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ACVIM General - Imp stuff > Renal > Flashcards

Renal Flashcards

1
Q

What’s unique about the kidneys arterial supply?

A

Capillary beds in kidneys drain into capillary beds, whereas capillary beds in the rest of the body drain into veins. This is why its called the renal portal system

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2
Q

What is the general job of the glomerulus?

A

Glomerulus filters almost everything out of the blood into the ultra filtrate (urine(

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3
Q

What is the general job of the proximal convoluted tubule?

A

Reabsorp almost everything from the utrafiltrate back into the blood

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4
Q

What is the general job of the loop of henle?

A

Dilute the urine and create a medullary concentration gradient

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5
Q

What is the general job of the distal convoluted tubule. and collecting ducts?

A

Concentrate the urine and control acid base. If ADH and a medullary concentration gradient

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6
Q

What are the 3 components/layers of the Renal Corpuscle?

A
  1. Capillary endothelium - faces lumen,
  2. GBM
  3. Podocyte - faces urinary side
    All negatively charged

Passage of material through filter depends on size and charge (small, positive molecules get through)

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7
Q

What is the route of blood to urine?

A

Arterial blood –> afferent arterioles –> glomerulus –> capillary endothelium –> GBM –> podocytes –> urinary space (Bowmans capsule) –> proximal tubule

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8
Q

Where is the macula densa located? What do they do when they sense low Na? High Na?

A

Distal convoluted tubule
Low Na: stimulates juxtaglomerular cells to release renin –> ultimately vasodilates afferent arteriole to increase GFR
High Na: no renin released. Vasoconstriction of afferent arteriole to reduce GFR

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9
Q

What is the job of the macula densa?

A

It senses Na+ and Cl- exiting the distal thick ascending LOH

Depending on this will respond

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10
Q

What type of cells produce and release renin? In response to what?

A

JG cells produce and release renin in response to low renal perfusion. Signal comes from the macula densa when the Na is low

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11
Q

How much is absorbed of each in the PCT?
glucose, AA, Na, K, urea, phosphate, Ca, bicarb, H2O

A

Glu: >99%
AA: >99%
Na and K: 2/3 in PCT, also reabsorbed in LoH + DCT
Urea: ~50%
Phosh: 80-90%
Ca: >90% ionized or chelated Ca absorbed
Water: >99%

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12
Q

Describe the resorption of bicarbonate in the PCT

A

Na gets counter transported with hydrogen ions (Na out, H+ in) - basolateral side. Uses 3Na-2K-ATPase pump (active)

As H+ comes into the cell it combines with H2CO3 inside the tubular lumen.

The enzyme carbonic anhydrase converts to H2O + CO2 (easily transported through membrane).

The CO2 is transported to the PCT and combines with H2O through carbonic anhydrase to form H2CO3 (BICARB!)

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13
Q

Describe the absorption of glucose in the PCT?

A

Luminal side: cotransported with Na
Basolateral side: facilitated diffusion according to concentration gradient

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14
Q

The renal threshold for phosphate is (low/high). What hormone increases renal phosphate excretion in the PCT?

A

LOW
PTH increases renal phosphate excretion

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15
Q

What type of transport is happening in the thin ascending LOH? Thick ascending?

A

Thin – passive transport
Thick – active transport

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16
Q

How is Na absorbed in the luminal side of PCT?

A

Cotransported with glucose, AA, phosphate

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17
Q

How is Na absorbed in the basolateral side of PCT?

A

NaK ATPase and Na-bicarb cotransporter

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18
Q

What is the MOA of furosemide?

A

Inhibits the action of Na-K-2Cl cotransporter in the thick ascending LOH. It works by not making the urinary concentration gradient.

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19
Q

What are the 2 main types of cells in the DCT? What distinguishes them?

A
  1. Principal cells
    - Resorption of Na, secretion of K based on ALOSTERONE (increases # of open luminal Na+ channels and basolateral Na+ pumps); resorption of H2O based on ADH (increases # of aquaporins)
    -Also play a role with ADH (remember that with ADH there is no active transport of H2O, just increase in the # of aquaporins)
  2. Intercalated cells - acid-base regulation
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20
Q

What’s the difference between alpha and beta intercalated cells in the DCT?

A

Alpha: secrete acid in the form of H_ ions on luminal side –> active transport
- This is broken in distal (type 1) RTA

Beta: secrete base in the form of bicarbonate ions on the basolateral side –> passive transport

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21
Q

MOA and SE of spironolactone

A

MOA: K-sparing diuretic or mineralcorticoid-receptor antagonist
-Competitively inhibits aldosterone in the DCT –> increase excretion of Na, Cl, water + decreased excretion of K, ammonium, phosphate

SE: GI, electrolyte (hyperkalemia, hyponatremia)

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22
Q

What is the major tubular site for aldosterone?

A

Principal cells in the distal portion of DCT and collecting ducts

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23
Q

What is the mechanism for aldosterone? What are the stimuli for aldosterone release?

