Intro to Kidney Diseases Flashcards

1
Q

define GFR

A

the amount of fluid filtered from the glomerulus into Bowman’s space per unit of time; a key determinant of kidney function

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2
Q

define azotemia

A

laboratory abnormality defined as an increase in nitrogenous products due to decreased renal excretion

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3
Q

define prerenal azotemia

A
  1. GFR is decreased due to decreased blood flow to the kidneys (hypovolemia due to dehydration or hemorrhage, circulatory shock, heart failure, etc.)
  2. if dehydration/volume depletion is the cause, functioning kidneys should be preserving water
    -so azotemia occurs frequently with well-concentrated urine
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4
Q

describe renal azotemia

A
  1. GFR is decreased due to decreased function or number of nephrons (intrinsic kidney disease, either acute or chronic)
  2. the kidneys, typically, also fail to concentrate the urine
    -azotemia occurs concurrently with minimally concentrated urine
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5
Q

describe postrenal azotemia

A
  1. GFR is decreased due to urinary tract blockage or urinary rupture has occurred, and urine is in the peritoneum
    -increased hydrostatic pressure in Bowman’s space decreases GFR
  2. urine concentration can vary
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6
Q

define chronic kidney disease

A
  1. abnormality of kidney structure or function that has been present for at least or longer then 3 months, with implications for health
  2. general/umbrella term for heterogeneous disorders of varying causes, histopath, severity, and rate of progression
  3. all disorders cause a PERMANENT reduction of the number of functioning nephrons which results in a decreased GFR (may detect this before creatinine rises)
  4. irreversible and slowly progressive
  5. predisposes to AKI
  6. most common form of kidney disease, more common in cats and senior animals (so hella common in OLD CATS)
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7
Q

define acute kidney disease

A
  1. an abrupt (within hours) decrease in kidney function, which encompasses both injury (structural damage) and impairment (loss of function)
  2. SUDDEN change in kidney structure, function, or both causes a decreased GFR that may be detected before creatinine rises
  3. potentially reversible, but not always and mortality rate is high
  4. predisposes to CKD
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8
Q

describe history and physical exam components that are supportive of AKI or CKD

A

AKI
1. recent change in urination
2. no change in weight/BCS
3. acute onset GI signs
4. recent reduction in appetite
5. healthy hair coat
6. normal to enlarged kidney

CKD:
1. PU/PD for >3 months
2. weight loss for >3 months
3. chronic/intermittent GI signs
4. reduced appetite for >3 months
5. poor hair coat
6. small, irregular kidneys
7. +/- chronic uremic breath, osteodystrophy, signs related to proteinuria/hypertension

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9
Q

describe labwork and imaging components of AKI and CKD

A

AKI

labwork:
1. more severe clinical signs for the same level of azotemia (no time to adjust)
2. hematocrit normal or increased

imaging:
1. normal or enlarged kidneys
2. changes in architecture vary with cause (neoplasia, obstruction, infection, etc.)

CKD

labwork:
1. clinical signs mild despite marked azotemia
2. non-regenerative (hypoproliferative anemia)

imaging:
1. small, irregular kidneys
2. degenerative changes (irregular margins, poor corticomedullary differentiation)

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10
Q

describe histopathology and response to treatment of AKI versus CKD

A

AKI:

histopathology: depends on etiology, but fibrosis is ABSENT

response to treatment: markers of GFR can improve over time (if animal survives) and even normalize in some cases

CKD:

histopathology: depends on etiology, but FIBROSIS indicative of CKD

response to treatment: after correcting for extrarenal/acute factors, markers of GFR (creatinine) tend to be stable or worsen over time

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11
Q

compare and contrast the short term and long term prognosis for AKI versus CKD

A

AKI:

short term survival: 50/50 (varies widely with etiology)

long term survival/QOL: depending on the degree of recovery/nephron loss, survivors may do very well! or may be left with advanced CKD

CKD:

short term survival: excellent if not in end-stage kidney disease

long term survival/QOL: varies according to etiology, CKD stage, and other factors, but likely life limiting (except some stage 2 cats live forever)

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12
Q

what are causes of CKD?

A
  1. AKI of any cause (months later)
  2. nepro- and ureterolithiases
  3. neoplasia (LYMPHOMA)
  4. immune complex glomerulonephritis
  5. glomerulosclerosis
  6. anyloidosis
  7. renal dysplasia
  8. polycystic kidney disease
  9. other congenital/hereditary familial disease
  10. pyelonephritis
  11. leptospirosis
  12. chronic infection wth FIV, FLV, or FIP
  13. idiopathic or literally so many other things
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13
Q

describe CKD lesions in dogs versus cats

A

dogs: most commonly primary lesions within the glomerulus

cats: most commonly primary lesions within the tubulointerstitial compartment

but primary lesions in any segment of the nephrons may occur in any species!

