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Urology > LA acute & chronic kidney dz (Reuss) > Flashcards

LA acute & chronic kidney dz (Reuss) Flashcards

1
Q

Pre-Renal Azotemia

A
  • Inadequate renal perfusion
    • hypovolemia
    • dehydration
      • GI fluid loss
    • hypotension
      • acute blood loss
    • dec CO
  • USG > 1.025
  • FCNa < 1%
  • >/= 50% reduction in azotemia w/in 24 hours of fluid therapy

*may be a back door determination

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2
Q

After starting IV fluids a patient should urinate in

A

8-12 hours

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3
Q

Renal azotemia

A
  • Acute kidney injury: abrupt decrease in GFR
    • Most common cause: Acute tubular necrosis (ATN)
      • vasomotor nephropathy (ischemia)
      • aminoglycoside toxicity
      • NSAIDS
      • Pigment nephropathy
      • lepto
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4
Q

Ischemia

‘vasomotor nephropathy’

A
  • Continuum of pre-renal azotemia
  • prolonged marked hypotension
    • endotoxemia (toxic line on MM)
  • Blood loss
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5
Q

Aminoglycoside toxicity

A
  • Bind to brush border of proximal tubule
    • pinocytosis
    • accumulate in renal cortex
    • inhibit phospholipase activity
    • impair organelle function
    • proximal tubular epithelial cell damange
  • Renal vasoconstriction
  • Toxicity Neomycin > Kanamycin > gentamicin > amikacin > streptomycin
  • Precipitated by concurrent dehydration
  • Binding saturable: once daily dosing preferred
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6
Q

Other nephrotoxic antimicrobials

A
  • Oxytetracycline
    • given to foals with tendon contracture
  • Polymyxin B
    • endotoxemia
  • Amphotericin B
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7
Q

NSAIDS

A
  • Medularry crest necrosis
    • medulla receives 10-20% Renal blood flow
  • COX inhibitors
    • dec prostaglandin formation
  • PGE2 and PGI2
    • renal vasodilators, especially when decreased RBF
  • Enhanced by dehydration
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8
Q

Pigment nephropathy

A
  • Myoglobinuria
    • rhabdomyolysis
    • crush injury
    • heat stroke
    • inc CK, AST
    • serum clear
  • Hemoglobinuria
    • intravascular hemolysis
    • serum pink
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9
Q

Pigment actions causing tubular necrosis

A
  • Pigment
    • vasoconstriction
    • ischemia
  • Tubular obstsruction by protein casts
  • Hydroxyl radicals
  • Cortex most susceptible d/t inc blood flow
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10
Q

Leptospira interrogans

Hosts

Exposure

Syndromes

A
  • Zoonotic
  • cause acute kidney injury
  • horses
    • incidental host (except bratislava)
    • maintenance hosts: rat, cow, skunk, opossum
  • Exposure
    • urine
    • aborted fetus
  • Clinical syndromes
    • AKI, tubulointerstitial nephritis
    • Uveitis
    • Abortion, stillbirths, neonatal death
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11
Q

Lepto

Diagnostics

TX

A
  • Diagnostics (organism or antibody)
    • Serum microscopic agglutination test (MAT) for antibody
      • rise in titer
    • Urine PCR
      • organism in urine
      • sheds more after furosemide
    • Dark field microscopy
    • Culture
      • takes months: clinically useless
    • Immunofluorescence on tissue sample
  • Treatment
    • doxycycline, ampicillin, penicillin, amoxicillin, ceftiofur

*Don’t use oxytetracycline ***nephrotoxic

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12
Q

Acute Glomerulonephritis

A
  • Rare in horses
    • usually sequela to other diseases
  • Marked proteinuria, red cell casts
  • Inciting antigens
    • Streptococcus
    • EIA
  • Immune complex deposition
    • complement activation
    • tissue damage
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13
Q

Post-Renal azotemia

A
  • Rare in adult horses
  • more common in neonatal colts
  • Dysuria, colic
  • Signs
    • neonatal uroabdomen
      • don’t rule out even if peeing thru normal hole
    • obstructive urolithiasis
    • bladder necrosis
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14
Q

Clinical Eval of AKI

A
  • Clinical signs non-specific
  • Rule out pre-renal and post-renal azotemia
  • Frequently oliguric
    • no urine within 6-12 hours of initiation of fluid therapy
  • Rectal palpation
    • kidney enlarged, painful
  • Ultrasound
    • perirenal edema
    • hypoechogenicity
    • loss of corticomedullary distinction
    • dilation of renal pelvis
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15
Q

Clin path AKI

A
  • Chem
    • inc BUN and Cr ( < 10:1 ratio)
    • dec Na, Cl, Ca
    • inc K, P
  • Urinalysis
    • hematuria, proteinuria, casts, glucosuria
    • inc UGGT
    • in FCNa, P
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16
Q

Treatment of AKI

A
  • d/c nephrotoxic drugs
  • treat concurrent dz
  • correct volume def and establish diuresis
    • balanced electrolyte solution
    • deficit = % dehydration x BW
    • maintenance = 40-60 ml/kg/day
  • monitor closely for urination or development of edema
17
Q

TX of hyperkalemia in AKI

A
  • 0.9% NaCl fluids
  • 5% dextrose
  • Calcium gluconate
  • Sodium bicarbonate
  • Insulin
18
Q

