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
2
Q
what is chronic renal failure
A
end stage process
azotemia and reduced urine concentrating ability
3
Q
what are degenerative causes of CKD (2)
A
- chronic interstitial nephritis
- renal infarcts
4
Q
what are developmental causes of CKD (2)
A
- familial renal dysplasia
- polycystic kidney disease
5
Q
what are metabolic causes of CKD (1)
A
- hypercalcemia
6
Q
what are neoplastic causes of CKD (2)
A
- renal lymphoma
- renal carcinoma
7
Q
what are iatrogenic causes of CKD (2)
A
- vitamin D supplementation
- nephrotoxic drugs
8
Q
what are idiopathic causes of CDK (2)
A
- renal amyloidosis
- primary glomerulopathies
9
Q
what are immune mediated causes of CKD (1)
A
- immune complex mediated glomerulonephritis
10
Q
what are infectious causes of CKD (2)
A
- pyelonephritis
- borreliosis (lyme nephropathy)
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
12
Q
what is the IRIS CKD classification
A
stage 1-4
13
Q
what is stage I CKD in dogs
A
non-azotemic
creatinine <125
14
Q
what is stage II CKD in dogs
A
mild renal azotemia
creatinine 125-180
15
Q
what is stage III CKD in dogs
A
moderate renal azotemia
creatinine 181-440
16
Q
what is stage IV CKD in dogs
A
severe renal azotemia
>440
17
Q
what is stage I CKD in cats
A
non-azotemic
<140
18
Q
what is stage II CKD in cats
A
mild renal azotemia
creatinine 140-250
19
Q
what is stage III CKD in cats
A
moderate renal azotemia
251-440
20
Q
what is stage IV CKD in cats
A
severe renal azotemia
creatinine >440
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
22
Q
what does prolonged injury in the kidney lead to
A
- infiltration of inflammatory cells
- profibrotic cytokine production
- hypoxia –> further injury
nephrons cannot regenerate or replicate
23
Q
what are the early pathophysiology changes in CKD
A
nephrons hypertrophy & single nephron GFR increase –> compensation
24
Q
what are the later pathophysiology changes in CKD
A
compensation is overwhelmed –> clinical kidney disease
25
what % of nephron loss causes urine concentrating ability to become impaired
1/3
26
what % of nephron loss causes azotemia to develop (CRF)
1/4
27
what are the physiological consequences of CKD (10)
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
28
why does CKD lead to hyperphosphatemia
phosphate excreted via filtration through glomeruli
reduced GFR --\> phosphate retention
29
what are the effects of hyperphosphatemia (2)
unlikely to cause clinical signs BUT
1. drives renal secondary hyperparathyroidism (increased PTH) --\> disease progression
2. leads to reduced survival
30
what are the effects of high PTH (3)
1. likely uremic toxin --\> depression
2. can cause osteopenia and tooth loosening and pathological features
3. renal cell tubular damage
31
how does decreased GFR lead to increase PTH
32
why does hypokalemia occur in CKD (3)
1. reduced intake
2. reduced renal potassium reabsorption
3. renal tubular acidosis
33
what does hypokalemia (6)
1. neuromuscular weakness
2. arrhythmias
3. metabolic acidosis
4. anorexia and impaired protein synthesis --\> weight loss
5. hypokalemic nephropathy
6. promotes PUPD
34
what type of anemia is present in CKD
non-regenerative, normocytic, normochromic anemia
35
why does CKD cause anemia (5)
1. erythropoietin deficiency (synthesized in kidneys)
2. reduced RBC lifespan
3. nutritional abnormalities
4. chronic GI hemorrhage
5. iron deficiency
36
what are the effects of anemia (3)
1. lethargy
2. inappetance
3. may cause progression of disease due to renal hypoxia
37
what is hemorrhage due to in CKD (2)
1. acquired platelet dysfunction (thrombocytopenia, impaired platelet adhesiveness to subendothelium)
2. GI hemorrhage secondary to ulceration
38
what is hypertension due to in CKD (2)
1. impaired excretion of sodium
2. activation of renin-angiotensin-aldosterone system (RAAS)
39
what are the effects of hypertension in CKD
damage to kidney, eye, brain, cardiovascular system
40
what is proteinuria due to in CKD (2)
1. increased glomerular capillary pressure
2. fewer tubules so less able to reabsorb filtered protein
41
what does proteinuria result in
progression of CKD and risk factor for mortality
42
what is metabolic acidosis due to (3)
1. reduced excretion of H+ ions by kidney
2. retention of phophate and other organic
3. increased loss of chloride (vomiting)
43
why is CKD progressive
1. ongoing presence of initial trigger
2. damage triggers secondary processes which perpetuate/contribute to the damage
44
what secondary processes perpetuate/contribute to damage in CKD (6)
1. systemic hypertension
2. glomerular hypertension
3. mineral imbalances (phosphate, PTH, CaPO4 precipitation)
4. proteinuria
5. renal fibrosis
6. renal inflammation
45
what are the presenting signs and examination findings in CKD (8)
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
what are the clinical examination findings of CKD (7)
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
what are the laboratory findings of CKD (2)
1. azotemia (reduced GFR, increased catabolism, GI hemorrhage)
2. inappropriately low urine specific gravity (unable to concentrate or dilute urine)
48
what are the USG values in the dogs with CKD
1.008 to 1.020
49
what are the USG values in the cats with CKD
1.008 to 1.030
50
what other tests would you perform when investigating CKD (5)
1. full biochemistry
2. full hematology
3. urinalysis including (sediment exam, protein:creatinine ratio, culture & sensitivity)
