Renal Flashcards
4 things GFR depends on:
1) adequate blood flow, 2) BP, 3) interstitial and intratubular pressures, 4) number of functioning nephrons
GFR has to be decreased by ____% before BUN and Cr increase.
75%
Urine concentrating ability is lost after ___% of nephrons are gone.
66%
After creatinine is increased, every doubling of Cr means there’s been loss of function of ___% of the remaining renal mass.
50%
What are some tests used to measure GFR?
endogenous/exogenous Cr clearance
insulin clearance
clearance of radioisotopes
measurement of fractional clearance of electrolytes
What is the formula for Cr clearance?
Cr clearance= [(Urine Cr x vol urine/time/kg)/ serum Cr]
What are 4 reasons that Cr is better than BUN for determining GFR.
1) rate of production and exertion of Cr is constant, 2) Cr isn’t metabolized by external or renal processes, 3) some BUN in the filtrate is reabsorbed, 4) rate of BUN resorption varies w/hydration status and speed of flow in tubules
Between BUN and Cr, which can be disproportionately higher in dehydration? Why?
BUN (rate of BUN resorption varies w/hydration status and speed of flow in tubules)
What does an increased BUN:Cr ratio indicate? (2)
dehydration of intestinal bleeding
What does a decreased BUN:Cr ratio indicate? (3)
diuresis, noncreatinine chromagens, or ability of cows/horses to excrete BUN from GI
What are the 5 locations that can have lesions leading to renal azotemia?
glomeruli, tubules, interstitium, renal pelvis, blood vessels
Creatinine: Made in the ____ from the spontaneous conversion of ____ and ____.
Made in the muscles from the spontaneous conversion of creatine and creatine phosphate.
What is a major mechanism of non-renal increases in Cr?
muscle catabolism
What are 3 scenarios where you could have incr Cr from incr muscle catabolism.
Sepsis, developing cachexia, rhabdomyolysis
What is are 3 scenarios where you could have dear Cr?
liver failure (rare), cachexia, hyperthyroidism
What should you think about in cattle and horses if the Cr is significantly increased and the BUN is normal or a little high?
Non-creatinine chromagens
What are 4 important non-creatinine chromogens?
ketones, glucose, carotenes, Vit A
Interpret the scenario in a cow/horse:
USG & Cr incr, BUN normal
non-Cr chromagens causing Cr increase
Interpret the scenario in a cow/horse:
USG & BUN incr but Cr disproportionately higher than BUN
prerenal azotemia & non-Cr chromagens causing incr
Interpret the scenario in a cow/horse:
Isosthenuria w/azotemia but Cr disproportionately higher than BUN
renal azotemia but the discrepancy could be b/c of non-Cr chromogens or the fact that they can excrete BUN in GI
Between BUN and Cr, which will be present in the abdominal fluid of an animal with ruptured bladder longer and why?
Cr b/c it takes longer for Cr to equilibrate with serum than BUN
Dialysis and diuresis promote greater excretion of ___ than ____ (BUN or Cr)
Dialysis and diuresis promote greater excretion of BUN than Cr.
___% of BUN is passively resorbed by the proximal tubules, ___% by the collecting ducts.
50% of BUN is passively resorbed by the proximal tubules, 10% by the collecting ducts.
What happens to the urea secreted in saliva of small animals?
goes to GI–> degraded to ammonia by back–> reabsorbed–> to liver–> turned back into urea
What happens to urea secreted in saliva of ruminants (and some degree in horses)?
goes to rumen–> bacteria turn urea into amino acids–> aas from the breakdown reabsorbed so get net protein gain and net urea loss
Why does rumen stasis cause increased BUN without Cr?
