Chronic Kidney Disease Flashcards
Is acute or chronic kidney disease more common?
chronic
Which terms should be used wrt kidney disease?
- CRF (chronic renal failure) indicates chronic azoteamia d/t renal disease
- > 3/4 nephrons need to be lost before azoteamia develops so significant renal disease can be present without azoteamia
- CKD (chronic kidney disease) = patients with longstanding disease ± azotemia
What is the IRIS staging scheme for kidney disease?
> plasma creatine concentration, proteinuria and blood pressure
only applicable to CKD patients (different staging system for AKI) with no pre- or post- renal causes of azoteamia (if not azoteamic other abnormality must be present to ID it as CKD)
values differ for cats and dogs
may have normal creatinine but other signs present
PL nephropathy and systemic hypertension may occur at any stage
1. Not azoteamic, Normal/near normal GFR - some other renal abnormality must be present eg. renal structure or proteinuria
2. Non-azoteamic to mildly azoteamic - clinical signs limited to PUPD or absent
3. Mild-mod azotamia - PUPD, extrarenal clinical signs (V+, dehydration, wt loss) MAY be present
4. plasma creatinine >440 - PUPD, external signs LIKELY
When is finding an underlying cause for CKD particularly useful? What would a biopsy show?
Initial stages 1 and 2
- often no underlying cause can be found
- if biopsy obtained = chronic tubulointerstitial nephritis with associated fibrosis [END STAGE KIDNEY] does not given inciting cause, not recommended. Esp common in cats.
See lecture for causes of intrinsic renal failure in dogs and cats
-
What are the most common causes of CKD in cats and dogs?
> Dogs - 50% tubulointerstitial nephritis - congenital/familial - 1* glomerular dz > Cats - 90% cases = Tubulointerstitial nephritis Some cases of.. - Polycystic kidney dz - Obstructive dz
What is big kidney little kidney syndrome?
- Ca oxalate crystal obstruction - no clinical signs when first kidney obstructs
- kidney fibroses and shrinks
- hyperplasia of second kidney to compensate
- signs only seen when 2nd kidney blocks
What is polycystic kidney disease?
- persians > 8mo can ultrasound - DNA test - autosomal dominant - azotaemia only develops middle age so hard to breed out without testing
What is a perinephric pseudocyst?
- small kidney surrounded by fluid filled cyst
Aim of tx of CKD. Why is this difficult?
> Tx for slowing the progression of CKD
- Beyond a certain point CKD is intrinsically progressive d/t maladaptive responses triggered by CKD that perpetuate renal injury
Which species progress at a more rapid rate with CKD?
- dogs worse
- most dogs with azotemia die within a year
- survival of cats 2-3y (only 50% die d/t renal dz)
Explain 2 maladaptive mechanisms with CKD? Tx?
> CKD mineral bone disorder (CKD-MBD)
- previously renal 2* hyperparathyroidism
- Tx: renal care diet
glomerular hypertension/hyperfiltration
- Tx: ACE-Is or Angiotensin R blockers
Tx indicated in patients with stage 2/3 dz
WWht is brenners theory?
Self perpetuating renal dz
What is CKD-MBD. Pathophysiology?
- systemic disorder of mineral and bone metabolism
- manifests as abnormalities in:
-Ca, Ph, PTH, Vit D metabolism - bone turnover, mineralization, volume, linear growth or strength
- vascular/other soft tissue calcification (inc kidney)
> pathophysiology - FGF23 involved in early stages (pre-azotaemic) d/t v clearance of phosphate
- FGF23 v active vit D
- PTH ^, and aong with FGF 23-> ^ phosphate excretion, normalising plasma Ph
- as dz progresses phosphate cannot be excreted anymore, clearance becomes dependant on GFR alone
- plasma Ph ^ -> hyperphosphateaamia (damaging to kidneys)
> no evidence as to whether changing levels of hormones (as opposed to phosphate) is beneficial so currently no need to measure levels
What is calcitriol?
Active vit D
What effect does PTH have on Ph?
Mixed
How can CKD-MBD be managed?
> feed phosphate restricted diet: VERY SIGNIFICANT EFFECT! ^ survival time
- no drugs will be as effective as diet
- feed renal diet/sernior diet/normalbalanced diet/homecooked food/milk WORST!
- aim for phosphate in lower half of reference range
- if renal failure severe, reference range Ph will have to suffice
intestinal phosphate binding drugs
- mixed in food
- not effective without concurrent dietary restriction
- aluminium ydroxide preparations (cheap and effective but not tasty and -> constipation)
- lanthanum carbonate (Renalzin) being discontinued
-calcium carbonate/acetate can be use (beware -. hyperCa in cats)
Do phosphate binding drugs have to comply with the cascade?
no as not absorbed
Tx of glomerular hypertension and hyperfiltration? Which animals are most likely to benefit from this?