A

Stimulation of NaK ATPase pump - basolateral
Stimuli for aldosterone:
1. Increased extracellular K
2. Increase Ag II levels (when hypotension)

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24
Q

Describe the pathogenesis for diabetes insipidus in the nephron

A

DI have a lack of ADH. Without ADH the permeability to water decreases in the distal tubules and collecting ducts. This leads to the kidneys excreting large, dilute volumes.

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25
Q

Name 4 sequelae of angiotensin II activation

A
  1. Blood vessel constriction (increase BP)
  2. Aldosterone release (increase Na and H2O resorption, increase ECF)
  3. ADH release (increase water resorption, increase ECF)
  4. Sympathetic NS stimulation (increase BP)
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26
Q

What is the pathogenesis of Type I renal tubular acidosis?

A

Alpha intercalated cells in the distal portion of the DCT and collecting ducts are not working. These cells usually secrete acid in the form of H.

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27
Q

What characterizes RTA? What are the types?

A

Hyperchloremic metabolic acidosis
Types:
-Proximal (type II) RTA
-Distal (type I) RTA
- Distal (type IV) RTA

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28
Q

What would the urine pH be for the Types:
-Proximal (type II) RTA
-Distal (type I) RTA

A

Types:
-Proximal (type II) RTA: acid pH (<6), no nephroliths or nephrocalcinosis, mild metabolic acidosis, can excrete other solutes such as AA, glu, phos, Na, K

-Distal (type I) RTA: alkaline pH ((>6), more severe metabolic acidosis, can have nephroliths and nephroclcinosis, no concurrent defects of PCT resorption

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29
Q

What is the pathogenesis for proximal (type II) RTA?

A

Defect in the basolateral membrane Na+ HCO3- cotransporter. HCO3- leaks into tubular lumen, preventing bicarb reabsorption and leading to metabolic acidosis. Can occur alone or with Fanconi syndrome or other proximal tubular defect.

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30
Q

What are the complications of proteinuria?

A

Azotemia
Hypoalbuminemia –> edema
Hypertension
Thromboembolism

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31
Q

What MHC is expressed in proteinic dogs as part of the inflammatory response?

A

MHC II - seen because of lymphocyte recruitment

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32
Q

What percentage of dogs with PLN are hypercoagulable?

A

~89%

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33
Q

What is the prevalence of thromboembolism in PLN dogs?

A

25%

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34
Q

What is the mechanism for hypercoagulaibility in PLN?

A

Antithrombin loss
Platelet activation
Hyperfibrinogenemiaa
Increased factors V, VIII
Thrombocytosis
Decreased RBC deformability
Increased vWF
Fibrinogen and alpha-2 macroglobulin accumulation
Inhibition of fibrinolysis

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35
Q

What is the incidence of hypercholesterolemia in glomerular disease?

A

79-86%

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36
Q

What is nephrotic syndrome?

A

Proteinuria
Hypoalbuminemia
Ascites
Hypercholesterolemia

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37
Q

What is nephritic syndrome?

A

2ry to renal inflammation and acute glomerular swelling
Common in humans, uncommon in dogs
Can see 2ry to Lyme disease - nephritis-like syndrome

Hematuria/RBC casts –> proteinuria

Edema
Hypertension
Azotemia
OLIGURIA

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38
Q

What is the major determinant of glomerular filtration? What is the limit of the GBM?

A

SIZE
but also negative charge
GBM limits 60-70,000 daltons
Albumin is 69,000 daltons AND has a negative charge

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39
Q

What are microscopic changes to the glomerulus that we see with glomerular disease?

A

-Podocyte effacement
-Enlargement of the diaphragm
-Loss of negative charge

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40
Q

Post-renal causes of proteinuria

A

Urinary system - no associated w/kidney
UTI
FLUTD/Cystitis
Urolithiasis
Prostatitis
Neoplasia (TCC, prostatic carcinoma, etc)
Intact male dog (semen can contribute, but eliminating seminal fluid is the only way to know – neuter)

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41
Q

Where does the proteinuria come from in pre-renal?

A

Overwhelm reabsorptive capacity of the PCT
-Hemoglobin
-Myoglobin
-Bence-jones proteinuria

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42
Q

Where does the protein come from in renal proteinuria?

A

Funtional/physiologic: transient changes in selectivity of glomerulus (seizures, fever, exercise, stress)
Pathologic:
-Glomerular: decreased per selectivity – most common cause of persistent high magnitude proteinuria (>5UPC)
-Tubular: decreased protein reabsorption (1-3UPC)
-Interstitial: exudation of proteins to the urinary space

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43
Q

Does hematuria affect the UPC?

A

Microscopic hematuria only minimally affects UPC. Blood does NOT affect UPC unless it changes the color of the urine

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44
Q

Does pyuria affect the UPC?

A

81% of dogs w/pyuria have normal. UPC

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45
Q

Does semen affect the UPC?

A

May cause false-positive results for protein and blood on dipstick

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46
Q

What is the level of protein detection in the dipstick, SSA, microalbuminuria?

