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Clin Path > Test 2- Renal > Flashcards

Test 2- Renal Flashcards

1
Q

What hormones do the kidney produce?

A

EPO, Renin

Kidney actively involved w/ activating calcitriol (vit D3) and also w/ the RAAS (regulates blood pressure)-

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2
Q

What waste products are excreted by the kidney?

A

Urea, creatinine, NH4+, K+, H+, P04, water soluble drugs, hormones and enzyme s like PTH, and in
• dogs- amylase and lipase are inactivated/excreted by the kidney

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3
Q

What important substrates does the kidney conserve?

A

Na, Cl, HC03, Ca, Mg, glucose, amino acids, water.

o Also regulates acid base, regulates water balance

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4
Q

What percentage of nephrons cease to function after losing ability to
concentrate urine?

A

66% nephron loss! renal insufficiency

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5
Q

what percentage of nephron cease to function after noting azotemia
in the body?

A

• 75% of nephron impaired! as wella s producing
unconcentrated urine
remember: lose ability to concentrate first, then renal azotemia
occurs

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6
Q

what occurs w/ renal dz?

A

Retention of nitrogenous waste products (BUN, Creatinine), inability
to dilute/concentrate urine (isothenuric 1.008-1.012) and greater
than 75% nephrons are affected

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7
Q

What test can you run on serum; run on urine for urine function?

A

Serum- BUN, and creatinine concentration
• Urine- USG, Urine protein concentration, urine protein:cratinine
ratio, fractional excretion of protein, fractional excretion of
electrolytes

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8
Q

What is the cycle of Urea?

A

Liver takes amino acids, deaminates and creates urea. Urea is
moved into the blood and is measured by blood urea nitrogen. Urea gets filtered by the glomeruli and is excreted
! but the Bun concentration is dependent on the rate of production,
reabsorption and excretionBUN changes w/ rate of production, reabsorption and excretion
Liver production- increase protein in upper GI (high protein diet, upper Gi bleed. Increase the prodctuion of BUN increases serum BUN.
If you have liver failure, decrease production of BUN therefore decrease serum BUN.
Renal resbsorption depends on resorption rate of flow thru tubules. Slow flow rate (more BUN resorbed. Fast flow rate- decrease serum BUN.

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9
Q

What percent of BUN is excreted by the kidney/ reabsorbed by the kidney?

A

60% is excreted, 40% is reabsorbed

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10
Q

can urea be a measure of GFR in ruminants?

A

No! salivary and blood urea enter the rumen and the rumen microflora create amino acids from deaminiating the urea.

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11
Q

What is the cycle of creatinine?

A

Produced by endogenous muscle catabolosim- muscle creatinine
phosphate (energy stored molecule), constant rate of production is proportional to muscle mass. Muscle cells release creatinine into plasma and is filtered by the glomerulus and not reabsorbed (unlike urea) and therefore is an indicator of GFR

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12
Q

If creatinine is increased in the blood, what does it imply?

A

A decrease in GFR, and possibly altered kidney function (nephron

function)

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13
Q

What is Urine specific gravity?

A

An estimate of urinary concentrating capacity
. Assess in conjunction
w/ serum BUN and creatinine. ! look at the USG along w/ BUN and
Creatinine! collect blood and urine at same time.

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14
Q

When would it be appropriate to obtain a sample and measure USG?

A

When suspected of renal dz, geriatric wellness, history of PU/PD

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15
Q

What is necessary by the kidney to create a concentrated urine?

A 
At least 33% functional nephrons, production and
responsiveness to ADH, and have the ability to create a
concentration gradient (medullary hypetonicity, production
of urea, and production of aldosterone)
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16
Q

What is necessary by the kidney to produce a dilute urine?

A

Ability to actively resorb sodium and chloride form ascending
limb of the loop of henle, and little to no water removed by the
colleting duct

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17
Q

What are the USG ranges by species?

A

Dog- 1.001- 1.060; cats 1.001-1.080; horse/bovine 1.001-1.055.
•  IF THE USG IS NOT REPRODUCIBLE, IT IS NOT
o If isothenurinic the kidney is incapable of altering the amount of water leaving the body.
o If hyposthenuric it is an active process and producing a dilute urine
o If USG is > than 1.017! some concentrating ability.

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18
Q

What are the minimum concentrating capacities for USG per species in a dehydrated state?

A

Dog 1.030; cat 1.035; horse/cattle 1.025 if you get these numbers you know the kidney is able to concentrate urine. If not something wrong
o The cause of increase BUN, and Increase Creatinine is prerenal when urine specific gravity is increased w/ these values due to dehydration

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19
Q

what is specific of urine protein concentration in dogs?

