Lecture 6 Flashcards
CKD vs CRF?
CKD= 66% loss CRF= 75% loss
Difference between CKD and AKI
CKD is permanent and progressive!
No recovery period like in AKI
Other than GFR markers, what other information do you want from your patient?
Blood pressure
UPC
Possibly imaging, culture
Underlying cause of CKD
Most are idiopathic (age related, accumulation of injuries)
Others might be toxicity, infection, cancer, obstructions
Why is it so important to recognize AKI vs CKD
Because there will be significant differences in treatment and prognosis
Compare/contrast AKI and CKD
History: Both have PU/PD, decreased appetite and vomiting. AKI might have oliguria/anuria but CKD is unlikely to have that
PE: Both have oral ulcers and hypertension. AKI does not have weight loss while CKD does. AKI does has large kidneys while CKD has small.
Lab: Both have high P, changes in Ca, low K, and active urine sediment. CKD will have anemia. AKI could have high K while CKD wont.
Imaging: CKD may have lost bone density. AKI has large kidneys while CKD has small.
Describe IRIS staging
At risk Stage 1 Stage 2 Stage 3 Stage 4
*substages- proteinuria, blood pressure
Goals of treatment for CKD
No cure
Good quality of life, slow progression, delay onset of uremic crisis, improve survival times
*pay attention to any nephrotoxic drugs or drugs excreted by the kidneys
Describe diet/nutrition for CKD pets
Renal diets are recommended for almost all patients- reduced P, omega 3 FA, vitamins
Good evidence for benefit in azotemic patients!
Still have questions about which diet and which cases/which to start?
General recommendation is to start when patient is stabilized and in stages 2-4
Even more important than renal diet though is that the patient is getting enough calories (appetite stimulants?). If won’t eat renal diet then feed them what you can
Describe fluids in CKD patient
Need to maintain normal volume and hydration!
This supports GFR and uremic toxin clearance, prevents clinical signs, and minimizes progression
Fluids for uremic crisis
IV fluids- replacement + maintenance + losses
Fluids for stable CKD
Fresh drinking water always available
Serial measurements of body weight to identify need for additional fluids
Give extra fluids as needed via SQ or E-tube
Disadvantages of feeding tubes
It keeps patients alive that maybe shouldn’t be alive anymore..can’t look at eating as a marker for quality of life
Describe P requirements in CKD patients
Control serum P within normal range
More P -> decreased serum Ca ->increased PTH and decreased calcitriol-> secondary mineralization of soft tissue and demineralization of bone and secondary hyperparathyroidism
How can you maintain normal phosphorus
Renal diets
Phosphate binders
Ideally you want to even be at low end of normal RI
Aluminum vs calcium based phosphate binders
Aluminum- effective, inexpensive, potential for toxicity, complexed with hydroxide, oxide, and carbonate
Calcium- may help minimize secondary high PTH, potential for toxicity, complexed with acetate, citrate, and carbonate
Describe control of hypertension in CKD patients
Incorporate BP measurements into regular diagnostics
Good evidence that controlling hypertension increases survival
Treat with anti-hypertensive if BP is greater than 160-170 or if evidence of end organ damage
Ways to control hypertension
Dogs- Na restriction, ACEi and calcium channel blocker and hydralazine
Cats- Na restriction, CCB and ACEi
*watch for signs that you overcorrected!
Describe proteinuria in CKD patients
Requires UPC measurements!
Treat with ACEi (enalapril, benzaepril)
Always treat this!
What are some other (noncore) treatment strategies for CKD patients
Acid-base balance (use potassium citrate unless hyperkalemic)
High or low potassium (high in end stage, low before then)
Acid blockers for GI symptoms (new evidence suggests maybe there isn’t increased gastrin)
Anemia (not making enough EPO)
Calcitriol reduces PTH but there are potential complications and frequent monitoring is required
Azodyl- probiotic that is claimed to be enteral dialysis. No evidence