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14
Q

describe the biological behavior of CKD

A
  1. primary renal disease: may or may not be active at time of diagnosis
  2. functional maladaptations: lead to self-perpetuating worsening of disease
    -reduced number of nephrons so each nephron now doing more work; how to increase GFR?
    -glomerular hypertrophy and hyperfunction/hyperfiltration/hypertension but these adaptations cause ongoing damage to remaining nephrons (tubular ischemia)
  3. superimposition of uremia: accumulation of substances normally excreted by the kidneys

GFR is decreases through each stage

in some cases there is linear progression through these stages (dogs more commonly) and in other cases there are periods of relative stability and episodes of precipitous decline (cats more commonly)

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15
Q

describe the functional maladaptations of CKD

A

the remaining nephrons undergo glomerular hypertrophy and hyperfunction/hyperfiltration/hypertension and subsequent tubular ischemia

they do this via
1. efferent arteriole constriction
2. increased single nephron GFR
3. tubular hypermetabolism
4. peritubular capillaries not providing enough O2 bc flow is limited so results in hypoxic/oxidative injury to nephrons

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16
Q

describe the pathophysiologic changes of CKD progression

A
  1. glomerular
17
Q

describe the stages of CKD

A
  1. primary renal disease
  2. functioanl maladaptations
  3. somewhere in between
  4. superimposition of uremia

early in the disease course you can have a really big drop in GFR but just a small increase in creatinine

in later stages, can have a really small drop in GFR but a dramatic increase in creatinine

renal azotemia is an indicator of a later stage!

18
Q

describe CKD diagnosis

A
  1. renal azotemia (azotemia + minimally concentrated urine)
    -a SMALL subset of cats maintain urinary concentrating ability in CKD
  2. inability to concentrate urine
    -USG < 1.030 (dog) or 1.035 (cat)
  3. palpable renal abnormalities
    -small and shriveled
  4. radiographic or ultrasound renal changes
  5. urinalysis abnormalities
    -persistent renal proteinuria +/- hyaline casts +/- nephrotic syndrome
    -chronic granular casts
    -chronic urinary tract infection localizable to kidney (pyelonephritis)
  6. serum creatinine or SDMA trending upward over years
  7. GFR measurement

in absence of extrarenal factors, each of 2-7 might help you diagnose CKD

19
Q

describe the relationship between acute and chronic kidney disease

A

it is common for CKD to co-exist with prerenal or postrenal azotemia, or with active kidney diseases (acute on chronic kidney disease)

unlike CKD, these pre or postrenal or acute kidney disease can be reversible, so you need to diagnose, identify, and correct these before staging the CKD

20
Q

describe the IRIS CKD staging scheme

A

stage 1: no azotemia, normal creatinine

stage 2: mild azotemia, normal or mildly elevated creatinine

stage 3: moderate azotemia

stage 4: severe azotemia

ideally based on 2 measurements, weeks apart, when the animal is fasted and well-hydrated

do NOT stage any animal NOT in the stable plane (dehydrated, recovering from AKI, acute on chronic, etc.)

21
Q

describe IRIS CKD sub-staging

A
  1. proteinuria: need UPC
    -is renal proteinuria present? if so, how much protein in urine/
  2. systemic arterial hyertension:
    -is the systemic blood pressure consistently elevated? if so, by how much?
22
Q

describe the full process of CKD staging

A
  1. diagnosis of CKD
  2. correct pre-renal and postrenal abnormalities
  3. stage based on fasted blood creatinine +/- SDMA concentration
  4. substage based on proteinuria (UPC)
  5. substage based on blood pressure menasurement
23
Q

describe CKD treatment goals

A
  1. identify and treat primary disease (primary therapy): most of the time this ship has sailed by diagnosis
  2. identify and correct factors for progression: renoprotective therapy
  3. correct metabolic derangements: decrease clinical signs and improve quality of life (supportive/systematic therapy)
24
Q

describe prognostic factors for CKD

A

degree of azotemia does not tell full story!

  1. pre and postrenal factors
  2. nature of primary disease
  3. AKI on CKD?
  4. severity of intrinsic renal and functional impairment
  5. rate of progression of kidney dysfunction