Chronic Kidney Disease Flashcards
(42 cards)
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)