Because the urea secreted in saliva goes to rumen but not broken down and reabsorbed as aas
How does GI bleeding cause an increase in BUN?
blood is broken down into aas and ammonia in the GIT–> reabsorbed and go to liver where they’re converted back to urea
4 nonrenal causes of increased BUN
1) high pr diet, 2) GI hemm, 3) sepsis/fasting (incr protein catabolism), 4) decr renal perfusion (increases renal tubular resorption)
6 causes of decreased BUN
1) liver failure, 2) shunts, 3) malnutrition or low pr diet, 4) hyperthyroidism (incr pr catabolism and incr GFR), 5) diuresis, 6) young animals (high anabolic state)
2 major mechanisms of prerenal azotemia
1) increased pr catabolism (small bowel hemm, necrosis, starvation, prolonged exercise, infection, fever, steroids); 2) hypovolemia (dehydration, cardiac insufficiency, shock)
5 nonrenal conditions where you have dehydration but can’t concentrate urine
primary and secondary DM hyperCa steroids pyometra medullary washout
What is the expected urine Cr:serum Cr ratio to distinguish renal from prerenal azotemia?
> 50:1 prerenal
Normal fractional excretion of Na is
T or F: With primary glomerular disease, you always get decreased concentrating ability before azotemia.
False: With primary glomerular disease, you may get azotemia before a decrease in concentrating ability because tubular disease usually follows glomerular.
Why might horses only get a moderate increase in BUN with renal failure?
Because they can excrete it in their GI– so if BUN is really high, likely has prerenal component
Why isn’t BUN a good indicator of renal disease in birds? What is a better indicator?
they don’t have a lot of urea in the blood to begin with. Uric acid is better
What is the main end-product of nitrogen catabolism in birds?
uric acid
What are 2 non-renal causes of hyperuricemia in birds?
ovulation and post-meal
The kidneys resorb ___% of H2O that enters the tubules.
99%
Water is resorbed passively in everywhere in the kidneys except the _____ where ____ acts.
Water is resorbed passively in everywhere in the kidneys except the collecting tubules where ADH acts.
What are 5 factors needed to make concentrated urine?
1) 1/3 renal mass functioning, 2) enough ADH made and able to respond to it, 3) medullary interstitium saturated, 4) conducive hydration status, 5) no concurrent diseases
T or F: Birds have a bladder.
False
6 mechanisms that can lead to decreased urine concentrating ability.
- lesions in 2/3 of the kidney
- decreased ADH production (CDI)
- refractory to ADH
- decreased medullary hypertonicity (washout)
- overhydration
- solute overload (DM, diuresis)
The water deprivation test is used to differentiate between which 3 diseases/conditions?
PD
CDI
RF (before azotemia)
A major contraindication to doing the water deprivation test is what?
azotemia
What is the mechanism of the water deprivation test?
Induces
What is the maximum weight loss stimulus for ADH release?
3-5%
What are 2 scenerios that using the water deprivation test would be indicated?
1) PUPD in an animal without azotemia, dehydration, or other biochemical abnormalities
2) repeated urine samples in nonazotemic patients with isosthenuria
When should you stop the water deprivation study (multiple)?
When they are concentrating to 1.025-1.035 or
5% of BW lost or
azotemia develops
When should you give ADH during a water deprivation study?
if the USG changes 310 most/kg or 3-5% weight loss
Water deprivation study: if the patient has PD, how fast should the urine start to become concentrated?
within a few hours
Water deprivation study: If the urine is not concentrating after a few hours, what are the differentials and what is ruled out?
Differentials are DI or renal failure
PD is ruled out
Water deprivation study: If a patient cannot concentrate their urine after a few hours but starts to concentrate after ASH is given, what is the dx?
CDI
Water deprivation study: If a patient cannot concentrate its urine after a few hours and ADH is given, but there is still no response, what are the differentials?
Renal failure or NDI but bloodwork should help differentiate between those
What is another test you can do to test concentrating ability if the water deprivation test is too risky (but is less sensitive than the WDT)?
ADH concentration test
Main differentials for persistent isosthenuria without azotemia?
CDI or NDI
PD
Urine specific gravity is an estimate of ______.
Urine specific gravity is an estimate of osmolality.
The urine filtrate starts with a USG of ____ and osmolality of _____.
The urine filtrate starts with a USG of 1.010 and osmolality of 300 most/kg.
Main differentials in a patient with persistent hyposthenuria without azotemia?
NDI/CDI
PD
USG is an estimate of _________.
osmolality
What is the relationship between osmolality and freezing temperature?
As osmolality increases, the freezing temp decreases (lower temp required to freeze).
T of F: Mucus, crystals, and cells affect USG.