4. abdominal imaging
5. blood pressure measurement
51
what might you find on biochemistry with CKD (4)
1. hyperphosphatemia
2. hypokalemia
3. hyper/hypocalcemia
4. metabolic acidosis
52
what would you find on hematology with CKD
non-regenerative, normocytic, normochromic anemia
+/- neutrophilic leukocytosis (concurrent renal infection)
53
what would be seen on sediment urinalysis
evidence of concurrent UTI
54
would you expect to find protein in urinalysis in CKD
proteinuria may be due to underlying cause of CRF (dogs)
CRF can cause proteinuria
55
what would you expect to find on culture and sensitivity in urinalysis with CKD
possibly
increased risk of concurrent infeciton
concurrent infection can lead to disease progression
56
what would be a non-proteinuria value in dogs and cats
UP:C \<0.2 in both
57
what is borderline proteinuric value in dogs and cats
UP:C
dogs: 0.2-0.5
cats: 0.2-0.4
58
what is proteinuric value in dogs and cats
UP:C dogs: \>0.5
cats: \>0.4
59
what does proteinuria increase the risk of
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
what can hypertension cause
kidney damage
can also lead to ocular, cerebral & cardiovascular damage (target organ damage)
61
what would the systolic blood pressure be in stage 0 CKD
\<150 mmHg
62
what would the systolic blood pressure be in stage 1 CKD
150-159 mmHg
63
what would the systolic blood pressure be in stage 2 CKD
160-179 mmHg
64
what would the systolic blood pressure be in stage 3 CKD
\>180 mmHg
65
on the basis of investigations what do you need to decide (5)
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
what are the aims of treating CKD (3)
1. treat underlying cause if possible
2. improve clinical signs/quality of life
3. slow progression
67
what underlying causes do you need to treat possibly (8)
1. hypercalcemia
2. renal lymphoma
3. removal of nephrotoxic drugs
4. glomerular disease
5. pyelonephritis
6. other infectious causes
7. ureteroliths
8. hypertension
68
how do you treat CKD (4)
1. ACE inhibitors
2. amlodipine
3. ARBs
4. moderate salt restriction
69
what clinical signs do you need to treat to improve quality of life (5)
1. dehydration
2. vomiting/nausea
3. anorexia
4. hypokalemia
5. anemia
70
how do you treat dehydration in the short term
IV fluids including KCl + control losses
71
how do you treat dehydration in the long term (4)
1. oral fluids (wet food/add water/broths/water fountain)
2. subcutaneous fluids
3. feeding tube placement
4. control losses
72
what are the causes of nausea (3)
1. stimulation of chemoreceptor trigger zone by uremic toxins
2. uremic gastritis
3. hypergastrinemia
73
how do you treat nausea (4)
1. antiemetics (maropitant, metoclopramide, ondansetron)
2. H2 antagonists (famotidine, ranitidine, cimetidine)
3. proton pump inhibitor (omeprazole)
4. gastric mucosal protectants (sucralfate)
74
how do you treat anorexia (3)
1. warm food, hand feed, quite environment
2. consider appetite stimulants (mirtazapine, capromorelin -- dogs only)
3. consider feeding tube placement
75
how do you treat hypokalemia (4)
1. supplement IV therapy
2. consider correcting metabolic acidosis
3. renal diets are potassium supplemented
4. oral potassium supplements
76
when is erythropoietin therapy indicated
symptomatic animals with PCV \< 20%
77
how do you treat hyperphosphatemia
IV fluids
restrict phosphate intake
78
how do you restrict phosphate intake
1. dietary restriction
2. intestinal phosphate binders
79
what are intestinal phosphate binders
aluminium hydroxide/carbonate (alucaps)
calcium carbonate/acetate (ipakitine/pronefra)
80
when are renal diets beneficial
in stage I and II CKD
definitely in III and IV
reduce the risk of uremic crisis
81
what are the components of renal diets (10)
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
how do you change a diet
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
how do ACE inhibitors work
inhibit the conversion of angiotensin I to angiotensin II
84
what are the benefits of ACE inhibitors
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
what are examples of ACE inhibitors
benazepril, enalapril
86
how are ACE inhibitors beneficial in CKD (4)
1. reduce proteinuria
2. slow progression of renal disease
3. improve appetite in proteinuric cats
4. mild anti-hypertensive effect
87
why can ACE inhibitors increase serum creatinine
due to reduced glomerular blood pressure
88
what are angiotensin receptor blockers
block angiotensin II from binding to receptors
89
what are examples of angiotensin receptor blockers
telmisartan
90
what are angiotensin receptor blockers licensed for
reduction of proteinuria associated with CKD and for treatment of hypertension in cats
91
what are side effects of angiotensin receptor blockers (4)
1. mild and transiet GI signs
2. elevated liver enzymes
3. reductions in blood pressure
4. decreases in RBC counts
92
what are the aims of long term monitoring (4)
1. assess disease progression
2. monitor for complications
3. assess management of prev diagnosed complications
4. provide client support
93
how do you treat acute decompensation of CRF
identify and treat underlying cause
IV fluids
94
what underlying causes should you treat in an acute decompensation
another disease --\> volume depletion
UTI
drugs (anesthesia, nephrotoxic drugs(
ureteral obstruction
blood loss
95
what should you treat acute decompensation with IV fluids
treat dehydration, optimize GFR
monitor urea, creatinine, phosphate, electrolytes
96