A

Dipstick: 30mg/dL
SSA: 5mg/dL
Microalbuminuria: 1mg/dL

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47
Q

Does pooling the urine for UPC change the magnitude compares to single catch?

A

No

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48
Q

Is there a difference between drip or dip in the urine dip stick results?

A

Dip > drip
Increases variability with drip method - pH, blood, glucose.

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49
Q

Which stain do we use for diagnosis of amyloidosis in renal biopsies using light microscopy?

A

Congo red

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50
Q

What can you see with the H and E stain using light microscopy?

A

Cellularity, wall thickness, inflammatory cells

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51
Q

What can you see with the PAS stain using light microscopy?

A

Basement membrane and matrix

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52
Q

Which stain do we use for diagnosis of immune complexes in renal biopsies when using light microscopy?

A

Masons trichrome

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53
Q

What does fluorescent stains in renal biopsies diagnose?

A

Immune complexes.

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54
Q

What part of the kidney do we obtain for a renal biopsy?

A

Cortex ONLY, no medulla
Run light microscopy, electron microscopy, immunofluorescence
Need 20-25 glomerular tufts for 90% confidence

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55
Q

What. are contraindications for renal biopsies?

A

IRIS Stage 4 or greater (crea >5)
Polycystic kidney dz
Renal abscess, infx
Hydronephrosis
Coagulopathy
Uncontrolled hypertension

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56
Q

What are the 3 most common types of glomerular diseases?

A

Membranoproliferative glomerulonephritis (MPGN)
Membranous nephropathy (MN)
Amyloidosis
Account to 66% of all glomerular diseases

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57
Q

What is the most common glomerular disease in dogs?

A

Membranoproliferative glomerulonephritis – 20-60%
No sex predilection
Mean age: 7-10Y
Slowly progressive, EXCEPT BERNESE MOUNTAIN DOGS

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58
Q

What % of dogs with MPGN are hypoalbuminemic?

A

75%

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59
Q

What % of dogs with MPGN are hypertensive?

A

40%

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60
Q

What % of dogs with MPGN have a UPC >1.6?

A

80%

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61
Q

What are the findings you can find in the electron microscopy in a dog with membranoproliferazive glomerulonephritis?

A

-Thickened capillary loops
-Mesangial hypercellularity
-Identification of immune complexes on the sub endothelial side of the glomerular basement membrane

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62
Q

What are the 2 types of MPGN? How do you tx it?

A

Type I (mesangiocapillary GN): often caused by infectious disease (mainly tick borne)
Type II (Dense Deposit Disease): rare in dogs. Not associated w/infectious dz.
TX: tx infectious dz or neoplasia

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63
Q

What is the most common cancer that causes proteinuria?

A

Lymphoma

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64
Q

What is the most common glomerular disease in cats? And the second most common in dogs?

A

Membranous nephropathy - NOT an inflammatory disease
M>F

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65
Q

The rate of nephrotic syndrome with membranous nephropathy is (high/low).

A

HIGH - 80% have mild to severe hypoalbuminemia

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66
Q

What are the 2 forms of membranous nephropathy? What is the tx?

A

Primary/Idiopathic - immune complexes on subepithelial aspect of glomerular basement membrane
-Reaction with unbound antibody and fixed antigen (podocyte) on urinary side

Secondary - circulating immune complexes also present in the mesangium and/or subendothelial space
-Circulating immune complexes and complement driven mechanism independent of inflammatory cells

Tx: IMMUNOSUPPRESSION

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67
Q

What are the common finings in electron microscopy in patients with amyloidosis?

A

Extracellular deposition of proteins with beta-pleated sheet

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68
Q

What’ the difference between reactive and familial amyloidosis>

A

Reactive amyloidosis – amyloid deposits in glomerulus
Familial amyloidosis – amyloid deposits in renal medulla

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69
Q

Who is predisposed to reactive amyloidosis? What’s the mean UPC?

A

F>M
Mean age: 7-9YO
Mean UPC: 12.7

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70
Q

What % of dogs w/reactive amyloidosis are azotemic?

A

50% have creatinine >1.6

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71
Q

What cat breeds are predisposed to familial amyloidosis? What dog breed is predisposed?

A

Abyssinian/Siamese
Shar Pei

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72
Q

What are the microscopic changes in the kidney of a cat with familial amyloidosis?

A

Medullary fibrosis and papillary necrosis

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73
Q

Where else do siamese deposit amyloid other than the kidney?

A

Liver

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74
Q

What is the tx of familial amyloidosis?

A

Colchine - impairs release of SAA from hepatocytes
DMSO - decreases SSA/decreases inflammmation

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75
Q

Is proteinuria common in Shar Pei fever?

A

Not as common given that the deposits are in the medulla

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76
Q

What systemic diseases are related to glomerular sclerosis (scarring of the gomerulus)?

A

DM, hypertensive nephropathy - end stage

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77
Q

What dog breed is predisposed to hereditary nephropathy? Where is the defect in the GMB?

A

X-linked in Samoyeds
Defect in GBM collagen type IV

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78
Q

What mutation to cocker spaniels have in their collagen chain of the kidneys?

