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Certifying Examination > Renal > Flashcards

Renal Flashcards

1
Q

Which is the urinary output and water intake to be considered as PU/PD?

A
  • PU:
    —- >50ml/kg urine
  • PD:
    —- >50ml/kg cats
    —- >100ml/kg dogs
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2
Q

Which are the causes of increase/decrease BUN/crea?

A

UREA:

  • Increased:
    —- AZOTEMIA (together with increase crea)
    —- NON RENAL:
    ——– GI bleeding
    ——– Portein catabolism (fever, tetracyclines)
    ——– High dietary protein
  • Reduced:
    —- Overhydration
    —- PU/PD: Addison, DI
    —- SIADH
    —- Low protein diet
    —- Hepatic dysfunction:
    ——– PSS
    ——– Cyrrhosis
    ——– Urea cycle abnormality

CREATININE:

  • Increased:
    —- AZOTEMIA (together with increased urea)
    —- NON RENAL:
    ——– High mm
  • Decreased:
    —- Low mm
    —- Overhydration
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3
Q

Which is the normal GFR in dogs and cats?

A
  • Dogs: 3.5-4.5 ml/kg/min
  • Cats: 2.5-3.5 ml/kg/min
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4
Q

Which are the different ways to evaluate directly GFR?

A
  • Urinary clearance: inulin (gold standard)
    —- Not practical into clinical point of view because continuous urinary samples are needed and inulin is not easily available
  • Plama clearance: inulin, exogenous creatinine, iohexol, radiolabeled markers
    —- Not practical because continuous blood samples are needed
    —- Development of punctual evaluations: iohexol evaluation at 2, 3 and 4h after iohexol IV administration
    ——– EAs: anaphylaxis, AKI, arrythmias, hypotension
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5
Q

Which variables can affect creatinine and SDMA?

A

Creatinine:
- Mm mass: + mm, + crea
- Diet: high meat diet, + crea
- Breed: Greyhound and Birman, + crea
- Age:
—- Dogs: lower crea at birth and increase during the first year to mantain stable
—- Cats: higher at birth and similar to adult values at 8w
- Non renal diseases: hyperthyroidism (hyperthyroidisim, - crea)
- No sex effect

SDMA:
- No mm effect
- No diet effect
- No sex effect
- Breed: Greyhound and Birman, + SDMA
- Age: Higher at birth
- Hemolysis: hemolysis, - SDMA
- Day to day variability: not considered a significant change until 6mcg/dl
- Non renal diseases:
—- Neoplasia: + SDMA
—- DM: - SDMA
—- Hyperthyroidism: SDMA is not a good biomarker

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6
Q

Which are the references for consider AKI?

A

Progressive increase >0.3mg/dl or >25% crea from basal value in <48h

Definition: damage to the kidney that produces a rapid decline on the renal function (waste and toxins accumulation, impairement of hydric/electrolytic/acid-base balance…)

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7
Q

Which is the cellular mechanism of AKI?

A
  • Tubular dysfunction:
    —- Ischemia –> reduced ATP –> unfunctional Na/K pump –> intracellular Na retention –> cell swelling –> cell death
    —- Increased intracellular Ca –> Ca enters mithocondria –> mithocondria swelling –> uncoupling oxidative dephosphorilation –> cell death
    —- Cytoeskelet injury
  • Increased endothelin and reduced NO

–> Reduced GFR

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8
Q

How can Na excretion fraction distinguish among causes of AKI?

A
  • Low (<1%) Na FE: prerenal
  • High Na FE: intrinsic
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9
Q

Which are the action mechanism of mannitol?

A
  • Osmotic agent –> increase extracellular volume
    —- Block RAAS –> no Na reabsorption
    —- Production natriuretic peptide
    —- Increase RBF –> increase GFR –> increase tubular flow –> relieve intratubular obstruction
  • Scavenger free oxygen radicals
  • Increase renal prostaglandines –> vasodilation
  • Reduce intramithocondrial calcium
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10
Q

Which are the indications for a renal replacement therapy?

A
  • Inadequate urine production
  • Overhydration
  • Resistance to diuretics
  • Hyperkalemia
  • Worsening azotemia
  • Overdose/intoxication with a drug that can be eliminated by dyalisis
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11
Q

Which drugs can be used when there is an AKI secondary to aminoglycosides?

