Vet 409 Renal

Front 1

Describe the position of the right kidney.

Back 1

Retroperitoneal. This means that only the ventral surface of the kidney is covered with peritoneum.
The R kidney is found between T12/13 and L2/3.

Front 2

Describe the position of the left kidney.

Back 2

Intraperitoneal. The kidney is covered with peritoneum on all sides.
Remember, the LEFT kidney hangs LOOSER. It's found between L2 and L4.

Front 3

Which animals have multipyramidal kidneys?

Back 3

Cattle --> Lack renal pelvis.

Pigs --> Have major and minor calyces and a renal pelvis.

Front 4

What arteries and veins service the kidneys?

Back 4

Kidney surface --> Phrenicoabdominal artery and vein.
Body of kidney --> Renal artery and vein, which branch from abdominal aorta.

Front 5

What are the components of a nephron?

Back 5

Glomerulus/Bowman's capsule/Renal corpuscle --> Proximal convoluted tubule --> Proximal straight tubule --> Thin descending limb of Loop of Henle --> Thick ascending limb of Loop of Henle --> Distal convoluted tubule --> Juxtaglomerular apparatus --> Distal collecting tubule --> Papillary duct

Front 6

Describe the structure of a renal corpuscle.

Back 6

A renal corpuscle includes the glomerulus and the glomerular capsule. The glomerulus consists of a basement membrane, thin endothelial cells with fenestrations, and mesangial cells in the core.The glomerular capsule has a parietal and visceral layer.

Front 7

Describe the juxtaglomerular apparatus.

Back 7

It is located between the distal part of the thick ascending limb of Henle's loop (or the distal straight tubule) and the renal corpuscle. Players in the apparatus include macula densa cells, which sense changes in NaCl in the tubule, and juxtaglomerular cells, which lie among the smooth muscle of the afferent arteriole and sense pressure + synthesize & release renin into afferent arteriole.

Front 8

Describe the micturition reflex.

Back 8

The bladder muscle (detrusor muscle) is innervated by both sympathetic (beta-adrenergic) and parasympathetic (cholinergic) fibers. Sympathetic stimulation causes relaxation of the detrusor m, leading to storage phase of urine. Parasympathetic stimulation causes contraction of detrusor m, leading to emptying phase.

The internal urethral sphincter is made up of smooth muscle controlled by sympathetic fibers; sympathetic stimulation causes contraction, increasing urethral tone during the resting state.
The external urethral sphincter is made up of striated muscle supplied by somatic neurons.

Front 9

What are the principles to imaging the bladder?

Back 9

Front 10

What are the principles of imaging the kidneys?

Back 10

Front 11

What structures form the "trigone" on the bladder?

Back 11

Trigone = Triangular area outlined bye the openings of the ureters and the origin of the urethra.

Front 12

What is the normal size for a kidney on ultrasound in a dog and cat?

Back 12

Dog: 2.5 to 3.5 x length of L2
Cat: 3.5 to 4.4 cm

Front 13

What is considered the normal echogenicity of a kidney in dogs and cats?

Back 13

Kidney echogenicity is evaluated by comparing it to other organs (My Cat Loves Sunny Places = kidney medulla < kidney cortex < liver < spleen < prostate).
Dogs under 2 yrs old follow the mnemonic, but once they get older, fat in kidney cortex makes it more hyperechoic than the liver.
In cats, the fat in the kidney cortex makes it equal in echogenicity with the liver.

Front 14

If we see retroperitoneal fluid when scanning the kidneys on ultrasound, what could that indicate?

Back 14

Ureteral trauma
Hemorrhage
Abscess formation
Ethylene glycol toxicity
Peri-nephric cysts

Front 15

What is pyelectasia? What does it indicate?

Back 15

Pyelectasia is renal pelvis dilation.

DDx: PU/PD, consequence of giving IV fluids, pyelonephritis, EARLY obstruction, lymphoma

Front 16

What is hydronephrosis? What could it indicate?

Back 16

Hydronephrosis is dilation of the renal papilla AND dilation of the renal calyces; we see splitting of the renal parenchyma.
DDx: Obstruction

Front 17

If you see a focal thickening at the APICAL end of the bladder, what does this suggest?

Back 17

Thickening at the apical end of the bladder is generally associated with inflammation due to trauma from urinary calculi, for example.