A

COL4A4 - GBM disease

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79
Q

What is the pathogenesis of minimal change disease nephropathy?

A

Dysfunction of T-cells –> increase lymphokines –> loss of (-) charge of GBM –> increased permeability

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80
Q

Why are omega-3 FA recommended in proteinuric patients?

A

Reduce inflammation and vasoconstriction
Lower mortality, increased renal function, reduced proteinuria and cholesterol

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81
Q

What’s the MOA of thienopyridines (Clopidogrel and Ticlopidine)?

A

-irreversibly inhibits binding of ADP to platelet P2Y12 receptor
-this impairs platelet release reaction and ADP mediated activation of GPIIb/IIIa, reducing the primary and secondary aggregation response
-metabolized by cytochrome p450
-platelet inhibition occurs 3 days after starting tx
-ticlopidine – but associated with unacceptable GI side effects

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82
Q

What is the MOA of aspirin?

A

Irreversibly inhibits COX-1 (catalyze conversion of arachidonic acid to PGH2- precursor for PGD2 - PGE2, PGI2, and TXA2 (thromboxane A2))

SE:
-GI upset
-acidosis (with OD)
-probably less common with lower anti-platelet doses)

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83
Q

What is the MOA of heparin?

A

Binds to AT –> inactivates procoagulant activity of factor IIa (thrombin). Also inhibits activatino of factor XIII and increases release of lipoprotein lipase –> clears circulating lipids

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84
Q

What is the MOA of unfractioned heparin?

A

-heterogenous mixture of molecules of differing molecular weights (3000-30,000 daltons)
-~1/3 of molecules that possess a pentasaccharide sequence that binds to AT and accelerates its interaction with thrombin (IIa), and Xa . (also IXa, XIa, XIIa but these aren’t as important
-thrombin inactivation requires formation of a ternary complex involving heparin, AT, and thrombin (only heparin molecules with more than 18 monosaccharide units can inactivate thrombin)
-indirect anticoagulant – exerts most of its activity through potentiation of AT
-anti-Xa:anti-IIa ratio: 1.0
-unpredictable anticoagulant effect in dogs and cats

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85
Q

What is the MOA of enalapril and benazepril?

A

-block ACE –> decrease formation of angiotensin II from angiotensin I (competes with AT I with higher affinity)
-preferentially dilate efferent arteriole (and thus may decrease GFR)
-may temporarily reduce aldosterone levels
-increase circulating bradykinin (inhibits bradykinin degeneration)
-balanced vasodilators (though weak)
-mostly renal excretion except benazepril (biliary excretion 50% in dogs, 85% in cats)
-enalapril 80% excreted through kidney

SE:
-hypotension
-decreased GFR
-hyperkalemia (due to decreased GFR and decreased aldosterone)
-GI – vomiting, diarrhea, anorexia

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86
Q

What is the MOA of telmisartan?

A

ARB - block angiotensin II subtype I receptors
-binding of subtype 2 is preserved
-Avoids ACE proteolytic pathways which can increase AgII production
-Telmisartan is more effective due to higher affinity and slower dissociation from the Ag-1 receptor
First line therapy for proteinuria

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87
Q

What’s the tx for immune mediated glomerual diseases?

A

Mycophenolate - recommended first choice
Cyclophosphamide
Glucocorticoids - recommended short term

88
Q

MOA and SE cyclophosphamide

A

Alkylating agent

Nitrogen mustards: N-7 position on guanine base most common site of alkylation; leads to mispairing with thymidine or strand breakage

SE: myelosuppression, GI, renal tox (sterile hemorrhagic cystitis, hematuria), cardiac, hepatic, pulmonary tox

89
Q

MOA mycophenolate

A

-pro-drug hydrolyzed in liver to form mycophenolic acid
-cytostatic for lymphos
-inhibits inosine monophosphate dehydrogenase (necessary for purine biosynthesis)
-selective inhibitor of T and B cell proliferation

90
Q

When would you expect to see improvement with immunosuppressive therapy?

A

At least 8 weeks before altering or abandoning immunosuppressive trial
If no response in 3-4 mo - d/c immunosuppression

91
Q

What will cause a false positive for protein in the urine dipstick test?

A

High pH or concentrated urineW

92
Q

What will cause a false negative for protein in the urine dipstick test?

A

Low pH, dilute urine, Bence-jones protein

93
Q

Describe the IRIS CKD Staging

A
94
Q

Name the DDX for an acute kidney injury

A

-Toxin: NSAIDs, grapes (dogs), Lillies (cats), EG, aminoglycosides, cisplatin, omnipaque, heavy metals, hemoglobinuria/myoglobinuria, envenenomation, melamine/cyanuaric acid, expired tetracyclines
-Infectious: Lepto, Borrelia, Leishmania, peel (bacterial, fungal)
-Ischemia: hypovolemia, decreased CO
-Inflammation: pancreatitis, trauma, sx
-Hypercalcemia
-Hyperviscosity
-UO

95
Q

Name the ddx for feline LUTD

A

-Bacterial cystitis
-Uroolithiasis
-Urethral stricture
-Urethral trauma
-Neoplasia
-Urethral plug
-FIC

96
Q

Risk factors for FLUTD in cats

A

Persian, Manx, Himalayan
Middle aged (4-7y)
Male
Overweight
Neutered

97
Q

Which crystal is implicated in the pathogenesis of FIC?

