inc in non-protein nitrogen compounds. So, could be an inc in urea or in creatinine
how much kidney damage until you see azotemia?
Less than 50% of nephrons functioning (slightly different for cats)--> called "renal insufficiency/failure"
two major signs of kidney failure?
azotemia and dec conc ability (USGref apprx 1.007–1.013, which is isosthenuric)
Explain the life of a urea molecule--> how does it begin, to how it ends
Protein gets broken down into ammonium. It is in blood and goes to the liver. The hepatocytes fix the ammonium into urea. The urea is filtered through the glom. Some is resorbed by tubules, most is excreted into urine, some is excreted into intestines.
Explain the life of a creatinine molecule---> how does it begin, to how it ends
creatine/creatine PO4 from MUSCLES is broken down to form creatinine and is then flowing through the blood. It is filtered in the glom. NONE is resorbed in the tubules, and it is then excreted into the urine (also some into intestine)
Prerenal azotemia can be caused by what two things?
(1) DEC RENAL BLOOD FLOW (like hypovolemia in dehydration or shock, or cardiac insufficiency) (2) significant inc in urea production
Renal azotemia is caused by what?
a dec in functional nephrons *>75% loss. This could be from Inflammatory causes (GNitis, pyelonephritis, tub-inter. nephritis), Amyloidosis, a toxic nephrosis (hypercalcemia, ethylene glycol, etc), or an ischemic/hypoxic situation--> poor renal perfusion (also could be a congenital hypoplasia/aplasia, hydronephrosis, or a metastatic neoplasia)
in who is it normal to have a small amount of protein and bilirubin in their urine?
you get the USGref how? how does this measurement work?
Use a refractometer. It measures the amount of light bending around solid particles in urine, which is inversely proportional to the USGref. Basically tells you the amount of particles in a volume of fluid
when is the USGref less accurate?
if there are high levels of protein and/or glucose in the urine (will overestimate the USGref, need to compensate for this)
what is the average, "normal" USGref?
about 1.030 (Lg animals about 1.025)
Hypersthenuria USGref values are?
apprx greater than or equal to 1.050
*Isosthenuria USGref values are?
What is Isosthenuria? what is it telling you?
when URINE osmolality is aprx equal to PLASMA osmolality, indicating that KIDNEYS HAVE LOST THEIR ABILITY TO CONCENTRATE OR DILUTE
Hyposthenuria USGref values are?
less than 1.007 (happens when LOH is working, so remove solutes, but ADH/distal tubular problem means it can't concentrate it again)
dehydration (they are dehydrated, so blood vol is low, so more ADH is released so the tubules respond by resorbing more water to conserve blood volume)
1.003, no other findings (NOT dehydrated)
OVERHYDRATION(too many IV fluids, maybe drinks too much) The blood volume is too high, so no ADH is released, so more water is excreted to get rid of excess water)) **note: its not isosthenuric, it's hypo. SO, proves kidney is still working b/c it's diluting to get rid of extra water.
1.010, no other findings
ISOSTHENURIC!!! Question--> IS THERE AZOTEMA? If no, just have extra water that body is getting rid of (they will be well hydrated, with slightly high blood volume, and a little release of ADH).
1.010, and there is azotemia/anemia/dehydration
CHRONIC RENAL FAILURE!! there is low blood volume, and lot's of ADH release, but the tubules arent responding well to resorb, so there is a poor water conservation (and a poor conc gradient also)
1.025, 4+ glucosuria/ dehydrated
OSMOTIC DIURESIS (DIABETES MELITUS). They are dehydrated and have low blood volume, and ADH is being released to try to get more water, and the tubules are responding to the ADH, but the conc gradient is low because all the glucose in the urine is drawing water towards the urine even though the aquaporins are open and responding to ADH. Thus, you still don't resorb enough water and are dehydrated with too much glucose.
1.002, other findings negative (DEHYDRATED)
hyposthenuric (so kidneys are working) but you are DEHYDRATED with lots of water in the urine. Why? DIABETES INSIPITUS. Two different types: (1) RENAL diabetes insipitus is when there is lots of release of ADH to try to conserve water, but the tubules aren't responding, so water is not conserved. (2) CENTRAL diabetes insipitus is when ADH is not being released for some reason, so although the tubules are working, they aren't being told to conserve water, so they're not.
If dehydrated and USGref > 1.030, what do you think?
this is an appropriate response. dehydration is not because of renal loss.