Front 18

If you see focal thickening at the trigonal area of the bladder, what does this suggest?

Back 18

Focal thickening at the trigonal area of the bladder is generally associated with neoplasia.

Front 19

Diffuse thickening of the bladder wall is almost always ______.

Back 19

Inflammation

Front 20

What would a focal thinning in the bladder wall indicate and what would a diffuse thinning indicate?

Back 20

Focal thinning of bladder wall generally associated with a rupture, whereas diffuse thinning is just indicative of a full bladder.

Front 21

What should the bladder look like ultrasonigraphically?

Back 21

The bladder should be very hypoechoic (black). If you see swirling debris, it could indicate RBCs, WBCs, proteinuria, or mucus inside the bladder. If you see hyperechoic (bright) things with shadowing, it could indicate crystalline debris or calculi.

Front 22

What factors influence glomerular filtration rate (GFR)?

Back 22

GFR is influenced by factors that both favor and oppose glomerular filtration. Forces that favor filtration include glomerular capillary hydraulic pressure (Pg) and oncotic pressure within Bowman's capsule (πb), which is negligible. Forces that oppose filtration include Bowman's capsule hydraulic pressure (Pb) and oncotic pressure within the glomerular capillaries (πg). So:
GFR = (Pg + πb) - (Pb + πg) = Pg - Pb - πg

Front 23

What factors influence net filtration pressure (NFP)?

Back 23

NFP = capillary hydraulic pressure - capsular hydraulic pressure - plasma oncotic pressure = Pg - Pb - πg

Front 24

How does dehydration affect GFR?

Back 24

Dehydration --> Increased [plasma protein] --> Increased πg --> Decreased GFR

Front 25

How does excessive drinking or fluid administration affect GFR?

Back 25

Excessive drinking / Fluid administration --> Decreased [plasma protein] --> Decreased πg --> Increased GFR

Front 26

How does an immune disorder influence GFR?

Back 26

Immune disorders cause pathologic increases in [plasma protein] --> Increased πg --> Decreased GFR

Front 27

What factors contribute to renal blood flow (Q)?

Back 27

RBF depends on arterial blood presure (Pa) and arterial blood resistance (R). So:
Q = Pa/R

Front 28

What autoregulatory mechanisms does the kidney have for maintaining RBF?

Back 28

Myogenic - Afferent arterioles vasoconstrict in response to stretch.
Tubulo-glomerular feedback - If RBF too high, NaCl concentrates in macula densa cells of juxtaglomerular apparatus. Adenosine is released, and afferent arterioles vasoconstrict.

Front 29

What extrinsic mechanisms does the kidney have to maintain RBF?

Back 29

Neural control - Norepinephrine release leads to constriction of afferent and efferent arterioles. RBF decreases. GFR also decreases and filtration fraction increases.
Humoral control - Epinephrine and angiotensin II have same effects as norepinephrine. Prostaglandins are vasodilatory and oppose the effects of the others.

Front 30

What does ADH / Vasopressin / AVP do? When is it released?

Back 30

ADH increases water reabsorption in the distal convoluted tubule and the collecting duct via insertion of more aquaporins into the tubule membrane. It is released when the body is dehydrated and wants to concentrate urine.

Front 31

What are the different mechanisms for ADH release?

Back 31

1. Baroreceptors - If arterial blood pressure is low, baroreceptors in arteries will sense the decreased amount of stretch.
2. Macula densa cells - If arterial blood pressure is low, GFR is decreased. Fluid spends more time in the tubules, and so, more NaCl is pumped out of tubule. MD cells see less NaCl, and renin is released. Renin turns into angiotensin II, which stimulates ADH release.
3. Increased plasma osmolality
3.

Front 32

What is aldosterone?

Back 32

Aldosterone leads to increased Na+ reabsorption in the distal convoluted tubule and the collecting duct and decreased K+ reabsorption.

Front 33

What causes increased secretion of aldosterone?

Back 33

ACTH
High plasma [K+]
Low plasma [Na]+
***Increased angiotensin (RAAS)

Front 34

Describe what happens in the kidneys following a drop in BP.

