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Module 17 > Approach to & Management of Chronic Kidney disease in SA > Flashcards

Approach to & Management of Chronic Kidney disease in SA Flashcards

1
Q

what is chronic kidney disease

A

often smoulders for months/years before becoming clinically apparent

loss of functional renal tissue due to prolonged process (generally >2 months)

usually progressive and irreversible

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2
Q

what is chronic renal failure

A

end stage process

azotemia and reduced urine concentrating ability

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3
Q

what are degenerative causes of CKD (2)

A
  1. chronic interstitial nephritis
  2. renal infarcts
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4
Q

what are developmental causes of CKD (2)

A
  1. familial renal dysplasia
  2. polycystic kidney disease
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5
Q

what are metabolic causes of CKD (1)

A
  1. hypercalcemia
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6
Q

what are neoplastic causes of CKD (2)

A
  1. renal lymphoma
  2. renal carcinoma
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7
Q

what are iatrogenic causes of CKD (2)

A
  1. vitamin D supplementation
  2. nephrotoxic drugs
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8
Q

what are idiopathic causes of CDK (2)

A
  1. renal amyloidosis
  2. primary glomerulopathies
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9
Q

what are immune mediated causes of CKD (1)

A
  1. immune complex mediated glomerulonephritis
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10
Q

what are infectious causes of CKD (2)

A
  1. pyelonephritis
  2. borreliosis (lyme nephropathy)
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11
Q

why is it important to stage CKD

A

CKD often progresses from initial non-azotemic stage to end-stage uremia (CKD –> CRF)

progression can take years

patient management varies substantially as disease progresses

prognosis changes as stage changes

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12
Q

what is the IRIS CKD classification

A

stage 1-4

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13
Q

what is stage I CKD in dogs

A

non-azotemic

creatinine <125

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14
Q

what is stage II CKD in dogs

A

mild renal azotemia

creatinine 125-180

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15
Q

what is stage III CKD in dogs

A

moderate renal azotemia

creatinine 181-440

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16
Q

what is stage IV CKD in dogs

A

severe renal azotemia

>440

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17
Q

what is stage I CKD in cats

A

non-azotemic

<140

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18
Q

what is stage II CKD in cats

A

mild renal azotemia

creatinine 140-250

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19
Q

what is stage III CKD in cats

A

moderate renal azotemia

251-440

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20
Q

what is stage IV CKD in cats

A

severe renal azotemia

creatinine >440

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21
Q

what is the pathophysiology of CKD

A

normal animals have more nephrons than necessary

CKD leads to nephron damage (glomeruli, tubules, interstitial tissue and/or vessels)

kidneys have limited ways of responding

as nephrons are lost, remaining nephrons have to filter more blood –> glomerular hypertension & hyperfiltration

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22
Q

what does prolonged injury in the kidney lead to

A
  1. infiltration of inflammatory cells
  2. profibrotic cytokine production
  3. hypoxia –> further injury

nephrons cannot regenerate or replicate

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23
Q

what are the early pathophysiology changes in CKD

A

nephrons hypertrophy & single nephron GFR increase –> compensation

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24
Q

what are the later pathophysiology changes in CKD

A

compensation is overwhelmed –> clinical kidney disease

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25
Q

what % of nephron loss causes urine concentrating ability to become impaired

A

1/3

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26
Q

what % of nephron loss causes azotemia to develop (CRF)

A

1/4

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27
Q

what are the physiological consequences of CKD (10)

A
  1. azotemia and uremia: due to reduced GFR
  2. PUPD: due to tubular damage & fewer nephrons
  3. hyperphosphatemia
  4. increased PTH (renal secondary hyperparathyroidism)
  5. hypokalemia
  6. anemia
  7. hemorrhage
  8. hypertension
  9. proteinuria
  10. metabolic acidosis
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28
Q

why does CKD lead to hyperphosphatemia

A

phosphate excreted via filtration through glomeruli

reduced GFR –> phosphate retention

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29
Q

what are the effects of hyperphosphatemia (2)

A

unlikely to cause clinical signs BUT

  1. drives renal secondary hyperparathyroidism (increased PTH) –> disease progression
  2. leads to reduced survival
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30
Q

what are the effects of high PTH (3)

A
  1. likely uremic toxin –> depression
  2. can cause osteopenia and tooth loosening and pathological features
  3. renal cell tubular damage
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31
Q

how does decreased GFR lead to increase PTH

A
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32
Q

why does hypokalemia occur in CKD (3)

A
  1. reduced intake
  2. reduced renal potassium reabsorption
  3. renal tubular acidosis
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33
Q

what does hypokalemia (6)

A
  1. neuromuscular weakness
  2. arrhythmias
  3. metabolic acidosis
  4. anorexia and impaired protein synthesis –> weight loss
  5. hypokalemic nephropathy
  6. promotes PUPD
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34
Q

what type of anemia is present in CKD

A

non-regenerative, normocytic, normochromic anemia

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35
Q

why does CKD cause anemia (5)