If dehydrated and USGref 1.014 –1.030, what do you think?
starting to have impaired ability to concentrate (since dehydrated, would want to conserve water, so should have very conc urine). you could suspect renal dz, OR, it could be diabetes mellitus (glucosuria-->osmotic duiresis) OR hypoadrenocortisism (dec Na and Cl would dec medullary tonicity which would dec conc gradient to pull water back in), OR diabetes insipitus (parital, central or renal)
If dehydrated and USGref 1.007 –1.013, what do you think?
ISOSTHENURIC RANGE!!! kidney cannot concentrate or dilute. (is dehydrated, so you know it's not from being overhydrated) If you also see azotemia, it is probably either renal failure or hypoadrenocortisism (will dec medullary tonicity and dec release of ADH by making plasma hyposmolar)
If dehydrated and USGref is less than 1.007, what do you think?
hyposthenuric range--> kidneys can dilute, there is too much water in urine but the animal is dehydrated--> diabetes insipitus
If oliguric, think
(low output of urine) prolly renal failure
if glucosuric, what's the diff between if the USG is 1.007-1.020 and if it's over 1.020?
both are diabetes, but when it's in isosthenuric range, it's DM AND medullary washout and or renal failure
if hyponatremic and hypochloremic, explain diff between USGref> 1.020, 1.007-1.013, and less than 1.007.
All are hypoadrenocortisism. In isotonic range, there is also a dec in medullary tonicity, and consider renail failure. If hyposthurnic, there is low medullary tonicity AND low plasma osmolality which leads to dec ADH release, causing the dilution
when you are interpreting semiquantative concentrations (the dipstick reading), what must you always consider?
CONSIDER VOLUME of urine being excreted per day (usually inversely proportional to USGref) because, your dipstick might say the dog is +3(300ml) protein, but it is only producing 100 mL of urine a day, so it's excreting 300mg of protein a day. Another dog's dipstick might say they are only a +1, but that dog is urinating 1000mL of urine a day, so this dog is ALSO excreting 300mg of protein a day, the same as dog one! (so, the amount of urine you're excreting in one day can dilute or concentrate whatever value you get on the dipstick, even if in the end you are excreting the same amount of protein)
pH of carnivore urine? pH of herbivore urine?
when is urine considered aciduria? when is it considered Alkalinuria?
acid= less than or equal to seven. alkaline= greater than or equal to 7.5
when would a reagent strip give you a false positive for protein?
in alkaline urine
(you can test presence of protein in urine with a SSA (sulfosalicylicacid) turbidity test. when would you get a false negative?)
in alkaline urine
what would you see in a prerenal proteinuria? causes?
high level of proteins from a problem before the kidney. Small proteins that can get through the glom are seen. Hemoglobinuria (intravascular hemolysis), Myoglobinuria (acute mm necrosis) BenceJones proteinuria (light chains of immunoglobulins, seen in lymphoid neoplasms)
what would you see in a renal proteinuria? causes?
usually in GLOM dz. you will see albumin and most globulins (except the largest globulins) can lead to hypoproteinemia & hypoalbuminemia (only one that causes hypoalbuminemia). Usually due to Glomerulonephritis, or Glomerular amyloidosis
what would you see in a tubular proteinuria? causes?
usually see small globulins, because prox tubule is not resorbing the small filtered globulins. Could be caused by acute tubular toxicity, or congenital disorders (fanconi's syndrome)
what would you see in a hemorrhagic/inflammatory/postrenal proteinuria?
Hematuria(UT hemorrhage), Pyuria (urinary tract inflammation-->exudation of plasma proteins)
what are two causes of glucosuria? what does this lead to?
(1) hyperglycemia glucosuria--> too much plasma glucose, exceeds renal resorption threshold and excess stays in urine. (2) renal glucosuria--> damaged/defective tubules arent absorbing norm amts of plasma gluc. (toxins, ischemia, congenital fanconi's in basenji) (they are normoglycemic in this case). IN EITHER CASE, you will get an OSMOTIC diuresis, where the excess glucose interferes with the conc gradient, and water stays in tubule instead of being resorbed
what are you detecting, if you find ketones in the urine? what does this mean?