A

Struvites. Over 80% of mineral urethral plug

98
Q

What pro inflammatory cytokines/chemokines are present in higher concentration in cats with FIC?

A

CXCL12
IL12
IL18
FIt3L

99
Q

MOA and SE of prazosin

A

MOA: alpha1 adrenergic blocker –> relaxes vascular smooth muscle

SE: high BW, GI, Neuro signs, nictitans elevation

100
Q

MOA and SE of bethanecol

A

MOA: cholinergic - increases tone of detrusor muscle in the bladder

SE: GI, CV (hypotension, tachycardia), elevated tbil, AST

101
Q

What diet do you use in FIC cases

A

Acidifying, low in Mg
Also have tryptophan (serotonin precursor) + alpha-casozepine (partial GABA agonist- anxiolytic)

102
Q

Considering the physiology of renal blood flow through the nephron, if a therapy decreased the blood pressure in the afferent arteriole a ______ in GFR might occur.

A

Decrease

103
Q

The proximal tubule reabsorbs what % of Na and water?

A

65%

104
Q

Tx for CDI
SE and MOA of drug

A

Desmopressin:
MOA: synthetic vasopressin (ADH) that acts on V2 receptors – increases urine osmolalality + decreasing net urine production

SE: ocular irritation, neuro signs with hypernatremia, hypersensitivity

NOTE: also causes dose-dependent increase in vWF by relesing vWF from endothelial cells and macrophages

105
Q

T/F: Vitamin D enhances the expression of apical calcium transport channels and intracellular calcium binding proteins within the cells of the distal convoluted tubule and collecting duct.

A

True

106
Q

What cell is primarily responsible for the selectivity of the glomerular filtration barrier?​

A

Podocytes

107
Q

What is the limit in daltons for the GBM?

A

Limits 60-70,000 daltons
Albumin: 69,000 daltons, negatively charged

108
Q

Which hormones are secreted by the posterior pituitary?

A

Oxytocin and ADH

109
Q

What are the common dog breeds for renal dysplasia?

A

-Lhasa Apso
-Poodles
-Shih tzus
-Soft coated wheaten terrier
-Chow Chow
-Alaskan Malamute
-Mini schnauzer
-Dutch kooiker (decoy dog)

110
Q

What are the 3 dog breeds predisposed to polycystic kidney disease?

A

-Bull terrier (dominant gene)
-Cairn terrier (recessive gene)
-Westie (recessive gene)

111
Q

What breed is predisposed to X-linked hereditary glomerular basement membrane defect?

A

Samoyeds

112
Q

What breed is predisposed to primary MPGN?

A

Doberman

113
Q

What dog breeds are predisposed to amyloidosis familial glomerulopathy?

A

Shar pei, English Foxhound, Beagle

114
Q

What dog breeds are predisposed to immune-mediated familial glomerulopathies?

A

Soft coated wheaten terrier
Bernese mountain dog
Brittany spaniel (type I MPGN secondary to C3 deficiency)

115
Q

What immune-mediated familial glomerulopathy do Bermese mountain dogs have?

A

Type I MPGN –> positive for C3 and IgM

116
Q

What breed is predisposed to Fanconi Syndrome?

A

Basenji

117
Q

Which breed is predisposed to reflux nephropathy with segmental hypoplasia?

A

Boxer

118
Q

Which breed is predisposed to multifocal cystadenocarcinoma familial glomerulopathy?

A

GSD

119
Q

Which breed is predisposed to telangiectasia familiar glomerulopathy?

A

Corgi

120
Q

Which cat breed is predisposed to polycystic kidney disease?

A

Persian (autosomal dominant)

121
Q

Which cat breeds are predisposed to familial amyloidosis?

A

Abyssinian, Siamese, Oriental

122
Q

What is the most common cause of primary polyuria in SA?

A

Secondary nephrogenic DI

123
Q

What are the ddx for PU/PD based on the mechanisms of action?

A

CDI
Primary NDI
Secondary NDI
-Cushings
-Addisons
-Hyperthyroidism
-Hyperaldosteronism
-Liver dz
-Pyelo
-Pyo/E coli endotoxemia
-Lepto
-Acromegaly
-Leiomyosarcoma
-Drugs (steroids, phenobarbital)
Osmotic diuresis
-DM
-CKD
-1ry renal glycosuria
-Fanconi
-Post-obstructive diuresis
-Drugs (osmotic diuretics)
-High salt diet
Low renal medullary tonicity
-Renal medullary washout
-Low protein diet
Other/unknown
-Polyuric phase of AKI
-Syndrome of inappropriate ADH secretion
-Splenic hemangiosarcoma
-Pheo

124
Q

What is important to have in mind in a patient with glycosuria?