Back 34

If BP is low, there is decreased stretch in the afferent arterioles, which is sensed by baroreceptors. Release of renin is increased.
If BP is low, GFR is decreased. Fluid spends more time in thick ascending limb, and more NaCl is pumped out. A lower [NaCl] is delivered to macula densa cells. MD cells release renin.
If BP is low, there's increased renal sympathetic nerve activity, and more norepi is released. This leads to increased renin release, and so, increased [angiotensin II]. The increased [angiotensin II] negatively feeds back on renin release, preventing extreme swings in [angiotensin] from BP fluctuations.

Front 35

What is atrial natriuretic peptide?

Back 35

ANP inhibits Na+ reabsorption in DCT and CD.

Front 36

What role does phosphate play in the animal's body?

Back 36

P is necessary for:
1. Skeletal structure
2. Metabolic and cellular functions - Kinases and proteases use it
3. Blood and urinary buffer as PO4
4. Formation of high energy bonds like ATP and GTP

Front 37

What are the main regulators of blood phosphate levels?

Back 37

1. Parathyroid hormone (PTH) - Increases excretion of P.
2. FGF-23 - Increases excretion of P and inhibits kidney conversion of vitamin D to active form.
3. Vitamin D - Increases intestinal absorption of P.
4. GI absorption - Dietary intake influences P levels.
5. Insulin - Promotes P reabsorption
6. Volume contraction / expansion

Front 38

How is P reabsorbed in the kidneys?

Back 38

Movement of P is an active process that occurs via NaPi transporters (Na is used for co-facilitated diffusion). 60-70% reabsorbed in PCT; 10-20% reabsorbed by distal nephron.

Front 39

What are the main regulators of blood Ca2+ levels?

Back 39

1. PTH - Increases renal Ca2+ reabsorption (via increased Ca channels) and bone release
2. *Vitamin D - Promotes reabsorption of Ca2+ (works in the nucleus; transcription factor)
3. Dietary intake of Ca2+
4. Metabolic acidosis - Interferes with Ca2+ transporter in late DCT/CCD

Front 40

Describe Ca2+'s reabsorption in the renal tubules.

Back 40

65% of Ca2+ is reabsorbed in the PCT, and 20% is reabsorbed by the thick ascending limb; both of these are passive/paracellular processes.

Up to 13% of Ca is reabsorbed in the late DCT and cortical collecting duct; this part is regulated via upregulation of the TRPV5 Ca2+ channel.

Front 41

True or false:
The diuretic, furosemide, leads to increased Ca2+ excretion, while thiazide does not.

Back 41

True

Front 42

What are the potential regulators of Mg2+?

Back 42

1. PTH - Causes reabsorption of Mg2+
2. Dietary Mg2+ intake
3. Others: calcitonin, vitamin D, insulin, ADH
4. Thiazide diuretics - Increase Mg2+ reabsorption

Front 43

Describe Mg2+'s reabsorption in the renal tubules.

Back 43

The kidney is the major regulator of Mg2+ levels.

20% is reabsorbed in the PCT/PST; this is a passive/paracellular process, linked to Na+/H2O transport.
70% is reabsorbed in the thick ascending limb; this is passive/paracellular AND regulatable process (PTH increases membrane channels
10% is reabsorbed in DCT; this is an active process via Mg2+ channels in membrane.

Front 44

What 2 endocrine compounds are produced and secreted by the kidneys?

Back 44

Erythropoietin (EPO)
Calcitriol (activated vitamin D / 1,25-dihydroxy vit D3)

Front 45

What are the effects of EPO? How is EPO regulated?

Back 45

EPO targets early progenitor cells in bone marrow, giving them immunity from programmed cell death, and sets them down the RBC pathway. EPO also regulates delivery of O2 to tissues.
EPO release is controlled by (-) feedback: high #s of RBCs in blood is inhibitory.
EPO production is controlled by HIF, a transcription factor.

Front 46

What are the actions of calcitriol?

Back 46

1. Decrease PTH secretion by parathyroid gland.
2. Increases Ca2+ transport & absorption in intestine (TRPV6).
3. Increases Ca2+ transport & absorption in kidney (TRVP5).
4. Increases bone accretion.
5. Increases intestinal P absorption.

Front 47

What things are reabsorbed in the PCT?

Back 47

65% of Na+, Cl-, H2O
80% Bicarbonate
50% Urea

Front 48

What happens in the descending limb of loop of Henle?

