How does the prognosis for CRF differ in dogs and cats?
cats usually stay stable longer, dogs get progressive CRF
With tubular>glomerular disease or if there is whole nephron loss what will biopsy show?
chronic tubulointerstitial nephritis, lymphocytes, plasma cells, super nephrons
What kinds of diseases cause tubular>glomerular damage?
renal dysplasia, end-stage fibrotic with fetal glomeruli
In which species is glomerular>tubular damage more common? What is seen in urine? What happens first, azotemia or PU/PD? What might biopsy show?
dogs, proteinuria, azotemia, glomerulonephritis, glomerulosclerosis, amyloidosis
What are the renal reserve numbers for dogs?
50% normal clinically, 67% become PU/PD, 75% PU/PD and azotemia
What happened with feline renal mass reduction experiments?
After 1 and 5/6 kidney reduction creatinine still only 2.5 and could still concentrate urine (1.035)
What are some morphologic changes of surviving nephrons in CRF?
super nephrons become hypertrophied, hyperplastic
What are some function responses of nephrons in CRF?
increased single nephron GFR (but still summation decrease GFR), stop regulating BUN/creatinine, keep regulating electrolytes
Give an example of the trade off hypothesis in CRF.
Mild hypertension helps increase GFR but can cause organ damage (retinal detachment and stroke)
Why might increasing PTH in CRF end up being a bad thing?
increases serum Ca dn phosphorus excretion, but is a uremic toxin
What are the four stages of chronic kidney disease?
non-azotemic (may be PU/PD, decreaed GFR); mild (azotemia, mild or no signs), moderate (azotemic, signs, hyperphosphatemia), severe (end stage)
What are the borderline proteinuric and proteinuric levels (for UP/C ratio) in IRIS guidelines?
0.2-0.4 in cats and 0.2-0.5 in dogs; greater than either is proteinuric
What three things are used to stage renal failure patients with IRIS guidelines?
azotemia, UP/C, blood pressure
Name 4 infectious causes of CRF
bacterial (pyelonephritis), spirochetes (Lyme, Lepto), rickettsial (RMSF), viral (FeLV, FIP)
Name 5 autoimmune causes of CRF
immune-mediated glomerulonephritis, lupus, lyme, HW (wolbachia), babesia
What are four things that contribute to the development of PU/PD in CRF?
osmotic diuresis (increased solute load), pressure diuresis (increased single nephron GFR), nephrogenic DI, medullary washout
What GI signs are seen with CRF?
vomiting/nausea (uremic toxins act on CRTZ), inappetance, ulcers (increased gastrin)
What happens with renal secondary hyperparathyroidism?
increased phosphorus causes increased PTH, and parathyroid hypertrophy and increased serum Ca++
What two processes happen to cause rubberjaw in young puppies?
decreased active vitamin D leads to hypocalcemia and decreased GFR leads to hyperphosphatemia, both lead to increased PTH levels
What Ca x Phos level can lead to soft tissue mineralization? Target organs?
70, renal tubules, gastric mucosa, small arterioles, aorta, CNS, lungs
What metabolic acid/base imbalance are CRF patients predisposed to?
metabolic acidosisj (can't excrete enough acid or resorb bicarbonate)
Chemistry changes with CRF? BUN? Creat? Phosphorus? Potassium?
all increased except potassium (can be high, low, normal)
What plasma clearance tests can show decreased GFR in PU/PD cases before azotemia is present?
iohexol or inulin
Two additional blood tests for differentiating ARF from CRF?
carbamylated hemoglobin or PTH/Vit D assay