A

Healthy dogs may have a measureable protein concentration
.Remember small proteins pass through the glomerulus- most
are reabsorbed by the proximal renal tubules (usually not detected in urine in most species)

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20
Q

How can urine protein concentration be measured?

A

w/ a regent strip- changes color w/ associated [protein] in urine. ! negative, trace, +, ++, +++,++++
o often UTI, pyelonephritis, urolith can cause some irritation in tissue to cause bleeding and see protein and inflammation in urine

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21
Q

what causes polyuria?

A

Inability to concentrate urine causes polyuria – implies that you
have a loss of 66% of functional renal mass w/ isothenuric urine
(low USG)

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22
Q

What are your DDX for polyuria?

A

Renal- renal failure, and pyelonephritis are your renal causes
• Extrarenal- diuresis, medullary washout, diabetes,
hyperadrenocritcism, pyometra

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23
Q

What is azotemia?-

A

75% renal function lossRetention of nitrogenous waste product in blood: increase [BUN] and/or increase [CREA]. Pre renal (blood, liver, GI), renal; post renal (ureter, bladder, urethra)

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24
Q

What values do you see w/ pre renal azotemia? what are some broad causes

A

Increase BUN, +/- increase creatinine, increase USG
• Decreased renal blood flow leads to decreased GFR (dehydration,
shock, cardiac insufficiency) ; increase urea production (upper Gibleed) high protein diet, endogenous protein catabolism, ruminants
(decrease ruminal motility)
REMEMBER- things increase w/ decrease elimination or increase production

25
Q

What cause pre renal azotemia w/ increase creatinine?

A

Increased muscle mass demonstrates mild increase in createinine
(greyhounds, males) and in neonatal foals often can have dysfunctional placenta and prevents normal clearance of fetal creatinine. -> normally cleared by kidney after birth
Dehydrated animal w/ normal renal function–. Urine volume decreased (less blood= less urine) and urine specific gravity increased.

26
Q

What are characteristics of renal azotemia?

A

Increase BUN, increase Creatinine, decrease USG (often Isothenuric)
o Increase waste products in blood, loss of 75% of functional nephrons! reaming nephrons undergo functional hypertrophy
o Renal azotemia results in a decrease GFR, increased BUN, Increase creatinine, increases phosphorous

27
Q

What does renal azotemia result in?

A

A decrease in GFR, increase BUN and Cretainine. Production in
a isothenuric urine w/ incrased water loss (even in dehydrated
animal) and isothenuria implies polyuria

28
Q

What are your causes of renal azotemia = renal damage?

A

Infectious- pyelonephritis, leptospirosis; toxins- ehtelyenglycool, drugs, grapes, Asiatic lilies, melamine, pigments (myoglobin, hemoglobin); hypoxia- decreased renal perfusion, infarction; neoplasia- primary or metastatic; congenital- hypoplasia or aplasia; miscilaneous- hydronephrosis

29
Q

Remember that an animal w/ azotemia and inappropriately low USG is not always in renal failure. What can cause this?

A

Imbalance of electrolyte metabolism, endocrine function, drugs: calcium, diabetes insipidus, medullary washout, endocrine;cortisol,glucose,pyelonephritis, fanconi syndrome, post obstructive diuresis, drugs, primary renal dz, non oliguric acute renal failure, 3+/4+ glucose, 4+ protine

30
Q

What are you values for post renal azotemia?

A

• Increase BUN, increase CREATinine, variable USG

31
Q

What are causes of post renal azotemia?

A

Urolithiasis in castrated males (FLUTD), goat urolthiiasis,
uroabdomen (from urolithiasis or trauma)
Polyuria occurs before azotemia!! Polyuria 66% nephrons gone, azotemia 75% nephrons gone
• Determine the origin of azotemia by the USG

32
Q

What are clinical sings to differentiate the azotemias?

A

Pre renal- other signs of dehydration (tachy mucous membranes,
skin tenting, look at blood work- increase PCV, TP and increase Na. Is there a reason for the patient to be bleeding, GI ulcer, bleeding
What are you values for post renal azotemia?
• Increase BUN, increase CREATinine, variable USG
into upper Gi, coagulopathy(DIC

33
Q

What if the animal is isothenuric and not azotmeic?

A

History , signalment, PE findings, what is the ydration status is it
appropriate. Is anyting interfering w/ kidneys concentrating ability

34
Q

What does a decrease in BUN demonstrate?