False
For every 1 g/dL of protein and glucose in urine, the USG increases by ____.
0.004
T or F: Hetastarch increases osmolality but not USG.
True
Urine volume and Spg are inversely correlated in health and most diseases except which 2?
DM (incr vol w/incr Spg) Oliguric RF (decr vol w/decr Spg)
Isosthenuria in dog, cat, cow, horse.
1.007-1.013
Hyposthenuria in dog, cat, cow, horse.
Adequate concentrating ability Usg in a dog.
> 1.030
Adequate concentrating ability Usg in a cat.
> 1.035
Adequate concentrating ability Usg in a horse.
> 1.025
Adequate concentrating ability Usg in a cow.
> 1.025
5 causes of NDI.
HyperCa Steroids HypoK Pyometra Congenital
4 causes of solute overload leading to PU/PD and dilute urine.
DM
acromegaly
Faconi’s
salt toxicity
Changes to urine when left at room temp: Cells and casts- Glucose- Ketones and bilirubin- pH- CO2- Bacteria-
Cells and casts- lyse Glucose-metabolized Ketones and bilirubin- decrease pH- increases (urea converted to ammonia) CO2-escapes Bacteria- proliferates
Normal urine production per day in a dog.
20-40 ml/kg/day (1 ml/kg/hr)
Normal urine production per day in a cat.
10-20 ml/kg/day
6 potential causes of red/brown urine.
hemoglobinuria myoglobinuria hematuria porphyria phenothiazine antihelmnitics aminopyrine (urinary analgesic)
What is unique about porphyrins in urine?
Fluoresce under UV light
Normal urine pH in dog and cat.
5-7
Normal urine pH in horse and cow.
7-8
Normal WBC or RBC seen in urine of dog, cat, horse, cow.
0-5
Proteinuria indicates a lesion in which part of the kidney?
Glomerulus
Casts indicate a lesion in which part of the kidneys?
Tubules
USG is lower in puppies
T or F: there is no difference in protein, blood, ketones, or bilirubin in puppy urine.
True
With paradoxical aciduria, what has to be corrected before the tubules can excrete bicarb?
HypoCl
What are the main chem/urine findings in paradoxical aciduria?
Profound hypoCl
Increased bicarb
Acidic urine
What is a differential to consider in a dog with acidosis but alkaline urine?
RTA
Struvites form in alkaline/acidic urine?
alkaline
Differentials in dogs with alkaline urine (4)
RTA
Urease splitting bacterial infections
long storage time at room temp
disinfectant contamination
How does the protein pad on the dipstick work?
it is kept at an acidic pH and when anionic proteins (albumin) hit it, it becomes alkalinized and changes color
Trace proteinuria is ____ g/dL.
Trace proteinuria is
1+ proteinuria is ____ g/dL.
1+ proteinuria is 0.03 g/dL.
Bence Jones proteins won’t case a + on the dipstick until ____ g/dL.
0.025- 0.05 g/dL
The SSA turbidity test is a test for what?
Proteinuria
T or F: The SSA test only picks up albumin.
False- it picks up all proteins
What can cause a false + on the SSA test?
Penicillin, sulfonamides, contrast media
What can cause a false - on the SSA test?
turbid or markedly alkaline urine
What causes a false + on the protein pad (dipstick) but a false - on the SSA test (if marked)?
alkalinuria
What can cause a false + on the blood pad of the dip stick because of lysis?
very dilute urine (
What are 2 causes of false +s on the glucose pad on the dipstick?
oxidizing cleaning agents or H2O2 touching the pad
cats with urethral obstruction (unknown compound causes it)
Renal threshold for glucose in dog.
200 mg/dL
Renal threshold for glucose in cat.
300 mg/dL
Renal threshold for glucose in horses.
150 mg/dL
Renal threshold for glucose in cattle.
100 mg/dL
Glucosuria without serum glucose over the threshold suggests what?
Renal tubular resorption defect or transient hyperglycemia causing glycosuria but blood taken after it has normalized
Differentials for glucosuria without serum glucose over threshold (non-transient).
nephrosis (toxic)
tubular injury
primary or familial glucosuria
fanconis
Ketones are measured on the dipstick via a ____ reaction.