A

Glycosuria can increase the USG by 0.04 for each g/dL of glucose in the urine. Urine can be marked as concentrated when it’s not

125
Q

What pH do struvites grow in?

A

Alkaline due to UTI

126
Q

How long do you tx struvite stones?

A

2-4 weeks post resolution of radiographic/US stones and negative urine culture

127
Q

What is different in dogs and cats w struvite stones?

A

Dogs - associated w/UTI
Cats - usually sterile/not associated with UTI

128
Q

What medication can you consider as adjunctive for struvite stones (other than antibiotics)?

A

Urinary acidifier such as D, L-methionine

129
Q

What are predisposing factors to CaOx stones other than breed?

A

Hypercalcemia
Hypercalciuria
Increased oxalate excretion
Acidic urine
Decreased urine vol/highly concentrated urine
High protein diet?

130
Q

What is the USG target for dogs with CaOx stones?

A

Dogs: <1.020
Cats: <1.030

131
Q

What medication can be considered for dogs with recurrent CaOx stones and why?

A

Thiazide diuretics (hydrochlorothiazide) - reabsorb filtered calcium
- If not hypercalcemic
Potassium citrate to alkalinize urine

132
Q

What is the target pH for minimizing recurrence of CaOx stones?

A

pH > 6.5
No crystalluria

133
Q

What type of pH do Calcium Phosphate Hydroxyapatite stones form in?

A

Alkaline (bc concomitant urease-producing UTI)

134
Q

What happens if you use allopurinol alone in a Dalmatian with urate stones?

A

Xanthine stones if not doing concurrent protein restricted diet

135
Q

What gene mutation causes urate stones in Dalmatians?

A

SLC2A9 Gene Mutation - inherited alteration of urate transported

136
Q

What gene mutation is associated with cystine uroliths in cats?

A

Missense mutation in SLC3AI gene

137
Q

Describe the purine metabolic pathway

A

Purine –> hypoxanthine –> xanthine –> uric acid –> allantoin

138
Q

What cat breeds are predisposed to forming CaOx stones?

A

Persian and Himalaysn

139
Q

What is the cause of cystine stones in dogs?

A

Genetic defect - reduced ability of the kidney’s proximal tubule to resorb cystine and other AA –> increased cystine in urine –> cystine stones

140
Q

What is thiola used for?

A

Thiola - tiopronin or 2-MPG - increase solubility of cystine
Can cause aggression, myopathy

141
Q

What dog breeds are predisposed to xanthine stones?

A

Toy Manchester terrier, KCCS, English springer spaniel - proximal tubular defect

142
Q

What’s the MOA of allopurinol?

A

Inhibits xanthine oxidase (enzyme that converts xanthine to uric acid)

143
Q

Which uroliths CANNOT be dissolved?

A

Xanthine, CaOx, Ca Phosphate (unless >70% struvite), Silica

144
Q

Which uroliths CAN be dissolved?

A

Struvite, urate (if no underlying liver dz), cystine

145
Q

What breeds are predisposed to silica cystoliths?

A

Yorkies <3, shih tau, Lhasa, Goldens, GSD

146
Q

What are predisposing factors for silica cystoliths?

A
  • Consuming diet or meds w/large amount of silica in soil or certain plants (corn gluten, whole grains, wheat hulls)
    -Active or inactive ingredient of meds containing silica
    -Some antacids: magnesium trisilicate
147
Q

What are causes of hypernatremia? List mechanism

A

Loss of water in ECF: CDI (lack of ADH), NDI (renal disease that does not respond to ADH)
Excess Na in ECF: over hydration, hypothalamic lesions

148
Q

How much can you correct hyponatremia per day?

A

<10-12 mmol/L

149
Q

What are causes of increase capillary pressure leading to edema?

A

-Excess renal retention of Na and water: acute or CKD, mineralocorticoid excess–> leads to SHT
-Increase venous pressure and venous constriction: CHF, venous obstruction, failure of pumps (paralysis, immobilization, failure of venous valves)
-Decrease arteriolar resistance: vasodilatory drugs, insufficiency of SNS, excess body heat

150
Q

What are causes of low plasma proteins leading to edema?

A

Nephrotic syndome
Denuded skin areas
Failure to produce proteins: liver disease, protein/caloric malnutrition

151
Q

Describe causes (cellular level) of increased GFR

A

-Increase glomerular capillary filtration coefficient
-Increase rate of blood flow to glomerulus
-Increase glomerular capillary hydrostatic pressure

152
Q

Describe causes (cellular level) that decrease GFR

A

-Increase Bowmans capsule hydrostatic pressure
-Increase glomerular capillary colloid osmotic pressure
-Increase resistance of afferent arteriole

153
Q

What’s the effect of efferent constriction on GFR?

A

Biphasic effect
-If constriction of efferent arteriole is severe –> colloid osmotic pressure exceeds the increase in glom capillary hydrostatic pressure caused by efferent arteriole –> decrease GFR
-If moderate level of constriction–> slightly increase GFR

154
Q

What’s the effect of afferent constriction on GFR?

