
* Polycystic kidney disease
* Pyelonpehritis
* Nephrotoxin exposure
* Neoplasia
Extra-renal:
* Hypertension
* Cardiac disease
* Hyperthyroidism
* Diabetes
* Urolithiasis/obstruction
* Cystitis
* Neoplasia
* Hypercalcaemia
What is pyelonephritis?
How is it diagnosed?
- Bacterial infection of the renal pelvis and parenchyma
- Uncommon in cats and dogs with normal urinary tracts but 5-8% prevalence if CKD
- Increased prevalence in other conditions e.g. AKI/ urolithiasis/ obstruction
- Can cause/ worsen underlying kidney disease
Diagnosis
* Compatible clinical signs (fever, abdo pain, pu/pd)
* Haematology - neutrophilia with left shift
* Ultrasound - renal pelvis dilatation with hyperechoic mucosa, altered cortex/ medulla echogenicity.
* Culture urine sample
