SA CKD

Question 1

1. CKD more commonly in cats or dogs?
2. Define CKD.
3. Aim of CKD management.

Answer 1

1. Cats - up to 20% geriatric cats will have clinically significant CKD.
2. Functional and/or structural disease of >3m duration.
   Gradual, progressive, irreversible nephron loss.
3. Protect remaining nephrons and manage clinical consequences.
   Can only decline and progress.
   Can stay static for some time too.

Question 2

Nephron loss and signs associated…
1. No nephron loss.
2. 50% loss.
3. 67% loss.
4. 75% loss.
5. 100% loss.

Answer 2

1. Normal kidney function.
2. Still subclinical.
3. Lose concentrating ability;
   - USG < 1.030 dogs.
   - USG < 1.035 cats.
   - PUPD – subtle and may be missed.
4. Become azotemic.
   - QoL decrease down to 100%.
5. Incompatible with life.

Question 3

CKD aetiology?

Answer 3

Chronic interstitial nephritis (CIN).
- end stage of many pathological processes.
Glomerulonephropathy.
Undiagnosed/untreated infections.
Chronic obstructive disease.
Congenital - PKD, renal dysplasia (dogs).
Neoplastic (lymphoma).

Question 4

Polycystic kidney disease (PKD).

Answer 4

Persian cats (and related breeds).
Autosomal dominant.
No cure - management as for CKD.
Aim to eliminate from gene pool.
Genetic test:
- cheek swab or (EDTA) blood sample.
- negative cats – ICC PKD register.

Question 5

CKD pathogenesis.

Answer 5

Asymptomatic/undiagnosed initial insult so reduced glomerular function.
- compensatory hypertrophy of remaining nephrons.
– progressive nephron loss and progressive decrease in GFR.
Loss of electrolyte/water regulation.
Loss of acid/base regulation.
Impaired renal hormone synthesis.
- Calcitriol (vitamin D).
- Erythropoietin (EPO).
Hypertension - cause vs consequence.

Question 6

CKD clinical presentation.

Answer 6

Increasing incidence with age.
- middle-older age more typical.
Young (<1yo) may be affected.
- usually due to congenital disorders.
It is a chronic disease i.e. longer-term signs (weeks, months).
OR
Diagnose incidentally (sub-clinical phase) during pre-op/geriatric wellness screening bloods.

Question 7

Historical findings for CKD?

Answer 7

Subtle/non-specific.
PUPD.
Weight loss.
Lethargy, weakness.
Inappetence.
V+/D+/haematemesis/melaena.
- may see constipation secondary to dehydration (cats).
+/- signs associated with hypertension (blindness, neuro).

Question 8

3 top differentials for PUPD nsd weight loss in geriatric cats.

Answer 8

CKD.
DM.
Hypertension.

Question 9

Exam findings in the CKD patient.

Answer 9

Catabolic state.
Typically dehydrated.
+/- weakness.
- hypokalaemic myopathy – neck ventroflexion.
+/- uraemic ulcers, +/- uraemic halitosis.
+/- hypertensive retinopathy.
Kidneys typically small and irregular on palpation.
- may be large if lymphoma.
‘Rubber jaw’ (renal secondary hyperparathyroidism).

Question 10

Renal secondary hyperparathyroidism.

Answer 10

Decreased GFR so decreased phosphate excretion.
So increased serum phosphate.
So parathyroid hormone secretion.
- to decrease phosphate (also increase calcium).
- ineffective as inadequate renal function to excrete increased phosphate.
So progressive increase in phosphate and persistent PTH release.
So bone resorption resulting from increased PTH activity so rubber jaw (R2PTH).
- clinically most recognised in renal dysplasia.

Question 11

1. What is the easiest approximation of GFR?
   - what should be noted when measuring this?
2. Gold standard measure of renal filtration?
3. What is another surrogate marker of GFR?

Answer 11

1. Creatinine (an inverse of GFR).
   - note muscle mass.
2. GFR.
3. SDMA - but is equally prone to all the limitations that creatinine is.

Question 12

Urinalysis for renal azotaemia.

Answer 12

Submaximally concentrated urine (USG) on refractometer.
Evaluate for proteinuria (UPC).
Sediment exam - casts and crystals.
Cytological exam - EDTA sample.
- inflammatory sediment or atypical cells.
Culture and sensitivity (cystocentesis, plain sample).

Question 13

Other diagnostics for renal azotaemia?

Answer 13

Haematology - anaemia (normocytic, normochromic).
Serum biochemistry:
- azotaemia.
- +/- increased phosphate.
- +/- increased (or decreased) calcium.
- +/- decreased potassium (at very end stage, it will increase).
FIV (+/- FeLV).
Systolic blood pressure.

Question 14

Imaging of renal azotaemia?

Answer 14

Ultrasound - renal size and architecture.
Radiography - ureteroliths – esp. cats.
Look for reversible causes:
- ureteric obstruction?
- pyelonephritis?
- lymphoma?