Nitroprusside
Excreted ketones include ___% beta-hydroxybutyrate, ___% acetoacetic acid, and ___% acetone.
78% beta-hydroxybutyrate, 20% acetoacetic acid, and 2% acetone.
7 differentials for ketonuria.
excessive fat catabolism (neg energy balance) low carb diet cachexia starvation hyperthryoidism preg toxemia DM
What might happen to Na and/or K with ketonuria?
It can cause hypoNa and/or hypoK because ketone needs to be excreted with a cation
Does biliverdin cause a + reaction on the bilirubin pad on the dipstick?
no
T or F: The bilirubin pad on the dipstick only detects unconjugated bilirubin.
False– only conjugated bilirubin
Does bilirubinemia or bilirubinuria come first?
bilirubinuria
RBC casts localize hemorrhage to the ____.
tubules
WBC casts localize inflammation to the ___ and indicate ____.
WBC casts localize inflammation to the tubules and indicate pyelonephritis.
If you see a bunch of squames in a free catch urine from a male dog, what differential should be considered?
Sertoli cell neoplasm (secreting estrogen and causing squamous metaplasia of the prostate)
5 reasons you may see bacteria in urine with pyuria.
contamination Cushings exogenous steroids dilute or alkaline urine (lyse WBCs) antibiotics
Lipid is common in the urine of ____.
cats– their renal tubular cells have a lot of lipid normally
T or F: Lipiduria is correlated with lipemia.
F
Hyaline casts are made from ___ and ___.
mucoprotein and albumin
An increase in hyaline casts implies what?
glomerular disease or Bence Jones proteinuria
Granular casts indicate ___, ___, or ____.
Granular casts indicate nephrosis, pyelonephritis, or infarction
Waxy casts indicate what?
Chronic progressive tubulointerstitial disease
___/lpf grabular casts in concentrated urine is normal
1-2/lpf
Waxy casts form in ____.
collecting tubules
Lipid seen in pathologic states (so not just in cats that normally have it) can occur with what 2 disease?
tubular disease/degeneration and DM
Ammonium biurate crystals can normally be seen in what breeds? What is the pathogenesis?
dalmations and bulldogs
defect in uric acid transporter into hepatocytes so excrete uric acid in urine
What are 2 pathologic states that you can see ammonium biurate crystals in?
Liver failure, shunt
Bilirubin crystals occur in alkaline/acidic urine?
acidic
What kinds of animals normally have Ca carbonate crystals?
herbivores like horses, rabbits, GPs
What kind of crystals are normally common in birds?
amorphous urates
In what situation may you see a non-pathologic increase in the number of Ca oxalate dehydrate crystals seen in horse and cow urine?
when they’re eating oxalate-rich plants
What differentials should be considered in dogs or cats with increased numbers of Ca oxalate dehydrate crystals?
can be normal
EG toc
hyperCa disorders
T or F: Ca oxalate monohydrate crystals can be seen in normal dogs, cats, horses, rabbits, and GPs
T
Ca phosphate crystals normally form in alkaline/acidic urine?
Alkaline
Why might you see cholesterol crystals in urine?
hypercholesterolemia
PLN
What drugs most often cause crystalluria?
sulfas, ampicillin, allopurinol, xanthine, contrast media
Hippuric acid crystals look like which other crystal?
Ca oxalate monohydrate
Leucine crystals suggest what?
liver disease
Tyrosine crystals can be seen with what?
liver disease
Uric acid crystals have the same pathology as what other crystal?
urates (can see in dalmatians or in liver disease)
What is the pathologic process that leads to formation of uric acid crystals in liver disease?
can’t concert uric acid to allantoin and ammonia to urea
xanthine crystals look exactly like what other type of crystal?
ammonium biurate
Xanthine crystals can be familial in what breeds?
doxies and cavies
Xanthine crystals can form with administration of what medication?
allopurinol
Most small animals with renal disease have increased/decreased/normal P and increased/decreased/normal Ca.
Most small animals with renal disease have increased P and normal Ca.
The second most common changes seen in small animal patients with renal disease in Ca and P are: increased/decreased/normal P and increased/decreased/normal Ca
The second most common changes seen in small animal patients with renal disease in Ca and P are: increased P and decreased Ca.