A

Ticarcillin and carbenicillin: complex AG and avoid renal uptake

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12
Q

How can diuresis be stimulated?

A
  • Mannitol
  • Loop of Henle diuretics
  • Fenodopam/Dopamine
  • Calcium channel blockers
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13
Q

Which is the prevalence of hypertension in AKI?

A

80%

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14
Q

Which is the prognosis of AKI?

A
  • 50% mortality
  • 50% survival
    —- 50% normal serum creatinine
    —- 50% creatinine persistence

Survival with hemodyalisis (used in those cases that not respond to medial tt): 60%

Parameters that affect survival:
- Etiology: survival obstruction (90%) > infection (80%) > ischemic (65%) > toxic (40%)
- No response to diuretics and no urine production: worse prognosis
- Hypocalcemia, anemia, hyperphosphatemia, lack of improvement of creatinine with medical tt, comorbid diseases (pancreatitis, SIRS) (dog)
- Hyperkalemia, low body temperature, hypoalbuminemia and decreased serum bicarbonate (cats)
- Presentation creatinine value not marker of prognosis (but there are other studies where AKI grade is associated with prognosis)

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15
Q

Which is the most common cause of AKI in dogs?

A

Inflammatory/ischemic (60%)

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16
Q

Which is the most common cause of AoCKD in dogs and cats?

A
  • Cats: uretheral obstruction > ischemic > pyelonephritis
  • Dogs: inflammatory > pyelonephritis > ischemic
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17
Q

Which percentage of dogs normalize creatinine value after an AKI?

A

75% (55% in the discharge moment and 20% later)

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18
Q

Which is the effect of acidosis of CKD in protein metabolism?

A

Acidosis promotes protein catabolism –> promotes protein malnutrition + increase BUN

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19
Q

Which is the relationship between azotemia, uremia and kidney disease?

A

Kidney disease can be present without azotemia or uremia
Azotemia can occur in the absence of kidney disease (prerenal or postrenal azotemia) or uremia
Uremia doesn’t occur in the absence of azotemia but it can occur in the absence of kidney disease

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20
Q

Which are the most common signs detected in each CKD IRIS stage?

A
  • IRIS I: non clinical signs a part of PU/PD
  • IRIS II: PUPD. Few cases can present with weight loss and hyporexia
  • IRIS III: PUPD + signs of loss of kidney function but use to no present with signs of overt uremia
  • IRIS IV: PUPD + signs of overt uremia and ureic crisis
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21
Q

Which are the renal diet characteristics?

A
  • Low P
  • Omega 3 fatty acids and antioxidants supplementation
  • Protein restriction: questioned
  • Low Na
  • Added vitamin B
  • Increased caloric density
  • Added soluble fiber
  • Neutral effect on acid-base
  • K supplementation (cats)
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22
Q

Which are the most used phosphorus chelants?

A
  • Aluminium salts: can produce Al toxicosis, neuropathies and mycrocitosis
  • Calcium based: can produce hypercalcemia
  • Lathanum based
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23
Q

Which are the most common additives to treat acidosis?

A
  • K citrate
  • Na bicarbonate
  • Diet
24
Q

Which are the mian reasons of hyperkalemia in CKD?

A
  • Inadequate intake
  • Urinary losses
  • Activation RAAS
25
Q

Which potential erythropoietin stimulating agents can be used?

A
  • Epoietin alfa
  • Epoietin beta
  • Darbopoietin
  • EPO receptor activator
26
Q

Which is the homology between human and pets EPO?

A

80%

27
Q

Which is the objective Hto reached with EPO treatment?

A
  • Dogs: 35-45%
  • Cats: 25-35%
28
Q

Which is the renoprotective effect of ACEi, ARB and MRA?

A
  • ACEi: block ACE (ACE increases ATII production as well as degrade bradikinin) –> ACEi reduce ATII and increase bradikinin –> vasodilation
  • ARB: block AT receptors 1 –> metabolites unite to AT receptors 2, with vasodilatory properties
  • MRA: block aldosterone –> inhibit their vasoconstriction and profibrotic activities
29
Q

Which are the main determinants of passage into filtrate?