A

Pre renal cause! 1. decrease urea production; decreased amino acid delivery to liver (decreased protein in diet or there his a shunt) or hepatic insufficiency (> 80% loss) or 2. Intestinal lost (in monogastric species, horse)
• Renal decreased BUN cause! decreased water reabsorption in prox tubule. Increased GFR (IVF, diuresis) or increased tubular flow (osmotic diuresis)! decreased the time to reabsorb BUN w/ increased tubular flow.

35
Q

What is the significance of decreased creatinine?

A

No significance

36
Q

Proteinuria:

A

Pre renal (increased protein in blood), renal (glomerular/tubular) and postrenal (hemorrhage/inflammation) can cause protein to appear in urine.

37
Q

Causes of prerenal proteinuria?

A

Increase in small protein in blood- paraproteinuira (bence

jones), hemoglobinuria, myoglobinuira, post colostral proteinuria

38
Q

what are the 2 causes of renal proteinuria?

A

Glomerular proteinuria- hypoalbuminemia, disease damage filtration barrier. (PLN). Tend to be more sever proteinurias
• Tubular proteinuria- normal or increased serum albumin (no hypoalbumineimia), if have hypoalbuminemia ! wont have this from renal tubular. Albumin will be normal to slightly increased if dehydrated. Usually associated w/ acute or congenital renal dz’s. proximal tubules are defective (filtered proteins not reabsorbed) or loss of low molecular weight proteins.

39
Q

What are causes of post renal proteinuria?

A

Hemorrhagic! impaired hemostasis, blood vessel damage from

inflammation, trauma, neoplasm.; inflammatory- will see pyuria

40
Q

What is the urine protein:creatinine ratio (UPCR)?

A

More often used in dogs. Normal is .5; glomerular >1.0. glomerular porteinurias tend to be more severe
o If approbation a UPCR of .5, something to keep an eye on

41
Q

In renal failure can be caused from hypercalcemia. What is associated w/ this?

A

Hypercalcemia impairs urine concentration ability causing primary PU. (interrupts ADH receptors) and you can commonly see mineralization of renal tubules w/ excess calcium which results in nephronal kidney dysufction. 95% of time, hypercalcemia caused the kidney dz. (5% of time you have hypercalcemia caused by kidney dz)
o Dogs, cat, and cattle can develop mild hypocaclemia b/c of dec. calcitriol. Horses fed hyperalcemic diet can demonstrate renal dz

42
Q

How can renal dz cause hyperphosphatemia?

A

w/ GFR less than 25% of normal! phosphorous excretion is impaired so ther is an accumulation seen. From this you can see decreased serum ionized calcium when can lead to renal secondary hyperparathyroidism and mineralization of soft tissuses. Number 1 differenatial for hyperphsophatemia is glomerular filtration rate- often seen in chronic. Have to have 75% nephron damage before seeing the actual levels increase.
o Dogs cats and horses!due to decrease GF. In horses- phsohprous tends to belost from the gut.
o Cattle may have hyperhphoastemia- slaviary phsohprous excretion is greater than renal phsohrous excretion

43
Q

Can an alkalosis or acidosis occur w/ renal failure?

A

Sever renal dz- tend to see metabolic acidosis due to increase
urinary loss of bicarb. And decrease tubular secretion of hydrogen
ions.
Random- cattle w/ renal failure can see hypochloremia

44
Q

In renal failure, what can your potassium values show on your biochem profile?

A

Can be normokalemic- potassium often normal w/ chronic renal failure, increased tubular secretion prevents hyperkalemia.
• Can be hypokalemic- uremic animals often eat less! decrease potassium intake.
o Also hypokalemic nephrpathy in cats- pathogeniesis uknown.
• Can be hyperkalemic- associated w/ oliguria/anuria! life
threatening in acutre renal failure or post renal condtions!
w/ this the outflow of urine is not occurring and you havebuild of potassium- can be life threatening! causeheart
arrhythmias.

45
Q

What occurs w/ a uroabdomen and electrolyte imbalances?

A

• Dogs, cats, and new born foals can have increase potassium,
phosphate and decrease sodium and chloride.
• Cattle- hyperkalemia does not occur and excess potassium excreted
in salivaUrea and potassium move quickly into plasma and plasma concentration increases
o Sodium and chloride move into urine quickly, plasma concentration decreases Creatinine takes a longer time to move across into the plasma! compare creatinine level in abodmen to the plasma level. A peritoneal [CRE] 2x serum [CRE] is diagnostic of a uroabdomen

46
Q

What are characteristics of acute renal failure?