A
  1. erythropoietin deficiency (synthesized in kidneys)
  2. reduced RBC lifespan
  3. nutritional abnormalities
  4. chronic GI hemorrhage
  5. iron deficiency
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36
Q

what are the effects of anemia (3)

A
  1. lethargy
  2. inappetance
  3. may cause progression of disease due to renal hypoxia
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37
Q

what is hemorrhage due to in CKD (2)

A
  1. acquired platelet dysfunction (thrombocytopenia, impaired platelet adhesiveness to subendothelium)
  2. GI hemorrhage secondary to ulceration
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38
Q

what is hypertension due to in CKD (2)

A
  1. impaired excretion of sodium
  2. activation of renin-angiotensin-aldosterone system (RAAS)
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39
Q

what are the effects of hypertension in CKD

A

damage to kidney, eye, brain, cardiovascular system

40
Q

what is proteinuria due to in CKD (2)

A
  1. increased glomerular capillary pressure
  2. fewer tubules so less able to reabsorb filtered protein
41
Q

what does proteinuria result in

A

progression of CKD and risk factor for mortality

42
Q

what is metabolic acidosis due to (3)

A
  1. reduced excretion of H+ ions by kidney
  2. retention of phophate and other organic
  3. increased loss of chloride (vomiting)
43
Q

why is CKD progressive

A
  1. ongoing presence of initial trigger
  2. damage triggers secondary processes which perpetuate/contribute to the damage
44
Q

what secondary processes perpetuate/contribute to damage in CKD (6)

A
  1. systemic hypertension
  2. glomerular hypertension
  3. mineral imbalances (phosphate, PTH, CaPO4 precipitation)
  4. proteinuria
  5. renal fibrosis
  6. renal inflammation
45
Q

what are the presenting signs and examination findings in CKD (8)

A
  1. PUPD, weight loss, depression/lethargy, dehydration
  2. hematuria
  3. abdominal distention
  4. edema/ascites
  5. acute blindness
  6. pathological fractures
  7. weight loss, poor body condition
  8. small or large kidneys
46
Q

what are the clinical examination findings of CKD (7)

A
  1. pale mucus membranes
  2. poor body condition
  3. loose teeth, deformable maxilla/mandible, fractures (rare)
  4. dehydration
  5. small kidneys
  6. hypertensive retinopathy
  7. hemorrhage (rare)
47
Q

what are the laboratory findings of CKD (2)

A
  1. azotemia (reduced GFR, increased catabolism, GI hemorrhage)
  2. inappropriately low urine specific gravity (unable to concentrate or dilute urine)
48
Q

what are the USG values in the dogs with CKD

A

1.008 to 1.020

49
Q

what are the USG values in the cats with CKD

A

1.008 to 1.030

50
Q

what other tests would you perform when investigating CKD (5)

A
  1. full biochemistry
  2. full hematology
  3. urinalysis including (sediment exam, protein:creatinine ratio, culture & sensitivity)
  4. abdominal imaging
  5. blood pressure measurement
51
Q

what might you find on biochemistry with CKD (4)

A
  1. hyperphosphatemia
  2. hypokalemia
  3. hyper/hypocalcemia
  4. metabolic acidosis
52
Q

what would you find on hematology with CKD

A

non-regenerative, normocytic, normochromic anemia

+/- neutrophilic leukocytosis (concurrent renal infection)

53
Q

what would be seen on sediment urinalysis

A

evidence of concurrent UTI

54
Q

would you expect to find protein in urinalysis in CKD

A

proteinuria may be due to underlying cause of CRF (dogs)

CRF can cause proteinuria

55
Q

what would you expect to find on culture and sensitivity in urinalysis with CKD

A

possibly

increased risk of concurrent infeciton

concurrent infection can lead to disease progression

56
Q

what would be a non-proteinuria value in dogs and cats

A

UP:C <0.2 in both

57
Q

what is borderline proteinuric value in dogs and cats

A

UP:C

dogs: 0.2-0.5
cats: 0.2-0.4

58
Q

what is proteinuric value in dogs and cats

A

UP:C dogs: >0.5

cats: >0.4

59
Q

what does proteinuria increase the risk of

A

causes renal injury

increases risk of developing end-stage CKD (dogs & cats)

risk factor for mortality

therapies to reduce magnitude of proteinuria often renoprotective

60
Q

what can hypertension cause

A

kidney damage

can also lead to ocular, cerebral & cardiovascular damage (target organ damage)

61
Q

what would the systolic blood pressure be in stage 0 CKD

62
Q

what would the systolic blood pressure be in stage 1 CKD

A

150-159 mmHg

63
Q

what would the systolic blood pressure be in stage 2 CKD

A

160-179 mmHg

64
Q

what would the systolic blood pressure be in stage 3 CKD

65
Q

on the basis of investigations what do you need to decide (5)

A
  1. identify presence of renal azotemia
  2. determine if acute or chronic
  3. stage CKD
  4. identify underlying causes of CKD (if possible)
  5. identify complications and treatable clinical signs of CKD
66
Q

what are the aims of treating CKD (3)