Question 15

Addressing reversible/manageable problems to manage CKD.

Answer 15

Discontinue any nephrotoxic drugs.
Dehydration:
- fluid therapy; replace deficit, maintain.
Hypertension.
Pyelonephritis?
Ureteroliths.
Hypercalcaemia (risk of mineralisation)/hyperviscosity?
- investigate and treat underlying cause.
Lymphoma - chemotherapy.

Question 16

1. Why is the outcome for geriatric cats with CKD that receive NSAIDs no worse than patients that do not receive NSAIDs?
2. What must be done if choose to give NSAIDs to a cat with CKD?

Answer 16

1. By giving NSAID, allow patient to be more mobile and means they are better able to hydrate and nourish themselves and therefore address some of the risk factors for kidney damage.
2. Advise owner that there is a risk of effect on renal perfusion, so if at any time their appetite drops off, drinking drops off, other GI losses (v+/d+) - fluid balance affected, may need to stop NSAID. But if other analgesia available, better to use that.

Question 17

IRIS (International Renal Interest Society) staging of CKD.

Answer 17

Only stage once any reversible problems have been addressed.
Used to determine disease progression over time and best treatment for the stage of disease.
Stage by:
- creatinine – NB. reference / thresholds
- proteinuria.
- BP.

Question 18

CKD management - fluid balance.

Answer 18

Encourage oral intake - e.g. fountains.
Wet food / slurry food / soaked food.
SC fluids.
Oesophageal tube (fluid, nutrition, medications).

Question 19

Delaying progression of CKD.

Answer 19

Renal diet - improve survival.
– restricts protein.
– reduce production of uraemic toxins.
– reduce escalation of their phosphate.
– supplements potassium and B vitamins.
Control parameters:
- hypertension.
- proteinuria.
- hyperphosphataemia.
- hypokalaemia.
Avoid further insults.

Question 20

Nutritional management of CKD.

Answer 20

Renal diets:
- minimise uraemic episodes .
- minimise uraemic crises/mortality.
- prolong survival.
Restricted:
- protein.
- phosphorus.
- sodium.
Supplemented:
PUFAs (polyunsaturated fatty acids), antioxidants (e.g. vitamin E) (synergistic with PUFAs), B vitamins, K+ (cats), soluble fibre.

Question 21

CKD management caloric intake.

Answer 21

Important ti avoid protein calorie malnutrition.
- MUST eat sufficient calories.
Address causes of inappetence:
- dehydration.
- hypokalaemia.
- nausea; mirtazepine, maropitant.
- uraemia gastropathy; omeprazole, sucralfate.
Tempt/warm/wet food.
Avoid introducing prescription diet in the hospital.
Avoid syringe feeding.

Question 22

CKD management - hyperphosphataemia.

Answer 22

Phosphate restriction slows progression of CKD and prolongs survival.
Target serum phosphorus depends on IRIS stage:
- renal diet.
- if inadequate, reduce phosphate by giving phosphate binder:
– must use with every meal.
– calcium vs non-calcium containing.
–> NB calcium:phosphorous product.
– adjust every 4w.

Question 23

CKD management - hypokalaemia.

Answer 23

Contributors:
- inadequate dietary intake.
- renal potassium wasting.
Hypokalaemia causes inappetence, lethargy, weakness, PUPD.
Manage with:
Renal diet.
+/- poassium supplementation.
- oral vs IV.
Adjust every 1-2w.

Question 24

CKD management - hypertension.

Answer 24

Can cause and be a consequence of KD.
Important to examine the retina in any patient with KD.
Aim for BP <140.

Question 25

CKD management - proteinuria.

Answer 25

Negatively associated with survival.
Manage where indicated.

Question 26

Management of anaemia in CKD patients.

Answer 26

Common / expected.
- usually mild and does not need specific tx.
Multifactorial:
- produce less EPO so less stimulation to produce RBCs.
Exacerbated by:
- GI haemorrhage – due to ulcers due to uraemic toxins.
- Reduced RBC lifespan - due to uraemic toxins.
Reduce GI losses (omeprazole, sucralfate)
If PCV <20% and symptomatic for anaemia:
- consider recombinant human EPO (darbopoeitin; DPO).
– stimulates bone marrow to produce more RBCs.
- generate antibodies to DPO overtime so do not start before clinically needed.
- ultimately over time anaemia will become refractory/progressive.

Question 27

Monitoring progress of CKD.

Answer 27

Refer to IRIS guidelines.
- individualise therapy.
Hx, exam.
BP.
Urinalysis.
PCV (haematology).
Urea, creatinine, phosphorous, calcium, sodium, potassium (biochemistry).
- fasted sample.
Consider dose reduction of any renally metabolised/excreted drug.

Question 28

CKD prognosis.

Answer 28

Address reversible component before prognosticate.
If specific disease, see that disease for prognosis.
Depends on IRIS stage.
Cats cope better than dogs:
- cats – often years.
- dogs – often very poor if significant clinical signs (usually months).