A
  • Molecular weight: big moecules cannot pass
  • Ionic charge: negative molecules cannot pass
30
Q

Which types of glomerular diseases can be distinguished?

A
  • Immunecomplexes glomerulonephritis
    —- Membranoproliferative
    —- Membranous
    —- Proliferative
    —- Lupus nephritis
    —- IgA
  • Glomerulosclerosis
  • Minimal change glomerulopathy
  • Hereditary neprhitis
  • Atrophy glomerulopathy
  • Podocytopathy
31
Q

Which dog breeds are predisposed to renal amyloidosis?

A

Shar Pei, Beagle, English Foxhound

32
Q

Which is the colchicine action mechanism?

A

It impair the release of SAA from hepatocytes and prevent the production of amyloid-enhancing factor.

Ideally colchicine must be administered in the predeposition phase. However, colchicine may lead to remission of proteinuria even after the appearance of amyloid deposits. No evidence support the effectiveness of colchicine once amyloidosis has resulted in persistent azotemia or hypoalbuminemia.

33
Q

Which breeds are predisposed to hereditary nephritis?

A
  • Cocker Spaniel/Springer Spaniel: autosomal recessive; bad prognosis (2y survival aprox)
  • Bull Terrier/Dalmata: autosomal dominant (good prognosis, 10y survival aprox)
  • Samoyed: X-linked dominant (poor prognosis, 2y survival aprox)
34
Q

Which is the progression of a glomerular disease?

A
  1. Glomerular damage due to immunecomplexes/protein deposits –> complement/coagulation cascade/inflammatory cells activation –> progression of the damage
  2. Proteinuria produce a tubular damage –> tubular cells death –> obstruction of the tubules due to protein casts –> progressive nephrons loss

–> a glomerular damage ends with a tubulointerstitial damage and reduced GFR

35
Q

Which is the prevalence of secondary glomerular diseases?

A

60%

36
Q

Which is the target of proteinuria treatment?

A

UPC <0.5 or >50% reduction of baseline

37
Q

Which are the immunosupressive of choice for glomerular diseases?

A

Mycophenolate or cyclophosphamide together with SHORT courses of steroids.

CsA was found to have no benefitl.

38
Q

In which situations without renal biopsy can be immunosupressive treatment considered?

A
  • No suspicion of amyloidosis
  • No suspicion of familial disease (except Bernese M or Soft Coated WT)
  • No contraindicated
  • Source of protein glomerular
  • Creatinine >3 or progressively increasing
  • Albumin <2

Monitoring:
- Complete response:
—- UPC <0.5
—- Crea < 1.4
—- Albumin >2.5
- Partial response:
—- UPC reduction >50%
—- Crea reduction >25%
—- Albumin increase >50% or 2-2.5

39
Q

In which tubule portion is absorbed/secreted every molecule?

A
  • Glucose and aa: completely reabsorbed in proximal tubule
  • Na/Cl/K/Mg/Ca/P: are reabsorbed in all portion, but specially in proximal tubule, except Mg that is mostly reabsorbed in thick loop of Henle
  • Urea: collecting duct
  • H+/bicarbonate: H+ is secreted in every portion and absorbed in distal/collecting ducts, whereas bicarbonate is absorbed in every portion and secreted in distal/collecting
40
Q

Which breeds are predisposed to cystinuria?

A
  • Slc3a1 mutation:
    —- Newfoundland, Labrador Retriever (autosomal recessive; develop cystine uroliths at very young age, 5m aprox)
    —- Australian Cattle Dog (autosomal dominant, develop disease at 5y aprox)
  • Slc7a9 mutation:
    —- Miniature Pinscher (autosomal dominant, develop disease at 5y aprox)

Other breeds: Bulldog, Jack Russel, Chiuahua, Staffordshire, Daschund, Welsh Corgi, Rotweiler

41
Q

Which are the reasons of hyperuricosuria in Dalmatians?

A

Slc2a9 mutation

  • Altered transport of uric acid to the hepatocytes to be converted to allantoin
  • No reabsorption of uric acid in proximal tubule
  • Increase tubular secretion of uric acid

But levels of uricase are normal

42
Q

Which breeds are predisposed to renal glycosuria?