A
  1. treat underlying cause if possible
  2. improve clinical signs/quality of life
  3. slow progression
67
Q

what underlying causes do you need to treat possibly (8)

A
  1. hypercalcemia
  2. renal lymphoma
  3. removal of nephrotoxic drugs
  4. glomerular disease
  5. pyelonephritis
  6. other infectious causes
  7. ureteroliths
  8. hypertension
68
Q

how do you treat CKD (4)

A
  1. ACE inhibitors
  2. amlodipine
  3. ARBs
  4. moderate salt restriction
69
Q

what clinical signs do you need to treat to improve quality of life (5)

A
  1. dehydration
  2. vomiting/nausea
  3. anorexia
  4. hypokalemia
  5. anemia
70
Q

how do you treat dehydration in the short term

A

IV fluids including KCl + control losses

71
Q

how do you treat dehydration in the long term (4)

A
  1. oral fluids (wet food/add water/broths/water fountain)
  2. subcutaneous fluids
  3. feeding tube placement
  4. control losses
72
Q

what are the causes of nausea (3)

A
  1. stimulation of chemoreceptor trigger zone by uremic toxins
  2. uremic gastritis
  3. hypergastrinemia
73
Q

how do you treat nausea (4)

A
  1. antiemetics (maropitant, metoclopramide, ondansetron)
  2. H2 antagonists (famotidine, ranitidine, cimetidine)
  3. proton pump inhibitor (omeprazole)
  4. gastric mucosal protectants (sucralfate)
74
Q

how do you treat anorexia (3)

A
  1. warm food, hand feed, quite environment
  2. consider appetite stimulants (mirtazapine, capromorelin – dogs only)
  3. consider feeding tube placement
75
Q

how do you treat hypokalemia (4)

A
  1. supplement IV therapy
  2. consider correcting metabolic acidosis
  3. renal diets are potassium supplemented
  4. oral potassium supplements
76
Q

when is erythropoietin therapy indicated

A

symptomatic animals with PCV < 20%

77
Q

how do you treat hyperphosphatemia

A

IV fluids

restrict phosphate intake

78
Q

how do you restrict phosphate intake

A
  1. dietary restriction
  2. intestinal phosphate binders
79
Q

what are intestinal phosphate binders

A

aluminium hydroxide/carbonate (alucaps)

calcium carbonate/acetate (ipakitine/pronefra)

80
Q

when are renal diets beneficial

A

in stage I and II CKD

definitely in III and IV

reduce the risk of uremic crisis

81
Q

what are the components of renal diets (10)

A
  1. phosphate restricted
  2. high energy
  3. high quality reduce protein
  4. sodium restricted
  5. potassium supplemented
  6. increased B vitamins
  7. neutral effect on acid-base balance
  8. omega-3 supplemented
  9. increased soluble fibre
  10. anti-oxidant supplemented
82
Q

how do you change a diet

A

not when in uremic crisis

not when hospitalized

diet change is for long term benefit not short term

educate owners about importance

implement early in disease

introduce over 3-4 weeks

83
Q

how do ACE inhibitors work

A

inhibit the conversion of angiotensin I to angiotensin II

84
Q

what are the benefits of ACE inhibitors

A

reduce the glomerular capillary pressure and glomerular size

reduce proteinuria

mild ant-hypertensive effect

reduces sodium and water retention

limit pro fibrotic effects of angiotensin II on kidneys

85
Q

what are examples of ACE inhibitors

A

benazepril, enalapril

86
Q

how are ACE inhibitors beneficial in CKD (4)

A
  1. reduce proteinuria
  2. slow progression of renal disease
  3. improve appetite in proteinuric cats
  4. mild anti-hypertensive effect
87
Q

why can ACE inhibitors increase serum creatinine

A

due to reduced glomerular blood pressure

88
Q

what are angiotensin receptor blockers

A

block angiotensin II from binding to receptors

89
Q

what are examples of angiotensin receptor blockers

A

telmisartan

90
Q

what are angiotensin receptor blockers licensed for

A

reduction of proteinuria associated with CKD and for treatment of hypertension in cats

91
Q

what are side effects of angiotensin receptor blockers (4)

A
  1. mild and transiet GI signs
  2. elevated liver enzymes
  3. reductions in blood pressure
  4. decreases in RBC counts
92
Q

what are the aims of long term monitoring (4)

A
  1. assess disease progression
  2. monitor for complications
  3. assess management of prev diagnosed complications
  4. provide client support
93
Q

how do you treat acute decompensation of CRF

A

identify and treat underlying cause

IV fluids

94
Q

what underlying causes should you treat in an acute decompensation

A

another disease –> volume depletion

UTI

drugs (anesthesia, nephrotoxic drugs(

ureteral obstruction

blood loss

95
Q

what should you treat acute decompensation with IV fluids

A

treat dehydration, optimize GFR

monitor urea, creatinine, phosphate, electrolytes

Module 17 (31 decks)

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