> ACE-Is and angtiotensin R blockers (ARBs more selective so ?better, no ^ renin like ACEI)
- cause preferential dilation of EFFERENT arterioles v glomerular capillary pressure, v proteinuria -> prevent glomerulosclerosis and ongoing renal injury
animals with more severe proteinuria and with a long term px (not end stage)
- if severely azoteamic animals/pre-renal azotaemia cases this may worsen decline
more evidence for dogs ^ survival (probs because 1* glomerular dz more common) but only LIC for cats (to v proteinuria, no evidence for survival effect )
Give a common example of an ACE-I
Fortekor (Benazepril)
Outline IRIS staging scheme for proteinuria
UPC 0.4 (cats)0.5 (dogs) = proteinuric
What complicating factors need to be addressed to reduce morbidity of CKD?
- Hypokalaemia
- Acidosis
- Anaemia
- UTIs
- Hydration sttus
- Laxatives
- Apetitie stimulatns
- Systemic hypertension
What part of the kidney does Amlodipine affect?
- AFFERENT arteriole (so should ^ pressure) only decreases d/t systemic effects v bP
Which animals more commonly get hypokalaemia? Why? Tx?
> Hypokalaemia
- 25% cats, not dogs
- not known why, should ^ with poor renal function
- often seen with IVFT and no supplementation
- maybe d/t relative ^ aldosterone?
- can induce histological lesions in the kidney
- improves apetite when tx
- tx not so easy cats don’t like supplements (renal diets supplemented)
When does acidosis occour? Tx?
> Acidosis
- metabolic acidosiss in severely azotemic animals (esp if suddednly decompensated from stable CKD)
- only tx (bicarbonate) if acid-base problems have been proven (unless part of CSL etc.)
Causes of anaemia in cats/dogs with CKD
- EPO deficiency
- Blood loss (GI ulcers, bblood samples, surgery)
- v RBC lifespan
- uremic inhibitors of erythropoiesis
- Fe deficiency
> in general severity of anaemia related to severity of azotaemia
> if symptomatic for anaemia other problems often at severe levels, poor px
Tx anaemia in CKD?
- recombinant human EPO
- BEWAARE: risk of Ab development against EPO cross-reactive w/ endogenous EPO
- can develop 1+ months after start of tx
-> anaemia that can only be tx with blood transfusion
> less common with darbopoietn (modified, administer less freuqneetly) - parenteral iron supplementation (iron dextram IM q 1 month) when starting tx
How is CKD related to UTIs?
May pdf pyelonephritis, and pyelonephritis may cause CKD
- cats with normal renal function rarely get UTIs d/t concentration of urine
- only see UTIs if underlying cause of v urine cconcentration present
- take samples regularly to monitor for occult infections
Why may fluids be useful? How can fluids be administered?
- prevent pre-rena element of CKD developing
> subcut - only indicated if ave a tendency to become dehydrated
- can teach owners to do at home
> gastrotomy/oesophagostomy tube - not common
- allows food and meds to be given
Why may laxatives be necessary for CKD patients? Egs?
- constipation common, may contribute to anorexia > d/t - dehydration - immobility (debilitated or concurrent ortho dz) - v food intake -phosphate binders > beware of causing D+ -> dehydration - liquid paraffin eg. katalax - lactulose (cats don't like) - miralax better for cats
Why may apetitee stimulants be needed? Egs?
- ureamic toxins v apetite
- ^ gastrin -> hyperacidity and GI ulcers
- mostly fibrosis and mineralisation
> cats mirtazapine (also v vomiting more effective than anti-emetics) and maropitant - less known about dogs
When is hypertension usually detected?
> Blind cat with hyphema
- blood vessels appear differnet thickness as they course closer to the cornea etc.
- retinal detachement
- retinal haemorrhage
- 3/4 cats w/ hypertnsive retinopthy will have mild CKD
- hypertension can also -> neuro signs and cardiac signs
Less common dogs
Aims wrt hypertension in CKD? How can this be achieved?
dx before clinical signs of end organ damage
- measure BP in all cats at risk of hypertension (CKD, hyperthyroid, geriatric cats)
What are the other 1/4 of hypertensive cats (that are not d/t CKD) d/t?
- idiopathic
- though may be sibclinical renl
wich types of BP measurement are best?
- Doppler best
- oscillometric has low correlation with direct BP measurmeents in awake cats
What is the IRIS staging system for hypertension with CKD? Is it helpful?
See lecture. Not that useful
How wide should a BP cuff be for a cat?
40% limb circumference
How should a blood pressure reading be taken?
Disregard first one, average 4/5
At what BP is tx for systemic hypertension initiated?
> 170mmHg or >160mmHg with concurrent ocular lesions - recorded on min 2 separate visits to the clinic
Normal BP cats?
125 sys
100 mean
90 dias
What tx is recommednedd for hypertension in cats?
> Amlodipine (v. efffective Ca channel blocker)
- Other tx (B blockers, ACEi) do not reduce BP significantly enough to prevent ocular lesions
Dogs with CKD poorly responsive to hypertension tx
- initial tx ACEI (esp if proteinuric)
+ amlodipine
Which term for kidney dz should not be used?
Renal insufficiency (too vague)