Other treatments AKI

establishing diuresis

A
  • Furosemide
    • loop diuretic: blocks Na/K/2Cl co-transporter
    • depends on GFR
  • Mannitol - NOT REALLY USED
  • Dopamine - NOT REALLY USED
  • Peritoneal dialysis
  • Hemodialysis: brutus the tiny cow
19
Q

Prognosis for AKI

A
  • Varies with underlying cause
  • if oliguria persists > 72 hours, prognosis guarded
  • secondary complications: laminitis
  • polyuria
    • transient
    • permanent
20
Q

Chronic kidney disease

A
  • irreversible
  • variable rate of decline
  • ‘end stage kidney dz’
21
Q

Causes CKD

A
  • Acquired
    • glomerular dz
      • glomerulonephritis
      • amyloidosis => more common in cattle
    • tubulointerstitial dz
      • chronic interstitial nephritis
        • incomplete recovery from ATN
        • pyelonephritis
        • obstructive dz
  • Congenital (dx with rectal, ultrasound, bx)
    • suspect if < 5 yo with CKD
      • renal agenesis
      • hypoplasia
      • dysplasia
      • PKD
22
Q

Clinical signs of CKD

A
  • Uremia: clinical manifestation of azotemia
  • Chronic weight loss
    • uremic toxins: appetite supp, oral and GI ulcers
    • Gastrin half-life prolonged
    • inc catabolic state
  • Rough hair coat
  • Poor athletic performance
    • anemia: dec EPO; dec RBC survival time
  • PU/PD
    • degree not correlated
    • collecting tubule can’t compensate for excess glom filtrate
  • Ventral edema
  • Uremic halitosis
  • urea exretion in sweat
  • dental tartar, gingivitis, oral ulcers
23
Q

Uremia

A
  • Uremia: clinical manifestation of azotemia
    • effects of uremic toxins on cell metabolism and function
      • BUN, other nitrogenous compounds
      • Cr and other guanidino compounds
      • products of intestinal bacterial metabolism
      • middle molecules
      • abnormal metabolism of hormones and trace minerals

*correlation btwn magnitude of azotemia and degree of uremic syndrome is poor

24
Q

Ventral edema

A
  • dec oncotic pressure
    • PLE
    • glomerular protein loss
  • inc vascular permeability
    • uremic toxins
  • inc hydrostatic pressure
    • renin release
25
Q

four mechanisms of edema

A
  1. dec oncotic pressure
  2. inc vascular permeability
  3. inc hydrostatic pressure
  4. dec lymphatic return
26
Q

Clinical evaluation of CKD

A
  • Azotemia
    • BUN: Cr > 10:1
      • > 15:1 = excessive protein intake
      • BUN actually helpful here
  • Electrolytes
    • hyperCa, hypoP
    • HypoNa, Cl
    • +/- K
    • metabolic alkalosis or neutral until terminal
      • metabolic acidosis late
  • hypoalbuminemia
  • hyperlipidemia
  • hematology
    • non-regenerative anemia
  • Urinalysis
    • isosthenuria (1.008-1.014)
      • develops before azotemia
    • enzymuria, proteinuria, glucosuria
    • pyuria, bacteruria
    • FCNa > 1 %
  • Rectal: small firm kidney
  • U/S: small, hyperechoic
  • BX: end stage kidney dz, congenital dz, immunfluor, EM
27
Q

CKD prognosis

A
  • Grave
    • 75% renal function loss if azotemic
  • doubling of Cr = 50% decline in GFR
  • Cr < 5 mg/dl => may manage for months - years
  • Cr > 10-12 mg/dl => marked compromise
  • Cr > 15 mg/dl => grave
28
Q

CKD prognosis

GFR measuring

A
  • Measure GFR
    • endogenous creatinine clearance
      • Requires timed collections
      • tubular creatinine secretion possible
    • plasma dissapearance of
      • exogenous creatinine sulfanilate
      • technicium 99 tag

*not done clinically

29
Q

acute exacerbation tx

A
  • treat like AKI
    • judicious fluid therapy
  • antimicrobials if pyelonephritis
  • discontinue nephrotoxic drugs
30
Q

CKD management

A
  • d/c alfalfa, legumes
    • use good grass instead
  • maintain normal protein intake (about 10%, not higher, deficiency can inc morbidity/mortality)
    • maintain BUN:Cr 10:1 - 15:1
  • maintain BCS
  • Only if necessary
    • NaCl
    • NaHCO3
  • omega-3 fatty acids
    • flaxseed oil
31
Q

AKI vs CKD

AKI signs

A
  1. Good BCS
  2. normal hematocrit
  3. kidney consistency normal to soft
  4. recent association with disease, drugs
  5. US: normal echogenicity or hypoechoic with loss of renal architecture
  6. BUN:Cr < 10:1
  7. HypoCa, hyperPh
32
Q

AKI vs CKD

CKD signs

A
  1. Poor BCS, weight loss
  2. Anemia
  3. Kidney size normal to decreased
  4. Kidney consistency normal to firm
  5. No recent history of other dz
  6. US: hyperechoic
  7. BUN:Cr > 10:1
  8. HyperCa, HypoPh

Urology (15 decks)

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