Renal Biochemistry Profile, Pt. 2 Flashcards
How is azotemia commonly determined by USG?
- pre-renal = hypersthenuria
- renal = isothenuria
- post-renal = variable
How can PE findings and bloodwork confirm pre-renal azotemia?
PE = tacky mucous membranes, poor skin turgor
BLOODWORK = increased PCV, increased TP, and increased ALB due to dehydration
Other than dehydration, what can cause pre-renal azotemia? What are 3 of the most common causes?
chronic bleeding (HYPOVOLEMIA)
- GI ulceration due to prednisone or NSAID therapy
- bleeding GI tumor
- coagulopathy due to decreased PLTs, DIC, warfarin, or liver failure
What are the 2 hallmark signs of renal disease (until proven otherwise)? What is unique in cats?
- azotemia
- isosthenuria
cats maintain some concentrating ability with renal failure
What is the best clue for determining renal azotemia?
USG —> concentrating/diluting ability of the kidney implies functional nephrons
- if urine is not concentrated or not appropriate for the patient’s hydration status, the cause of azotemia is probably renal
What signalment is most susceptible to post-renal azotemia? What are the 3 most common PE findings?
castrated males
- straining to urinate
- large turgid bladder
- distended abdomen (uroabdomen)
- all due to blockage
What should be considered when an animal’s USG is isosthenuric, but they are not azotemic?
- history, signalment, PE
- hydration status
- possible interference with kidney concentration ability (calcium, cortisol, etc.)
Azotemia approach:
What are the 2 tiers of evaluating a patient with renal azotemia?
FIRST TIER = BUN, creatinine, USG
SECOND TIER = phosphorus, calcium, potassium, sodium, chloride, bicarbonate, anion gap
How should phosphorus levels change with renal azotemia? What is the mechanism? What 2 species show variation?
hyperphosphatemia
GFR drops below 25% and phosphorus excretion is impaired, allowing for its accumulation and a risk for mineralization of soft tissues (Ca x P > 70)
- HORSES - lose P from the gut
- CATTLE - lose P in saliva
What must be measured to get an accurate calcium reading during renal azotemia? Why?
ionized calcium
total calcium may be increased, but ionized calcium will be more accurately normal or decreased
How do the calcium levels change with renal azotemia? What is the mechanism? In what animals is this most common?
normocalcemic at the early/mild stages that develops into hypocalcemia
renal damage causes decreased renal tubular calcium resorption, which results in renal tubular production of vitamin D and hyperphosphatemia —> physiologic response of decreasing calcium and deposition into tissues
dogs, cats, ruminants
What does the hypocalcemia resulting from renal azotemia commonly result in? What 4 biochemical changes are observed?
renal secondary hyperparathyroidism due to decreased calcium causing the stimulation of PTH release
- azotemia
- increased P
- normal to decreased Ca
- increased PTH
How does the calcium response in horses with renal azotemia compare? Cats?
hypercalcemia - diet and excretion
hypercalcemia - chronic renal failure thought to be caused by receptor abnormalities (tertiary hyperparathyroidism)
How do patients with hypercalcemia and renal failure present on USG? Why?
hyposthenuric - calcium interferes with ADH receptors
How are potassium levels commonly altered with chronic renal failure? What is the mechanism in the 2 species this occurs in?
hypokalemia
- CATS - unknown hypokalemic nephropathy
- CATTLE - renal loss, salivary loss, anorexia, metabolic acidosis
What are the 2 mechanisms of hyperkalemia in renal azotemia? When is this life-threatening?
- oliguria/anuria - kidney unable to excrete potassium in end-stage and acute renal failure
- metabolic acidosis - hydrogen ions move intracellularly and potassium ions move extracellulary
acute renal failure and urethral obstructions
Sodium and chloride are most commonly normal in cases of renal failure. How are they altered if observed? In what 2 situations is this most common?
hyponatremia and hypochloremia
- chronic kidney failure, especially in horses and cattle, causing them to eat less (decreased Na/Cl intake)
- always a finding in uroabdomen
How is bicarbonate and the anion gap commonly affected by renal failure? What are the 3 mechanisms?
severe renal disease causes metabolic acidosis
- increased urinary loss of bicarbonate
- decreased tubular secretion of H+ ions
- production of sulfates and phosphates
DECREASED bicarb, INCREASED anion gap
What 2 characteristics affect glomerular filtration? What type of proteins pass?
- size (<68 kDa)
- electrical charge (negative charge at podocyte)
small proteins with positive charges —> most resorbed i the proximal tubule and not detected in the urine sample
How is proteinuria measured? What are the 6 levels? What protein is it best at detecting?
reagent strip - negative, trace, +, ++, +++, ++++
albumin
When is protein (albumin) measurable in the urine? What are the 4 categories of proteinuria?
protein either got past the glomerulus or entered after the glomerulus
- pre-renal
- glomerular
- tubular
- post-renal
What are the 2 main causes of pre-renal proteinuria?
- physiologic - hypertension, fever, seizure, strenuous exercise
- increase in small protein in the blood - hemoglobin, myoglobin, paraproteins (Bence-Jones)
What are the 2 types of renal proteinuria? What causes each?