Back 48

Permeable to H2O.
Impermeable to Na+ and Cl-.

Front 49

What happens in the thin and thick ascending limb of loop of henle?

Back 49

Impermeable to H2O.
Permeable to Na+, Cl-, urea. Increased [urea] outside of limb causes NaCl to flow out of limb.

Front 50

How is urea excreted from the renal tubules?

Back 50

Urea is freely filtered and moves with its osmotic gradient. Most of the concentrating occurs in collecting ducts.

Front 51

What happens in the distal convoluted tubule?

Back 51

Not very permeable to Na+ or Cl-.
This is where aldosterone acts to reabsorb water & Na+, and excrete K+. If no aldosterone present, not much changes.

Front 52

What happens in the cortical and medullary collecting duct?

Back 52

Aldosterone acts here. If present, Na+ & H2O gets pumped out of tubules / reabsorbed.
ADH acts here. If present, H2O is reabsorbed / pumped out of tubules via increased presence of aquaporins.

Front 53

Why are diuretics used in vet med?

Back 53

Diuretics are used mainly to treat edema caused by hepatic, pulmonary, or renal DZ. Diuretics that work on different parts of the nephron can be used together synergistically.

Front 54

How do diuretics enter renal tubular cells to exert their effects?

Back 54

Via glomerular filtration and active transport from blood.

Front 55

What are the different categories of diuretics?

Back 55

Osmotics
Carbonic anhydrase inhibitors
Loop / High ceiling diuretics
Thiazides
K+ sparing / Aldosterone antagonists

Front 56

How and where do osmotic diuretics work?

Back 56

Osmotics work mostly in the PCT, but also has some effect throughout the rest of the tubule. Osmotics trap water in tubule with osmosis. [K+] remains unchanged.

Front 57

How and where do carbonic anhydrase inhibitors work?

Back 57

Carbonic anhydrase inhibitor diuretics work in the PCT. They prevent carbonic anhydrase from reabsorbing Na+ and HCO3-, instead, trapping it in the tubule/urine. This means that the macula densa cells see a higher [Na+], causing them to release more aldosterone. Aldosterone will try to lower [Na+] in the tubule by reabsorbing Na+ and swapping it out for K+. This is why CA inhibitors are K+ wasting.

Front 58

How and where do loop / high ceiling diuretics work?

Back 58

Loop diuretics work in the ascending limb of the loop of Henle. They are the most efficacious diuretics, since they work even when GFR is low.
Loop diuretics work by preventing Na/Cl symporters from doing their job: Decrease in Na+ reabsorption. As a result, there's more Na+ and Cl- in the DCT and less in the interstitium, preventing the formation of the hyperosmotic interstitial gradient. There is nothing to pull water back into interstitium; water stays in tubules and is peed out.

Front 59

How and where do thiazide diuretics work?

Back 59

Thiazides work in the distal tubule.
They are moderate diuretics; better than carbonic anhydrase inhibitors, but worse than loo diuretics.
Thiazides block Na+ reabsorption by the NaCl symporter. MD cells sense the increased [Na+] and release aldosterone. Aldosterone causes Na+ to be reabsorbed in exchange for K+ to be excreted. This is why thiazide is a K+ wasting diuretic.

Front 60

How and where do aldosterone antagonists work?

Back 60

Aldosterone antagonists act in the distal tubule and collecting duct.
The AAs bind to aldosterone receptors and competitively block aldosterone. K+ is not exchanged for Na+, and so, cannot be excreted. As a result, we risk creating hyperkalemia when using these drugs. Example: Spironolactone

Front 61

How and where do ACE inhibitors (diuretic) work?

Back 61

ACE inhibitors are used in human medicine to reduce blood pressure in treating congestive heart failure.

ACE inhibitors are slow onset, but have good half lives. Can cause GI problems, hypotension, and hyperkalemia. Never use with K+ supplements or K+ sparing diuretics.

Front 62

What animals use ammonia (ammonium ion) as their metabolic waste product?

Back 62

Bony fishes and amphibian larvae are ammonotelic. Ammonia is highly toxic and very water soluble; fish are surrounded by water, so they can afford to be ammonotelic. Their urine is very dilute.

Front 63

What animals excrete uric acid as their metabolic waste product?