A

Decrease GFR

155
Q

What’s the effect of strong activation of sympathetic NS on GFR?

A

Constriction of renal arterioles –> decrease renal blood flow –> decrease GFR

156
Q

What’s the effect of NE and Epi on the kidney

A

Constriction of afferent and efferent arteriole = decrease GFR

157
Q

What’s the effect of angiotensin II on afferent and efferent arterioles of the kidney

A

Constricts the EFFERENT
Increases glomerular hydrostatic pressure while decreasing renal blood flow –> helps prevent decreases in glomerular hydrostatic pressure and GFR

158
Q

What does urinary excretion =

A

Excretion = Filtration - Reabsorption + Secretion

159
Q

How much of the CO is filtered through the kidney?

A

20%

160
Q

Electrolytes with nephrogenic DI – which electrolyte could be decreased?

A

Cl low
Na, Ca HIGH

Nephrogenic DI – kidneys unable to respond to ADH
ADH 🡪 reabsorb water in distal and cortical tubules
Plasma osmolarity should be high normal to increased

161
Q

MOA of mannitol (osmotic diuretic)

A

Increase ECF and plasma volume –> increase renal blood flow –> traps water in tubule –> diuresis

162
Q

WHats the gold standard for diagnosing anti-GBM diseases?

A

Direct immunofluorescence for immunoglobulin – typically show a strong linear ribbon-like appearance

163
Q

What is ANCA?

A

Anti-neutrophilic cytoplasm antiBODY disease
-Autoantibodies specific for neutrophils and monocyte granule proteins
-Neutrophil degranulation causes small vessel vasculitis

164
Q

With glomerulonephritis associated with SLE, where would we see the defect?

A

sub endothelial and/or subepithelial

165
Q

Main extracellular electrolyte

A

Na

166
Q

Main intracellular electrolkyte

A

K

167
Q

What factors regulate the NaK ATPase?

A

Insulin (moves K into cell)
Catecholamines
Thyroid hormone
K balance in body
Chronic disease (heart, renal)

168
Q

How do catecholamines affect K?

A

Alpha: impair K entry to cell
Beta: promote K entry to cell

169
Q

How does K shift in acidemia? Alkalosis?

A

Adisosis: movement from ICF–>ECF
Alkalosis: movement from ECF–>ICF

170
Q

Where do the thiazide diuretics work? How?

A

Distal convoluted tubule

Inhibit Na/Cl cotransporter in the distal convoluted tubule; actions: 1) block electrolyte resorption and loss of H20, 2) increased K and H secretion in the distal tube,

-initially have a hypercalciuric effect, but with continued therapy calcium excretion is significantly decreased (in normal dogs, hydrochlorothiazide by not chlorothiazide had this effect); causes subclinical volume depletion resulting in proximal tubule reabsorption of Na and Ca; this effect is blunted when using high Na diet
-paradoxically decrease urine production in dogs with diabetes insipidus

171
Q

Which cells are responsible for K excretion in the kidneys?

A

Principal cells in the collecting tubule

172
Q

Which cells in the cortical collecting ducts secrete bicarb?

A

Intercalated type B cells

polarity reserved com0ared to type A cells

173
Q

WHats the most important hormone for urinary K excretion?

A

Aldosterone

174
Q

What promotes aldosterone release?

A

AgII
Hyperkalemia
ACTH
Hyponatremia
Acidemia

175
Q

What inhibits aldosterone release

A

Dopamine and atrial natriuretic peptide (ANP)

176
Q

What step is carbonic anhydrase required for?

A

dissolved CO2 -> carbonic acid (H2CO3)

177
Q

What is the strongest stimulus for aldosterone?

A

Hyperkalemia

178
Q

What stimulates ADH?

A

Osmoreceptors in the supraoptic nuclei due to high osmolarity, dec. blood volume, dec. blood pressure

179
Q

What does the juxtaglomerular apparatus secrete?

A

Renin

180
Q

Which factor decreases GFR?
Kf
Glomerular onc pressure
Glom hydrostatic pressure
Hydrostatic pressure of bowman’s capsule
Decreased onc pressure of Bowman’s capsule

A

Low Kf, high glomerular onc pressure, low glom hydrostatic pressure, increased hydrostatic pressure of bowman’s capsule, decreased onc pressure of Bowman’s capsule

181
Q

Effect of hormones on GFR:
-Epi/NE and endothelin
-NO
-Prostaglandin
-Bradykinin

A

-Increased Epinephrine/NE and endothelin secretion = decrease GFR
-Decreased Ang II (constricts efferent arterial, normally as a BP protective measure) = decreased GFR
-Decreased NO (dilates afferent art.) = decreased GFR
-Decreased prostaglandins and bradykinin (increase renal blood flow) =decreased GFR