What are the 6 mechanisms that lead to hypocalcemia in renal disease (SA)?
not enough tubular cells to resorb it decr Vit D production decr albumin soft tissue mineralization secondary to P increase chelation from oxalate with EG tox
Only about __-__% of small animals with renal disease have hyperCa.
10-20%
HyperCa more commonly occurs in renal disease in small animals with what condition?
familial renal nephropathy
Horses most commonly have increased/decreased/normal Ca in renal disease. P is 50/50 incr and decr.
increased
Are cows with RF more likely alkalotic or acidotic?
Alkalotic because of ruminal atony & ileum from uremia
Ill cows are often hypoCa…why is this?
Ill cows often get ruminal atony and ileus which causes alkalosis. Alkalosis causes a shift of iCa to protein bound Ca.
___% of P is resorbed in the prox tubule, ___% excreted.
80% of P is resorbed in the prox tubule, 20% excreted.
A P >___ mg/dL is considered severe.
15 mg/dL
What are 4 common sites that become mineralized with a high Ca x P?
blood vessels, midzonal gastric mucosa, heart, lungs
What is the mechanism for developing metabolic bone disease, osteopenia, renal fibrous osteodystrophy from CRF?
CRF–> decr Vit D–> can’t resorb Ca or get from bones–> parathyroid hyperplasia–> incr PTH–> Ca resorbed in kidneys and get more from bones
How correction of metabolic acidosis cause hypoCa?
Ca will go from ionized in acidosis to protein bound in alkalosis.
Why aren’t patients with hyperCa of malignancy hyperP?
because PTH-rp acts like PTH which is phosphaturic
If you have hyperP with a much higher hyperCa with azotemia, is renal failure or a primary Ca disorder (like hyperCa of malign or primary hyperPTHism) more likely?
Primary Ca disorder b/c Ca is much higher
If you have hyperP with a much higher hyperCa with azotemia, a primary Ca disorder is more likely than renal failure. Between hyperCa of malign and primary hyperparathyroidism, which is more likely in this case?
HyperCa of malignancy because only 5% of patients with hyperparathyroidism have azotemia.
What do you think is going on if you have a patient with normal P, hyperCa, and azotemia?
Think primary Ca disorder (hyperCa of malign or primary hyperPTHism) that’s causing phosphaturia.
What are 4 mechanisms that hyperCa causes dilute urine?
Interferes w/ADH action
Decreases movement of AQP2 to apical membrane to prevent H2O resorption
Blocks receptors on renal epis
Mineralization of cells
Cows and horses are usually hyper/hypo/normo Na and hyper/hypo/normo Cl with renal failure.
Cows and horses are usually hypoNa and hypoCl with renal failure.
___% of Na is resorbed in the kidney– __% in prox convoluted tubule, __% in the ascending LOH, ___% in each distal tubule and collecting duct.
100% of Na is resorbed in the kidney– 65% in prox convoluted tubule, 25% in the ascending LOH, 5% in each distal tubule and collecting duct.
What are 2 differentials when the FE of Na is over 1%?
RF or decreased aldosterone
Most cases of small animal renal failure have hyper/hypo/normo Na and hyper/hypo/normo Cl unless chronic and then there may be hyper/hypo/normo Na and hyper/hypo/normo Cl.
Most cases of small animal renal failure have normoNa and normoCl unless chronic and then there may be hypoNa and hypoCl.
Cl and Na are expected to be high/low/normal in cases of uroabdomen in all species.
low Na and Cl
Most K is resorbed in the ____ and excreted in the ___ via _____.
Most K is resorbed in the pro tubule and excreted in the CD via aldosterone.
HypoK in cats with renal failure put them at risk for what?
kaliopenic polymyopathy-nephropathy syndrome
SAs with chronic renal failure are more likely to have hyper/hypo/normo K?
hypo
What are the mechanisms responsible for hypoK in cows with RF?
renal loss, salivary loss, anorexia, met alkalosis from ruminal atony causes K to shift into cells
How does hypoK make renal failure worse?
causes tubular degeneration and decreased responsiveness to ADH
Where is most Mg resorbed?
prox tubule and thick ascending LOH
Mg is usually high/low/normal in patients with RF.
high
Ca and Mg pattern in blister beetle tox?
severe hypoCa and hypoMg
P in horses with CRF is usually high/low/normal?
low (different than SAs & cows)
Formula for determining FE of an electrolyte?