Back 63

Birds and reptiles are uricotelic. 4 Ns are excreted per uric acid molecule, making uricotelism more efficient than ammonotelism or ureotelism.
Non-human primates are also uricotelic - Uric acid is reabsorbed and secreted in the PCT. bit tje rate pf secretion is greater than the rate of reabsorption so that most uric acid is excreted.

Front 64

Which animals excrete urea as their metabolic waste product?

Back 64

Many terrestrial vertebrates and sharks are ureotelic. Only 2 Ns are excreted per urea molecule, so it's not as efficient as uricotelism.

Front 65

Why are dalmatians susceptible to urinary stones?

Back 65

Uric acid precipitates in acidic urine, forming uric acid crystals. Dalmatians have a genetic defect in their renal and hepatic transport of uric acid (they have no uricase, which turns uric acid into allantoin). Since not all filtered uric acid is reabsorbed in the kidneys of dalmatians, urinary stones form.

Front 66

How is the term "fluid" different from "water"? What are the primary cation and anion found in interstitial fluid?

Back 66

"Fluid" means that there's water + solute.
ISF is 15% of body weight.
Primary cation is Na+.
Primary anion is Cl-

Front 67

Describe intracellular fluid (ICF).

Back 67

Intracellular fluid is 40% of an animal's body weight.
Low Na+
High K+
High Mg+
High protein content

Front 68

Describe plasma.

Back 68

Plasma is 5% of an animal's body weight.
Osmotic pressure of plasma is generated by the proteins in it (oncotic pressure).
The oncotic pressure in plasma is >> oncotic pressure interstitial fluid, which is important for maintaining vascular volume.

Front 69

Describe total body water: What percentage of body weight does it make? What are the components of total body water?

Back 69

Total body water is 60% of an (adult) animal's weight. 66% of total body water is intracellular fluid, and the remaining 33% is extracellular fluid.
Of the extracellular fluid compartment, 25% is plasma/intravascular space, and the remaining 75% is interstitial fluid space.

Front 70

When a patient is considered "X% dehydrated," what does this mean?

Back 70

The animal is dehydrated X% of its total BODY WEIGHT, not total body water.

Front 71

Where does fluid loss happen from in a patient?

Back 71

Fluid is always lost from the interstitial space (a component of extracellular fluid compartment), unless the source of dehydration is due to a hemorrhage. If hemorrhage, fluid loss is from the intravascular space.

Front 72

When we gain fluid, as in edema, where does water accumulate?

Back 72

Edema is an accumulation of interstitial water; we can visualize the accumulation once 5% is accumulated. Intracellular fluid volume increases in relation to extracellular fluid volume in a ratio of 2:1.

Front 73

What does TCO2 tell us on blood-gas results?

Back 73

Total CO2 is an estimate of bicarbonate in the blood.

Front 74

What does the SBE value tell you on blood-gas results?

Back 74

SBE is the standardized base excess, and it is a better indicator of the metabolic system than TCO2. A normal SBE is about 0. The more (-) the SBE, the more suggestive it is of metabolic acidosis; the more (+) the SBE, the more suggestive it is of metabolic alkalosis.

Front 75

True or false:
Respiratory compensation is slow (hrs to days), while renal compensation is fast (minutes).

Back 75

False; it is the opposite.

Front 76

How do we decide what the primary acid/base disorder is?

Back 76

Look at:
1. pH: Is the animal acidemic or alkalemic?
2. PCO2: Is it low? If yes, then respiratory alkalosis. Is it high? Then, respiratory acidosis.
3. HCO3-: Is it low? If yes, then metabolic acidosis. Is it high? Then, metabolic alkalosis.
4. Which parameter matches up with the blood pH? The matching one is the primary disorder.

Front 77

What are the 2 kinds of metabolic acidosis?

Back 77

High AG metabolic acidosis
Normal AG metabolic acidosis

Front 78

What causes a high AG metabolic acidosis?

Back 78

High AG metabolic acidosis is caused by a gain of acid.
Think DUEL when you see it:
Diabetic ketoacidosis
Uremic acids
Ethylene glycol toxicity
Lactic acidosis

Front 79

What causes normal AG metabolic acidosis?

Back 79

Normal AG metabolic acidosis is caused by renal losses or intestinal losses (via diarrhea; more common in LA).
We usually see high Cl- levels.

Front 80

What buffers are found in the tubules to regulate pH?

