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
