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
when are antibiotics used in chronic renal disease?
Up to 33% dogs and 25% cats with CKD have a positive urine culture – subclinical bacteriuria .Only treat if clinical signs of cystitis/ pyelonephritis
Treatment of UTIs/ pyelonephritis
* Choose renally excreted drugs e.g. amoxycillin/ amoxyclav
* TMPS- beware many adverse effects
* Fluoroquinolones?- NOT Enrofloxacin in cats
* 3rd Gen Cephalosporins (e.g. cefotaxime)?
* AVOID NEPHROTOXIC ANTIBIOTICS when treating any infection in patient with CKD e.g. aminoglycosides, enrofloxacin
What are the beningn and malignant renal neoplasias?
Benign primaries: adenomas, lipomas, fibromas, and papillomas- usually incidental
Malignant:
* Lymphoma: usually multifocal or diffuse, interstitial, and bilateral > large, irregular kidneys. May only be in the kidneys (esp. cats), may be multicentric.
* Carcinoma: Usually at one pole and well demarcated. Metastasise early to other kidney/ lungs/ liver/ adrenals
* Less common- Transitional cell carcinomas, renal sarcomas
what is polycystic kidney disease?
what are the predispositions?
how are they diagnosed?
- Autosomal dominant hereditary condition
- Fluid filled cysts present from birth in the kidney +/- organs (e.g. liver and pancreas). Size and number gradually increase with age > CRF.
- Breeds-Persians (34%), Exotic Shorthair, Himalayan, British/American Shorthair, Burmilla, Ragdoll, Maine Coon
- All Persians/exotic shorthairs should be screened before breeding
- Average age clinical signs 7 yrs
- Exam- as CRF but large irregular kidneys
- Diagnosis -ultrasound -hypo/anechoic spherical cavities
What is Faconi’s syndrome?
what are the causes?
what are the Signs:
how is it diagnosed?
what is the treatment?
- Disease of proximal tubule > reduced resorption of solutes>loss of glucose, Na+, K+, phosphorus, bicarbonate, albumin, and amino acids
- Causes: Idiopathic, hereditary (Basenji’s, gradual onset), gentamicin nephrotoxicosis, chicken jerky treats, copper metabolism diseases, infection
- Signs: PU/PD and weight loss +/- signs of uraemia
- Diagnosis: glucose, Na+, K+, phosphorus & bicarbonate in urine despite normal plasma concs. Can do fractional excretion tests.
- Treatment: remove cause if possible
- Supplement oral NaCl, K+, and bicarb if serum concentration is low
What is Glomerular disease?
what does it cause?
what are the signs?
how is it diagnosed?
Can be secondary to advanced CKD or primary and cause/worsen CKD
Causes protein-losing nephropathy (PLN)
Signs consistent with CKD/ uraemia or can be non-specific (weight loss/ lethargy).
Diagnosis:
* Haematology/biochem
* Likely as for CRF +/- azotaemia; likely hypoproteinaemia
* Urinalysis
* Proteinuria; may still be able to concentrate urine; hyaline casts common as protein lines tubules
*
What are the causes of primary glomerular disease in cats and dogs?
CATS- less common than in dogs. Most common causes: neoplasia, systemic inflammatory diseases, chronic FeLV/ FIV/ FIP
DOGS- a leading form of renal disease, most common in middle age
* Immune complex glomerulonephritis- idiopathic (most) or associated with neoplasia, rickettsial diseases, SLE, heartworm, pyometra, chronic septicaemia or adenovirus.
* Familial glomerulopathies in several breeds including Bernese Mountain Dogs, English Cocker Spaniels, English Springer Spaniels, Doberman, Greyhounds and more.
* Amyloidosis (non familial form)- chronic inflammation results in protein deposition in glomerulus
* Glomerulosclerosis- currently poorly characterised but IDed at histology
how is glomerular disease investigated?
- Assess proteinuria via Urine Protein Creatinine Ratio (UPCR)
- UPCR >0.5 (dog) or >0.4 (cat) –Likely caused by glomerular leakage
- IF no inflammation/haematuria
- Higher UPCR = more likely primary glomerular disease-
- > 3.5 investigate for Glomerular disease
- Imaging findings may be non-specific. Possible to see small kidneys, increased cortex echogenicity, loss of corticomedullary definition
- Renal biopsy- definitive diagnosis
What are the indications and contraindications of renal biopsy?
GA and operator skill required!
Indications- Only if will alter patient management (generally not CKD) e.g.
* Protein Losing Nephropathy – unexpected/doesn’t respond to treatment
* AKI- cause and prognosis
* Mass lesions
Contraindications: late stage CKD, severe anaemia/ azotaemia, uncontrolled hypertension/ coagulopathy, severe hydronephrosis/ many large cysts, pyelonephritis/ perirenal abscesses, NSAIDs in last 5 days
How are renal biopies performed?
what is the aftercare?
16-18G 9cm biopsy needle. Ultrasound guided, laparoscopic, surgical wedge biopsy, (blind/palpation - cats only )
Only sample CORTEX or bleeds/ infarctions/fibrosis
Ideally cranial or caudal pole for best sample of glomeruli
Ask lab what to fix samples with for histo/ electron microscopy/immunofluorescence
After care-IVFT 24 hours post to reduce renal pelvis clots. Rest patient for 72 hrs and monitor PCV.
What is nephrotic syndrome?
what are the clinical signs?
What is the treatment?
Uncommon result of PLN. Pathognomonic for glomerular disease.
Excessive loss of protein via the kidneys –> hypoalbuminaemia –> hyperlipidaemia and 3rd spacing of fluid (ascites/oedema)
Clinical findings (in addition to usual signs of renal disease)
* Pitting oedema /ascites/ pleural effusion
* Hypoalbuminaemia
* Hyperlipidaemia (TGs and cholesterol)
Treatment:
* Antiproteinurics - slow nephron damage and increase plasma oncotic pressure
* ACE inhibitors e.g. Benazepril/ Enalapril
* Anticoagulants – because of risk of thromboembolism - as regulatory proteins (e.g. antithrombin and protein S) lost
* Aspirin or Clopidogrel- minimize spontaneous platelet aggregation.
* Fluid removal- only if severe impairment of resp/ heart/QoL as result
* Will reform as RAS upregulates and worsens hypovolaemia
* Abdominal/ pleural tap
* Diuretics- frusemide? Spironolactone (K+ sparing)
What are the similarites and differences with CKD in rabbits?
how is it diagnosed?
What is the treatment?
Same underlying disease processes as dogs and cats (but also can be due to E. Cuniculi)
Similar clinical signs - PU/PD, weight loss, occasional haematuria (renal infarctions, uroliths due to high calcium)
Diagnosis
* Urinalysis (don’t cysto if possible)
* Inappropriate urine concentration (ref 1.003-1.035- should be >1.035 if dehydrated).
* Proteinuria common in CRF
* Biochem - hypercalcaemia and azotaemia (use lab reference ranges for rabbits). If severe also ^K+ and Phos.
Treatment
* Treat underlying causes if possible
* Discontinue nephrotoxic drugs
* Treatment as dogs/cats BUT dietary management different
* 2ndary hypertension common- diagnose as dogs/cats and treat with ACEi