FE = [serum Cr/urine Cr] x [urine electrolyte/serum electrolyte] x 100
HypoNa azotemic animal with FE of Na
GI Na loss
What does a FE of P >20 in a dog and >73 in a cat indicate?
increased PTH or PTHrp
What is the typical pattern of Na, Cl, K, and acidosis vs alkalosis in cows w/RF?
hypoNa, hypoCl, hypoK; usually met alk b/c of ruminal atony but can have acidosis from uremia
3 conditions that have to occur for paradoxical acuduria to happen.
hypoCl, dehydration, met alkalosis
What is the mechanism for paradoxical aciduria?
dehydration–> RAAS triggered–> aldosterone to kidney–> Na/H2O resorbed but K has to be excreted for this to happen–> at same time aldosterone triggers H excretion which wants to leave with Cl but hypoCl prevents that–> so leads to bicarb formation in tubules which is resorbed in exchange for H
Some of the highest fibrinogen concentrations in cows are seen with what condition?
RF
2 main glomerular diseases?
glomerulonephritis and amyloidosis
What are some sources/causes of preglomerular proteinuria?
overloading– myoglobin, Hg, paraproteins
transient from fever, stress, seizures, and exercise
Hypoalb + persistent proteinuria + inactive sediment indicate a lesion in which part of the kidney?
glomerular
What changes are seen with nephrotic syndrome?
hypercholesterolemia, proteinuria, hypoalb
also edema, ascites, thrombi
Why might kids, foals, calves, and lambs
colostrum ingestion
Creatinine is usually measured via the ___ reaction.
Jaffe
UPUC: >___ indicates renal proteinuria
> 1
A normal UPUC is
What is the point of the microalbuminuria test?
To detect trace protein that might be present in early renal disease
What are 2 ways that glomerular disease can lead to a prothrombotic state?
- AT lost in urine
2. albumin lost in urine–> increases plt sensitivity
Why isn’t hyperP as significant in a cow with dear GFR as other species?
Because they secrete P in other locations other than the kidney.
Why is PTH important in renal failure?
It increases because of decreased GFR which can lead to fibrous osteodystrophy or osteopenia. Also, PTH acts as a uremic toxin.
Does Vit D increase or decr in renal failure?
Decrease because it can’t be converted to active form in the nonfunctioning kidneys.
An increase in the amount of GGT or NAG in the urine in renal disease indicates what?
indicates ongoing proximal tubular lesion because this is where most of these enzymes are and are washed out with each urination when released in tubular injury
Ormolu gap is defined as-
the difference between the measured osmolality and calculated osmolarity
What is the formula to calculate osmolality?
1.86 ([Na + K] + Glucose/18 + BUN/2.8)
What are the osmole gap RIs?
___= normal
___= suggestive of EG tox
___= diagnostic of EG tox
What are the osmole gap RIs?
20= suggestive of EG tox
>30= diagnostic of EG tox
What is the AG calculation?
AG= (Na + K) - (Cl + HCO3)
What is the toxic metabolite with diethylene glycol toxicity?
HEAA
What are the expected serum BUN, Cr, K, P, Na, & Cl in uroabdomens?
incr BUN, Cr, K, P
decr Na, Cl
What makes up the counter current multiplier system?
hypertonic medullary interstitium and the vasa recta
Fanconi syndrome is from a defect in what?
defect in proximal tubule resorption in glucose, Na, Ca, bicarb, amino acids, and/or P
What are some findings in the urine in a patient with Fanconis?
dilute urine, glucosuria, proteinuria, increased FE of electrolytes, cystinuria, aminoaciduria
Patients with nephrotic syndrome have a lesion at the level of ____.
the glomerulus (from amyloidosis, glomerulonephritis, or end stage RF)
Puppies/young dogs with progressive renal nephropathy/dysplasia typically have increased/decreased/normal Ca and P.
hyperCa and hyperP
Why would one consider running a bFGF test on urine?
if bladder cancer is suspected