Back 80

HPO42- and NH3

Front 81

Describe chronic kidney DZ.

Back 81

Chronic kidney DZ persists for > 3 months and indicates a decrease in GFR of more than 50%. Symptoms occur due to erosion of kidney mass.

Front 82

What are the early historical findings of chronic kidney DZ.

Back 82

PU/PD, anorexia, nausea, vomiting, progressive weight loss, lethargy, nocturia, halitosis, diarrhea, dilute urine, urinary incontinence, periodontal DZ.

Front 83

What is uremia?

Back 83

Uremia is seen with chronic kidney failure. Kidney function is insufficient to compensate and adapt to the functional mass that is lost. At this point, we have less than 25-30% of functional capacity left. We see accumulations of metabolic wastes (like uremia toxins) and impaired endocrine and metabolic functions.

Front 84

What are the clinical consequences of chronic kidney DZ?

Back 84

Progressive weight loss
Uremia
Increase in serum creatinine
Hyperparathyroidism
NNN Anemia
Systemic hypertension (High blood pressure)

Front 85

Why does chronic kidney DZ cause hyperparathyroidism?

Back 85

With chronic kidney DZ, you see accumulation of P. P will form complexes with Ca2+, reducing the [ionized Ca2+]. This stimulates the bone marrow to increase FGF-23 levels to stimulate increased excretion of P. Also, production of calcitriol decreases, and PTH levels increase. Ca2+ is taken from bones, which can lead to renal osteodystrophy.

If the kidneys worked properly, P would be excreted by the kidneys and calcitriol levels would rise back up, leading to (-) feedback on the parathyroid gland to stop production of PTH. But alas, P remains high and parathyroid gland hypertrophies.

Front 86

why does chronic kidney DZ lead to anemia?

Back 86

Erythropoietin is made in the inner and out cortex of the kidneys by peritubular interstitial cells. When an animal suffers from CKD, lots of kidney mass is replaced with scar tissue, reducing the amount of PICs available for EPO production.

Also, as creatinine levels in blood rise, hematocrit decreases.

Front 87

What do we look at to evaluate the kidneys' ability to concentrate urine?

Back 87

USG + Hydration status + Presence of azotemia + Urine volume

Front 88

What defines hypersthenuria? What does it suggest?

Back 88

Hypersthenuria in:
Dogs = USG > 1.030
Cats = USG > 1.035
Other = USG > 1.025

Indicates that the kidneys CAN concentrate urine. Hypersthenuria is expected in dehydrated patients.

Front 89

What defines isosthenuria? What does it suggest?

Back 89

Isosthenuria is a USG between 1.008 and 1.012.
Isosthenuria indicates that the urine is the same as unmodified plasma filtrate. It can be normal, but is always ABNORMAL in dehydrated or azotemic animals.

Front 90

What defines hyposthenuria? What does it indicate?

Back 90

Hyposthenuria is a USG that's < 1.008. It can be normal, but is abnormal in a dehydrated patient. In a dehydrated patient, it can indicate defective concentrating ability due to ADH deficit or lack of response to ADH.

Front 91

How do we evaluate renal blood flow (RBF) clinically?

Back 91

We look at BUN and creatinine values.
BUN rises because there's increased protein catabolism and urea synthesis going on. BUN is not as sensitive as creatinine b/c gut flora can convert urea into protein, lowering BUN falsely.
Creatinine is a molecule that's released from muscle into the blood at steady state. It's more sensitive test for renal failure.
BUN:Cr ratio - The 2 should go up proportionally, but certain things will cause BUN to increase faster than Cr. These include: a high protein diet & GI hemorrhage.

Front 92

What is azotemia?

Back 92

Azotemia is an increase in both BUN and Cr values. A lot of renal damage is required to see azotemia, since it's not a very sensitive test.

Front 93

Describe pre-renal azotemia.

Back 93

Pre-renal azotemia can occur b/c of (1) increased urea production or (2) decreased renal perfusion.

(1) occurs with high protein diets or GI hemorrhage.
BUN ↑↑↑, while Cr stays the same.

(2) occurs with dehydration and shock.
BUN ↑, Cr ↑, USG ↑.

Front 94

Describe renal azotemia.