- glomerulonephritis - damages barrier by antigen-antibody complexes or amyloid
- tubular proteinuria - acute renal disease, Fanconi’s syndrome
What is Fanconi’s syndrome?
defective proximal tubules where filtered proteins are not resorbed, causing renal proteinuria
What are 2 causes of post-renal proteinuria?
- hemorrhage - RBC in urine caused by vessel damage from inflammation, trauma, neoplasia, or coagulopathies
- inflammation - WBC in urine caused by UTIs or cystitis
How is proteinuria quantified? What type is most severe?
urine protein:creatinine ratio (UPCR)
- normal < 0.5
- tubular or glomerular > 0.5
- glomerular > 1.0
GLOMERULAR
What is characteristic of glomerular proteinuria?
decreased serum albumin (hypoalbuminemia)
What are the main 2 signalments to patients with glomerulonephropathy? How do most patients present?
- familial often manifests young
- secondary causes, like chronic infectious disease, noninfectious inflammatory disease, or neoplasms, manifests middle-aged to older
many are asymptomatic, some are sick with underlying disease
What is the pathogenesis of glomerulonephropathy? What does this result in?
damage to podocytes, most commonly by deposition of antigen-antibody complexes or amyloid, causes the podocytes to retract and allow the filtration of larger, negatively charges proteins
protein loss exceeds protein production, especially albumin and antithrombin —> hypoalbuminemia, hypercoagulability
What 3 biochemical markers are observed with glomerulonephropathy?
- moderate to marked hypoalbuminemia
- moderate to marked proteinuria
- +/- evidence of renal insufficiency
What is nephrotic syndrome? What 5 conditions are characteristic?
protein-losing nephropathy that leads to abdominal effusion
- proteinuria (glomerular disease)
- hypoalbuminemia
- abdominal effusion (decreased oncotic pressure)
- hypercholesterolemia
- hypercoagulable state (antithrombin loss)
What differentiates acute from chronic renal failure?
speed of development NOT severity
What patients are most commonly presenting with acute renal failure?
any signalment - acute onset of clinical signs (get sick fast)
How will patients with acute renal failure commonly appear? What are the 3 most common signs?
good BCS
- GI: anorexia, vomiting, diarrhea, halitosis (NH3)
- renal: oliguric to anuric
- neuro: depressed to obtunded to non-responsive, seizures
What are the 3 most common etiologies of acute renal failure? What is the characteristic feature?
- toxicants - lily toxicity in cats
- renal ischemia
- infection - leptospirosis
- (things that damage the kidneys swiftly!)
marked decrease in GFR leading to azotemia
What are the 3 most common bloodwork findings with acute renal failure?
- azotemia (occurs fast, within hours to days)
- +/- hyperkalemia
- +/- acidemia
What are the 4 most common urinalysis findings with acute renal failure?
- oliguria to anuria due to an abrupt decrease to GFR
- variable USG
- +/- proteinuria
- +/- cellular casts due to tubular epithelial cells
How do patients commonly present with chronic kidney failure?
extremely common in cats and geriatric animals with a poor BCS and dehydration —> slow onset of clinical signs
What is the etiology of chronic kidney disease in cats? What are 4 common clinical signs?
irreversible chronic interstitial fibrosis
- GI: anorexia, vomiting, diarrhea, halitosis (NH3)
- renal: polyuric
- neuro: depressed
- cardio: hypertension
What are the main 2 differences in end-stage chronic kidney failure compared to earlier chronic kidney failure?
- hyperkalemia
- oliguria to anuria
What gender most commonly presents with uroabdomen? What are the 2 most common causes? How will these animals present?
males
- trauma: birth (foals), HBC (dogs)
- chronic urethral obstruction
abdominal effusion
What are the most common serum electrolyte imbalances with uroabdomen?
hyperkalemia and hyponatremia
How does the kidney retain and excrete electrolytes and proteins? How is this affected by uroabdomen?
HEALTHY: kidney conserves Na and Cl (plasma); excreted CREA, urea, and K (urine)
UROAB: Na and Cl move into urine, causing their decrease in plasma (hyponatremia and hypochloremia); urea and K move into the plasma (azotemia, hyperkalemia); CREA remains in urine since it is a larger molecule and moves slowly
What are the 5 common bloodwork findings in uroabdomen?
- hyponatremia
- hyperkalemia
- hyphochloremia
- azotemia (increased BUN)
- +/- increased CREA from previous post-renal disease
What is characteristic of the abdominal effusion in uroabdomen? When is it diagnostic?
modified transudate (non-inflammatory) with high CREA concentration
when CREA concentration of the effusion is 2x the CREA concentration in the plasma
Categorized the azotemia:
normal - all within RI
Categorize the azotemia:
renal azotemia - urine is diluted with increased BUN and CREA
(USG is the best value used to categorize azotemia!)
Categorize the azotemia:
pre-renal - urine in concentrated
(use USG to categorize azotemia!)
How do the values in the renal failure cases prove the bladder is still intact?
cases 4 and 5 have azotemia and abdominal effusion CREA is about the same as serum CREA