A

ARF, AKF, ARI, AKI. On physical exam- patient usually have a good
BCS vs CRF patients. Any animal and very quick progression of signs
o GI- anorexia, vomit, diarrhea, halitosis (NH3).
o Renal- oliguric to anuric (worry aobut potassium at the
heart)
o Neuro- depressed, obtunded, nonresponsive, seizures

47
Q

What are causes of ARF?

A

Commonly associated w/ toxins, renal ischemia, infection. Things
that damage the kidney quickly.
o Often marked decreased in GFR leading to azotemia-
may be reversible or irreversible

48
Q

What are laboratory blood findings of ARF?

A

Abrupt decrease in GFR can leads to:! azotemia! speed of
development differentiates ARF from CRF (fast increase w/ ARF
(days to hours) where as slow increase in CRF (weeks to months)
• +/- hyperkaelemia and acidemia! impaired excretion of both
cations leading to metabolic acidosis. Failure to recapture bicarb.
• On urinalysis- oliguria or anuria, urine specific gravity is variable.
+/- proteinuria, +/- cellular casts

49
Q

What are characteristics of chronic renal failure?

A

CRF, CKF, CRI, CKI!usually patient is geriatric and frequent in cats. Slow onset of clinical signs.
o Poor BCS (thin, cachexic),
o GI- anorexic, vomiting, diarrhea, halitosis o Renal- polyuric
o Neuro- depressed
. A peritoneal [CREA] 2x serum [CREA] is
diagnostic of uroabdomen
o CV- hypertension
“ Often irreversible kidney injury, renal function is
inadequate to maintain patient health, decreased GFR,
azotemia, isosthenuria

50
Q

What are laboratory blood findings n CRF?

A

GFR

51
Q

What lab findings are seen w/ end stage renal dz? (GFR

A

Nonregen anemia, marked dehydration, marked azotemia
(uremia probably present) hyperphosphatemia, metabolic acidosis, hyperkalemia (acute-on-chornic b/c anuric/oliguric). Urinalysis demonstrated isosthenuria, oliguria to anuria

52
Q

What is glomerulonephritis?

A

Renal glomerular damage due to amyloid deposit or immune complex deposition There is either a retraction of podocotyes or loss of the selective permeability of the glomerular basement membrane which allow proteinuria (protein enter filtrate faster than reabsorbed) and hypoproteinemia (protein loss exceeds production – ie. albumin

53
Q

What are laboratory findings w/ glomerularnephritis?

A

mild to marked hypoproteinemia, and hypoabluminemia and

normoglobulinemia. Moderate to marked proteinuria. And +/- renal insufficiency (azotemia, isothenuria0

54
Q

What is nephrotic syndrome?

A

PLN leading to abdominal trasudatoin.
• Glomerular dz, hypoalbuminemia(leakly glomeruli),
hypercholesterolemia, edema (loss of plasma oncotic
pressure), and hyepercoaguable stae – loss of antithrombin

55
Q

what are biomarkers?

A

Any substance, structure, or process that can be measured in the
body or its products and influence or predict the incidence of
outcome or dz.

56
Q

What are conventional biomarkers in renal dz?

A

BUN, Creatinine.

57
Q

What are ideal biomarkers for kidney injury?

A

Detect kidney injury at an early stage, localizes kidney injury (glomerular vs tubular vs both), differentiates renal injury from pre/post/non renal injury, predicts the severity of renal injury, and monitors the effects of intervention
• Clinically applicable- accurate, easy to measure, noninvasive and notexpensive

58
Q

What are other biomarkers?

A

Albumin- not supposed to be filtered. Often sene in sick patients.
• Microalbuminura- in borderline and proteinuric patients,
microabluminuria may be present. Not clinically sign. Yet. Usg 1.101 and urine albumina >1 and 30mg/dl
• Cystatin C! cysteine protease inhibitor- produced constantly and released by nucleated cells. Freely filtered by glomerulus. Reabsorbed and catabolized by renal tubulars- does not reenter blood, not excreted inurine.Symmetric dimethylarginine(SDMA)! methylated from of arginine-
releaed into circulation by nucleated cells and filtered by the
glomerulus. Excreted exclusively by the kidney >90%. Increase w/
40% loss of renal tubular function. 100% sensitivity in all cats
w/CRF. If it is a ture negative reading- means it is a true negative
b/c 100% sensitive
o increase in the SDMA! it suggests renal tub. Dz..
always interpret along w/ history clinical signs, PE
fidings, other markers of renal injury
o 100% sensitive all cats w/ CRF detected
o 91% specific for some cats w/ out chornic renal failure
had positive result

Clin Path (20 decks)

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