Back 94

Renal azotemia occurs with a decrease in functional nephrons by 75%. Will see it with acute or chronic renal failure.
BUN ↑, Cr ↑, USG ↓

Front 95

Describe post-renal azotemia.

Back 95

Post-renal azotemia can be caused by a post-renal obstruction, a uroabdomen, or from anuria.
BUN ↑, Cr ↑, USG variable.

Front 96

What do you look at clinically to evaluate glomerular function?

Back 96

Look at proteinuria (albumin) and UPC (urine protein:Cr).

Front 97

What is nephrotic syndrome?

Back 97

With glomerular dysfunction, we see PROTEINURIA. If it's profound enough, we'll deplete the plasma of proteins, leading to HYPOPROTEINEMIA. Blood in the vessels lose oncotic pressure, and fluid leaks out of them, leading to EDEMA &/or CAVITARY EFFUSION. The liver goes into overdrive to try and make more proteins; lipoproteins are one of those proteins, and we see HYPERCHOLESTEROLEMIA.

Front 98

What do we look at clinically to evalulate tubular function?

Back 98

Look for glucosuria and proteinuria. This would suggest defective renal tubular resorption or secretion.

Front 99

True of false:
Hyponatremia is always due to an addition of H2O, NOT a loss in Na+.

Back 99

True

Front 100

Electrolyte panel comes back; animal has hyponatremia. What should be your next thoughts?

Back 100

(1) What is the osmolality? Low osm indicates a true hyponatremia; move on to (2). Normal osm means you should look to see whether there are high lipid or cholesterol levels causing artifactual decrease; if none, move on to (2). High osm means you should look for hyperglycemia or consider whether you just gave mannitol; sugar can pull water from osmotic space, causing false hyponatremia. If none, move on to (2).
(2) Where did the water come from? The animal could have drunk a lot, but primary PD is rare. Other option is that the water is retained in kidneys from severe renal DZ or too much ADH. Are ADH levels appropriate or excessive?

Front 101

Electrolyte panel comes back; animal has hypernatremia. What should be your next thoughts?

Back 101

(1) How was the hypernatremia generated? Na+ can be acquired via ingestion (toxins, playdoh, paintballs, etc.). Or, the animal could have lost water (GI / renal / insensible loss).
(2) How is the hypernatremia being maintained? Why can't the animal drink to fix the hypernatremia? An animal that can drink will always do so to self-correct. Patient must be obtunded, unconscious, injured, or have no access to H2O.

Front 102

Blood work returns and shows hyperkalemia. What could've caused it?

Back 102

Always think 1 of these 3 things:
1) Cells --> a) Acidemia, though this doesn't happen clinically. b) Cell death, which leads to K+ release from cells. C) Insulin deficiency/antagonism, which means that K+ can't get taken up into cell. d) Beta blockers, which block Na+/K+ ATPase so that K+ stays outside of cells.
2) Kidneys --> a) Decreased GFR, preventing clearance. b) Decreased DCT flow, which leads to increased time for K+ reabsorption. c) Decreased aldosterone.
3) GI intake --> Iatrogenic.

Front 103

Bloodwork returns, and shows hypokalemia. What could've caused it?

Back 103

Always think 1 of these 3 things:
1) Cells --> a) Alkalosis, in which cells hoard K+ with lack of H+ buffer. b) Insulin excess, causing movement of all K+ into cells. c) Beta agonists, which increase Na+/K+ ATPase activity.
2) Kidneys --> a) Increased GFR & GFR clearance. b) Increased aldosterone. c) Non-resorbable ions like bicarb and ketones in DCT will pull K+ in
3) GI loss --> a) Severe diarrhea. b) Anorexia.

Front 104

What is Cl-'s role?

Back 104

Cl- stalks Na+ to maintain electric neutrality.

Front 105

When you see hypochloremia on bloodwork, what should you do to find out what's causing it?

Back 105

Calculate the Na - Cl difference. If the difference is < 42, the hypochloremia is a result of Cl- following Na+. If the difference is > 42, the hypochloremia is due to selective Cl- loss from vomiting, stomach tubes, etc.

Front 106

What methods of urine sample collection are preferred in large animals? Small animals?

Back 106

LA: Free catch
SA: Cystocentesis

Front 107

How long does a urine sample last?

