Chronic Renal Failure Flashcards
Chronic renal failure (4)
Loss of functional renal tissue due to a prolonged process (generally >2 months)
Usually progressive & irreversible
Chronic renal disease (CKD) often smoulders for many months or years before it become clinically apparent
CRF is end stage of process that has gone on for much longer
Causes of CRF
Degenerative - Chronic interstitial nephritis - Renal infarcts Developmental - Familial renal dysplasia - PKD Metabolic - Hypercalcaemia - Neoplasia - Renal lymphoma - Renal carcinoma Iatrogenic - Vitamin D supplementation - Nephrotoxic drugs Idiopathic - Renal amyloidosis - Some forms of glomerulonephritis Immune-mediated - Immune-complex mediated glomerulonephritis Infectious - Pyelonephritis - Lyme (Borreliosis) nephropathy
Sequel of post-renal failure
Sequel of acute renal failure
Pathophysiology
CKD leads to nephron damage & loss
Normal animals have more nephrons than necessary
If number of nephrons falls below:
1/3 - urine concentrating ability becomes impaired (renal insufficiency)
¼ - azotaemia develops (CRF)
Further progression of damage & azotaemia leads to signs of uraemia
effects of CRF
Failure of excretion of nitrogenous waste uraemia
Failure of urine concentration PUPD
Failure of synthesis of calcitriol (vit D3) hypocalcaemia & renal secondary hyperparathyroidism
Failure of erythropoietin synthesis anaemia
Failure to catabolise peptide hormones (eg gastrin) uraemic gastritis
Can initiate systemic hypertension
Can result in defective haemostasis
WHy is CRF progressive?
Regardless of initial cause, once CRF develops, secondary processes are activated that contribute to renal damage
These include:
- Systemic and glomerular hypertension
- Mineral imbalance
- Proteinuria
- Renal fibrosis
–> these are what you treat!
Presenting signs of CRF
x
Clinical examination findings
x
Lab findings
Azotaemia
- Reduced GFR
- (Increased catabolism)
- (GI haemorrhage)
Inappropriately low urine specific gravity
- Unable to concentrate (or dilute urine)
- Cats SG: 1.008 to 1.030
- Dogs SG: 1.008 to 1.020
staging
CKD often progresses from initial non-azotaemic stage to end-stage uraemia (ie CKD CRF)
IRIS classification for CKD
Uses creatinine concentration in a normally hydrated animal as estimate for degree of decline of GFR
Only applies in chronic disease where creatinine is reasonably stable
1) Non-azotaemic CKD
2) Mild renal azotaemia
3) Moderate renal azotaemia
4) Severe renal azotaemia
Biochemistry
- Hyperphosphataemia
- Hypokalaemia
- Hyper/hypocalcaemia
- Metabolic acidosis
Hyperphosphataemia
Kidneys are primary route of phosphate excretion
Reduced renal function phosphate retention
Stages I & II CKD:
- Compensatory mechanisms lead to increased phosphate - loss from surviving nephrons
- Phosphate rarely increased
Stages III & IV CKD
- Compensatory mechanisms fail
- Phosphate increases
Hyperphosphataemia effects
Unlikely to directly cause clinical signs BUT…
- Drives renal secondary hyperparathyroidism
- Causes progression of disease
- Leads to reduced survival
Hypokalaemia
- due to (2)
- results in (6)
Due to:
- Reduced intake
- Increased renal potassium loss
Results in:
- Neuromuscular weakness
- Anorexia –> weight loss
- Impaired protein synthesis –> weight loss
- Decreased renal function (reversible)
- Promotes lymphoplasmacytic intersitial lesions
- Promotes PU/PD
Other biochemical changes
Calcium:
- Total calcium often unchanged or slightly decreased
- Hypercalcaemia can be secondary to renal failure or cause renal failure
Metabolic acidosis
- Due to reduced excretion of H+ ions by kidney
- Tends to mild relatively mild in CRF
- Tends to be a later complication