182
Q

Parasympathetic innervation to the urethra

A
  • Pelvic nv
183
Q

Renal hemorrhage

A

normal serum, + occult blood, red supernatant

184
Q

What does oxaloacetate depletion lead to in terms of diabetes

A

= ketone formation

185
Q
  1. Pressure natriuresis with increased aldosterone to prevent increased sodium
A
186
Q

Fractional excretion (urinary) of Na <1%

A

🡪 relative volume decrease (SIADH, low aldosterone, Lasix admin)

187
Q

Fractional excretion of K - what’s normal, what’s the use

A

Less than 4% in non-renal causes
Can help distinguish between renal and non renal causes of HYPOkalemia

188
Q

What is affected with amino glycoside toxicicty

A

aminoglycoside toxicity - proximal convoluted tubule

189
Q

Syndrome of inappropriate ADH- effect on GFR

A

Normal GFR

190
Q

Diagnosis: High sodium, low serum osmolality

A

: central diabetes insipidus

191
Q

What GN is least likely to be responsive to immune suppressive therapy?

A

Amyloidisis

192
Q

DDAVP in psychogenic PD dog - what would you expect to see in BW?

A

—low sodium

193
Q

Calcitriol in CKD

A

Vitamin D analog – with PTH and calcitonin will regulate Ca homeostasis

194
Q

What would concentrated urine or a high pH do to the dipstick protein measurement

A

False positive

195
Q

What would dilute urine, low pH, or hence jones proteins do to the dipstick

A

Fasle negative

196
Q

Phenylpropanolamine MOA

A

Alpha agonist - inducing norephinephrine release (indirect sympathomimetic, affects alpha more than beta receptors)

197
Q

What nephropathy do dogs with GI or liver disease get?

A

IgA nephropathy –> mesengial proliferative GN

198
Q

Factors that influence renal K excretion

A

Na intake
K intake
Mineralcorticoids
Hydrogen ions
Diuretics

199
Q

What’s the high K+ phenotype? Inheritance? Breed

A

Active NaK ATPase maintains intracellular K
Autosomal recessive trans
Shibas, akita, kinda
May also accumulate glutathione – increases susceptibility to oxidative injury

200
Q

How can low K affect the kidneys

A

Hypokalemic nephropathy
Renal vasoconstriction of afferent arteriole –> decreased renal blood flow and GFR
impaired responsiveness to ADH –> PU/PD

201
Q

What will albuterol toxicity do to the K?

A

Hypokalemia

202
Q

What breed of cats is predisposed to HYPOkalemia periodic paralysis

A

Burmese

recurrent episodes of limb weakness, cervical ventroflexion
increased CK

203
Q

What changes to bloodwork would vomiting lead to?

A

Hypochloremic metabolic ALKALOSIS – tx with 0.9% NaCl and KCL

204
Q

What causes hyperaldosteronism in a cat?

A

50/50 - adenomas or adenocarionmas

205
Q

What’s the anion gap formula? Whars normal

A

AG = (Na+ + K+) - (CL- + HCO3-)

Norma;: 18-24
Strong ion gap increases with unmeasured strong anions

206
Q

Strong anion gap formula

A

Dog = (alb) x 4.9 - AG
Cat = (alb) x 7.4 - AG

Normal: -5 to +5 mEq/L

207
Q

DDX for High AG metabolic acidosis

A

Ketoacidosis
Lactic acidosis
Uremic acidosis
Intoxication (EG, salicylates, metaldehyde)

208
Q

Ddx for normal AG metabolic acidosis

A

Addisons
Diarrhea
Renal tubular acidosis
Post-hypocapnia
Iatrogenic (CAIs, ammonium, chloride, TPN)

209
Q

Describe the classic metabolic acidosis pattern

A

Low pH
Low bicarb
Low CO2 (compensation)

210
Q

Describe the classic respiratory acidosis pattern

A

Low pH
High bicarb (compensation)
High CO2

211
Q

Describe the classic metabolic alkalosis pattern

A

High pH
High CO2 (compensation)
High bicarb

212
Q

Describe the classic respiratory alkalosis pattern

A

High pH
Low CO2
Low bicarb (compensation)

213
Q

DDX for respiratory acidosis

A

Large airway obstruction
Small airway disease
Pulmonary parenchymal disease
Restrictive pleural space disease
Neuromuscular dz causing resp muscle failure
Increased CO2 production w hypoventilation
Iatrogenic (mechanical underventilation)
Marked obesity

214
Q

DDX metabolic alkalosis

A

Hypochloremic alkalosis: loop/thiazide diuretics, vomiting, iatrogenic (sodium bicarb)
Concurrent alkalosis: pure water loss, hypotonic fluid loss
Chloride resistant alkalosis: HAC, hyperaldosteronism
Hypoalbuminemic alkalosis: PLE, PLN, liver failure

215
Q

DDX respiratory alkalosis

A

Hypoxemia - stimulation of peripheral chemoreceptors
Non-hypoxemic activation of pulmonary stretch/nocireceptors: pulmonary embolism, fibrosis, edema
Fear, pain, anxietty
Spesis
fever
activation of central resp center – hyperventilation

ACVIM General - Imp stuff (11 decks)

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