Back 107

Ideally, you want to analyze the urine within 1 hr of collection. If that is not possible, can refrigerate the urine for up to 12 hrs, but make sure to bring it to room temperature before analyzing. If the urine is cold, the dipstick rxns are inhibited + can see false increase in USG.
Keep in mind that delayed analysis leads to bacterial overgrowth, increased pH, crystal formation/dissolution, degradation of cells and casts, and salt precipitation leading to turbidity.

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What is a reflex test?

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Reflex testing refers to testing performed after an initial lab test result is positive. This initial test result requires follow-up/confirmatory testing, and so, a reflex test is done.
Ex: Reflex culture is done if >3 WBCs or bacteria are found in urine.

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How does the normal range for urine pH in a carnivore or omnivore differ from that in an herbivore? What about in a bird?

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Carnivores/omnivores have more acidic urine than herbivores (or birds) because they undergo protein catabolism.
Carnivores & omnivores: 5.5 - 7.5
Herbivores: 7.5 - 8.5
Birds: 7 - 8

Front 110

When would we run a reflex Urine protein : Creatinine (UPC) ratio?

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You would do a reflex UPC when you see proteinuria in order to quantify the protein loss.
Normal UPC: < 0.5
Borderline: 0.5 - 1.0
Proteinuric: > 1.0

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What are examples of causes of pre-renal proteinuria?

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Hemoglobinuria
Myoglobinuria
Light chains

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What are examples of causes of renal proteinuria?

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Glomerular DZ
Tubular DZ

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What are examples of causes of post-renal proteinuria?

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Inflammation
Hemorrhage in bladder or urogenital tract

*Most common type of proteinuria.

Front 114

You get a sample of urine, and it is red. Your DDx are: hematuria, hemoglobinuria, & myoglobinuria. How do rule out?

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Hematuria indicates whole RBCs in the urine, whereas hemoglobinuria indicates Hgb from intravascular lysis of RBCs. Myoglobinuria indicates myoglobin from muscle damage.
Centrifuge the urine sample; if it separates into a clump of RBCs at the bottom and yellow/pink plasma, then it's hematuria. If no separation occurs, it's hemoglobinuria or myoglobinuria.

Front 115

What is glomerular DZ?

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Glomerular DZ presents clinically as significant proteinuria without inflammation elsewhere in the urinary tract. There are 2 types of glomerular DZ:
1) Glomerulonephritis. Usually immune mediated. Can be membranous (capillary loops thickened; unchanged cellularity) or membranoproliferative (thickened capillary loops and increased cellularity).
2) Glomerular amyloidosis. Beta-pleated sheets deposited in mesangium and subendothelial space of glomerular capillary walls.

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How can we tell the 2 types of glomerular DZ apart?

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Look at UPC. It will help you rule out pre-renal and post-renal proteinuria.
If glomerulonephritis, UPC will be b/t 5-15. if amyloidosis, UPC will be > 18.

Front 117

What percentage of renal function must be lost to see azotemia?

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75%+

Front 118

What is an ectopic ureter?

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Ureter comes out from kidney and doesn't connect properly with the bladder. Leads to incontinence and needs surgical correction.

Front 119

What are the 4 most common types of neoplasia to see in the kidneys?

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1) Renal carcinoma - A primary renal tumor in older animals. Oval masses in renal cortex. Can see increased EPO production in the form of erythrocytosis/polycythemia.
2) Nephroblastoma - A primary renal tumor common in pigs and chickens. Usually occurs in young animals.
3) Lymphoma - A secondary renal neoplasm.
4) Metastatic osteosarcoma - A secondary renal neoplasm due to the fact that kidneys see 25% of body's blood supply. (Really, any cancer that travels hematogenously can met to kidneys.)

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What are the primary calculi in dogs?

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CaOx
Struvite
Urate
CaPhos/Cysteine/Silica

Front 121

What are the primary calculi in cats?

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Struvite
CaOx (if upper UT stone, usually this.)
Urates/Dried blood/CaPhos

Front 122

What DZ are horses that are given NSAIDs while dehydrated susceptible of?

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Renal medullary necrosis

Front 123

What causes hypercalcemia?

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G - Granulomatous
I - Idiopathic
H - Hyperparathyroidism
A - Addison's DZ
R - Renal failure
D - Vitamin D toxicity
O - Osteolysis
N - Neoplastic (Paraneoplastic)
S - Spurious