A

Basenji, Scottish Terrier, Norwegian Elkhound

43
Q

Which are predisposing factors of pyelonephritis?

A
  • Bacterial factors:
    —- Ab resistance
    —- Adherence capacity
    —- Biofilm formation capacity
  • Renal impairment:
    —- Preexisting UTI
    —- Vesiculoureteral reflex
    —- Ureteral osbtruction
    —- Ectopic ureters
    —- Pyelectasia
    —- Renal glucosuria
    —- Renal scarring
  • Immunesupression
    —- Congenital
    —- Acquired: FIV, DM, Cushing…
44
Q

Which is the reccommended treatment for a pyelonephritis?

A
  • Antibiotic (beta lactamics +/- quinolones)
  • 4-6w of treatment was first reccommended, but last consensus stated 2w of tt is enough
  • Favorable response should be detected in <72h of tt
45
Q

Which breeds are predisposed to renal agenesia? And renal dysplasia?

A
  • Agenesia: Beagle, Shetland, Doberman Pinscher
  • Dysplasia: Lhasa Apso, ShiTzu, among others
46
Q

Which dogs and cat breeds can be predisposed to PKD?

A
  • Dog: PKD1 mutation
    —- Bull Terrier: autosomal dominant; cysts only on kidneys, develop signs in the first years of life
    —- Cairn Terrier and WHWT: autosomal recessive; cysts on kidney and liver, develop signs in the first months of life
  • Cat: PKD1 mutation
    —- Persian: autosomal dominant
47
Q

Which miscellanoeus renal familial diseases can be distinguished?

A
  • Cystadenocarcinoma:
    —- GSH: mutation in BHD gene, autosomal dominant
    —- Cystadenocarcinoma + dermatofiboris nodular + leiomiosarcoma
  • Telangiectasia:
    —- Pembroke Welsh Corgi
    —- Hematuria
  • Reflux neprhopathy with focal hypoplasia:
    —- Boxer
    —- Pyelonephritis due to vesico-ureteral reflux cauisng renal hypoplasia
48
Q

Which is the composition of ECF and ICF?

A
  • ECF: Na, Cl, Ca, glucose, bicarbonate
  • ICF: K, Mg, PO4-, proteins
49
Q

Which are the criteria to diagnose SIADH?
Which are the main causes?

A

Criteria to diagnose:
- Hypotonic normovolemic hypoNa
- High urinary Na –> osmolarity urine > plasma
- Absence of edema or diseases causing low effective circulating volume
- Adrenal and renal function normal

Causes:
- Hypothalamic neoplasia
- Cyst
- Congenital hydrocephalus
- Acanthamoeba meningitis
- Liver disease
- Dirofilaria
- Vinblastine overdose

50
Q

Which are the functions of magnesium?

A
  • Stabilizing phosphorilation reactions
  • Enabling glucose utilization and synthesis
  • Supporting ion transport
  • Enhanching macromolecules synthesis
51
Q

How is absorbed/secreted Mg and K and where are they mostly found?

A

Potassium:
- LIC (95%) > LEC (5%)
- Absorbed by GI and secreted by kidneys (90-95%) and GI (colon, 5-10%)

Magnesium:
- LIC (99%) > LEC (1%)
- Found in bone (70%) > mm (20%) > soft tissue (10%)
- Absorbed by GI (colon) and bone resorption, and secreted by kidneys (thick loop of Henle mainly) and GI

52
Q

Which are the causes of hyperchloremic acidosis?

A
  • Renal tubular acidosis (loss of bicarbonate)
  • Diarrhea (loss of bicarbonate)
  • NaCl administration
53
Q

Which is the normal pH of urine?

A

5.5-7.5

54
Q

Which are the causes of aciduria and alkaluria?

A

Aciduria:
- Acidosis
- Paradoxical aciduria (in cases of gastric obstruction with alkalosis)
- Meat rich diet
- Protein catabolism
- Acidifiers

Alkaluria:
- Alkalosis
- Distal renal tubular acidosis
- UTI
- Vegetable rich diet
- Post prandial
- Aged sample
- Alkaliniziers

55
Q

What indicates a granular cast?

A

A renal tubular injury/necrosis due to inflammation/ischemia/toxins

56
Q
A

Certifying Examination (10 decks)

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