Hepatocytes make ketone bodies: acetoacetate, β-hydroxybutyrate, acetone but only AcAc and acetone(degraded quickly) are detected by strip b/c only they are "true" ketones. So, AcAc gets into urine when there is excess ketogenesis by liver, which usually happens when there is Excess catabolism of fatty acids by hepatocytes (Promoted by dec insulin activity and inc glucagon activity). Common in diabetes mellitus and bovine ketosis. *also important to note that excess ketones in urine causes obligate loss of cations and can contribute to hyponatremia or hypokalemia. (Ketones are virutally non-resorbable, they have an extremely low threshold of resorption)
Hematuria--> see what? happens when?
see RBCs in urine sediment, bc RBCs added to the fluid. usually post renal (hemorrhage in bladder, in urethra) but can occur in the tubules
Hemoglobinuria--> see what? happens when?
see anemia, hemoglobinemia. Can be from intravascular hemolysis, or if there were RBCs in urine but they were lysed (if alkaline urine, or if dilute urine, or if in urine for a long time) or were lysed in vitro after collection.
Myoglobinuria--> see what? happens when?
see myoglobin in urine, happens when there is myglobin in plasma from MUSCLE DAMAGE
when would you find bilirubin in the urine?
(1) hemolytic icterus...there is more bilirubin being formed from the broken down RBCs than what is able to be excreted into bile. (2) hepatobiliary dz (cholestatic icterus) is when there is impaired bilirubin excretion (can't excrete it, so regurgitated into plasma and filtered into urine). (NOTE: strip usually only detects CONJUGATED bilirubin, b/c the unconjugated is bound to albumin)
casts in urine
what should you look for if you see bacteria in the urine?
Are there WBCs? if there are, there is prolly a UT infection or inflammation. If there isn't, the bact are prolly a contaminant (like getting flushed out of system after tx with abx)
what should you know about hyaline casts?
not pathogenic, can be in healthy pts, it's made from a mucoprotein
what should you know about fine/coarse granular and epithelial casts?
PATHOGENIC. generally indicate TUBULAR DEGENERATION
Epithelial cells in urine--> squamous cells. What are you thinking?
from distal urethra/genital tissues
Epithelial cells in urine--> transitional cells. what are you thinking?
from renal pelvis to urethra (genito-urinary tissues)
Epithelial cells in urine--> renal cells. what are you thinking?
loss of tubular cells (rare).
three main reasons there might be lots of epithelial cells?
iatrogenic damage, hyperplastic mucosa due to inflammation, neoplastic mucosal cells (rare)
Urinalysis PU/PD (wasn't mentioned on review, but...)
polyuria---> how does chronic renal failure cause this?
to few functional nephrons--> solute diuresis (too much solute for remaining functional nephrons) (there is damaged medullary tissue or poor blood flow, which decreases Na and Cl xport in the LOH whch reduces the medullary tonicity and thus the conc gradient) (Damaged renal tubular cells cant respond to ADH)
polyuria---> how does acute renal failure cause this?
the tubules wont respond to ADH (Damaged renal tubular cells can't respond to ADH)
polyuria---> how does post-obstructive diuresis cause this?
Tubules not responding to ADH & solute diuresis (Solute accumulates during obstruction -->overloads nephrons after removing obstruction) (Damaged renal tubular cells can't respond to ADH)
polyuria---> how does diabetes mellitus cause this?
Solute diuresis (possible dec in medullary tonicity) (Glucose in tubular fluid reduces osmotic gradient) (a persistant diuresis (solute overload) can lead to a medullary washout--> dec medullary tonicity which reduces gradient)
polyuria---> how does hypercalcemia cause this?
Ca2+interferes with tubule response to ADH
polyuria---> how does Canine pyometra cause this?
tubules not responding to ADH (endotoxins might interfere with ADH activity)
polyuria---> how does hypokalemia cause this?
tubules not responding to ADH (because not enough K+ for them to be able to respond)
polyuria---> how does Hypoadrenocorticism cause this?
dec medullary tonicity &/or dec release of ADH (hypoadreno--> less aldosterone--> hyponatremia and hypochloremia--> less resorption of Na and Cl--> dec medullary tonicity) (also, dec conc of Na and Cl --> hyposmolar plasma--> less stimulus for ADH release)
polyuria---> how does Liver failure cause this?
dec medullary tonicity &/or NH4+interferes with ADH (dec production of urea means less urea is able to contribute to the the medullary tonicity, so it dec)
polyuria---> how does Central diabetes insipidus cause this?
dec release of ADH (brain problem means cant release ADH from pituitary)
polyuria---> how does Hyperadrenocorticism cause this?
inc Cortisol --> dec release of ADH
polyuria---> how does Psychogenic polydipsia cause this?
inc H2O consumtion-->dec Plasma osmolality (diluted)--> hyperosmolar plasma means dec release of ADH b/c dec stimulus for it