Diagnosis and Management of Different CKD Stages Flashcards

1
Q

describe uremia

A

uremia: accumulation of substances (uremic toxins) usually excreted in the urine under normal physiologic conditions

origin of many uremic toxins:
-dietary protein: amino acids are metabolized by GI bacteria, then liver

with uremia, we have concerns for:
1. clinical signs (dysrexia, nausea, vomiting)
2. CKD progression
3 CV disease
4. microbial diversity altered in CKD; increase of bacteria that produce uremic toxins

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2
Q

desribe antiuremic therapy

A
  1. therapeutic renal diets:
    -reduced protein substrate and soluble fiber
  2. pre/probiotics: improve bacterial metabolism
  3. uremic toxin binders: bind toxin precursors in GI
    -reduces serum uremic toxin concentrations in cats
    -unknown if meaningful clinical benefit
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3
Q

describe uremic syndrome

A
  1. most prominent clinical signs of uremia in patients are related to GI tract (due to chemoreceptor trigger zone): nausea, vomiting, dysrexia are common
  2. this is problematic bc adequate caloric support is crucial for chronically ill patients and CKD results in an increased metabolic state
  3. urea in saliva can be degraded to ammonia by urease producing bacteria and cause gastric ulcers
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4
Q

describe uremic gastropathy

A
  1. decreased renal excretion leads to hypergastrinemia which leads to hyperacidity and uremic gastritis (ulcers, edema)
  2. not as severe in dogs and cats
    -dogs show gastric edema and mineralization
    -cats show gastric fibrosis and mineralization

-antacids? yes if clinical suspicion of GI ulceration; not automatically need gastric acid suppression

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5
Q

describe CKD nutritional therapy

A
  1. renal diets: most likely to enhance longterm survival and QOL for patients in stage 3 and 4
  2. key nutrients:
    -high quality, reduced quantity protein: beneficial for balance of nitrogenous waste, reducing uremic crises,
    proteinuria/glomerular hypertension

-supplemented with omega 3 faty acids: beneficial for glomerular hypertension, proteinuria, inflammation

-reduced phosphate: beneficialy for phosphate retention, CKD mineral and bone disorder

reduced sodium: beneficial for sodium retention and SAH

supplemented with potassium: beneficial for hypokalemia

-added antioxidants: beneficial for nephron hyperfunction, oxidative damage

-added soluble fiber: nitrogenous waste balance (colonic bacteria), constipation

-increased caloric density: acceptability, cachexia

-alkalinizing agents: metabolic acidosis

-supplemented with B vitamins: wasting of water-soluble vitamins

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6
Q

describe the controversies of protein restriction

A

potential benefits:
-decrease uremia
-decrease renal ammoniagenesis
-decrease tubular hyperfunction by decreasing renal acid load
-decreasing phosphate load
-decreasing TGF-B
-decreasing intraglomerular progression
-decreasing proteinuria

potential detriments:
-loss of lean body mass
-decreased protein synthesis
-protein energy wasting

goal: to decrease dietary protein enough to achieve these benefits but now so much as to contribute to lean body mass loss

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7
Q

describe hypokalemia and CKD

A
  1. polyuria causes excessive kaliuresis (less opportunity for reabsorption)
  2. RAAS activation causes potassium loss
  3. metabolic acidosis causes intracellular potassium depletion
  4. common in cats with stage 2 and 3 CKD
  5. less common in cats with stage 4 bc GFR so reduced that is isn’t lost as much
    -less common in dogs on RAAS blockers
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8
Q

describe clinical signs of hypokalemia

A

moderate: muscle weakness, lethargy, inappetence, constipation

severe: myopathy: cervical ventroflexion and plantigrade stance; arrhythmias

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9
Q

describe treatment of hypokalemia

A
  1. renal diets: supplemented with Kt and alkalinizing
  2. further supplementation:
    -oral route is safest and preferred
    –potassium citrate (alkalizing) or potassium gluconate daily to effect
    –parenteral: KCl; IV for hospitalized patients; may be added to SQ fluids
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10
Q

describe metabolic acidosis

A
  1. retention of acids that are normally excreted by the kidneys
    -the kidneys lose the ability to excrete the daily acid load as ammonium and titratable acid
  2. can contribute to malaise, inappetence, skeletal muscle loss, and muscle weakness, and hypokalemia
  3. treatment:
    -most renal diets are alkalinizing = first step

-if acidosis persists:
–sodium carbonate
–potassium citrate
–daily supplementation

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11
Q

describe inappetance and CKD

A

possible reasons:
1. acid-base and electrolyte imbalances
2. severe anemia
3. uremic toxins stimulating CTZ (nausea/vomiting)
4. uremic gastropathy
5. oral disease
6. multiple medications

possible solutions:
1. treat acid-base and electrolyte derangements
2. correct severe anemia
3. treat oral disease
4. modify pilling technique for medication aversion
5. antiemetics/antinausea therapies: ondansetron, maropitant citrate, mirtazapine, capromorelin
6. feeding tubes

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12
Q

describe CKD challenges with water balance

A
  1. if animals are obligatorily polyuria they are prone to dehydration
  2. provide hydrations support:
    -fresh water available at all times for drinking
    -use canned food, add warm water if needed
    -regular SQ fluid admin: LRS more common, only if challenges with oral hydration
  3. dehydration management:
    -if there are fluid losses, correct clinical dehydration with isotonic polyionic replacement fluid solutions
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13
Q

describe constipation and CKD

A
  1. common in cats with CKD, likely a dysfunction of water balance
    -chronic subclinical dehydration increases colonic absorption of water
    -hypokalemia decreases colonic motility
    -phosphate binders may promote constipation
    -concurrent osteoarthritis may affect posturing
  2. evaluation:
    -thorough history and PE
    -serum biochem
    -abdominal radiographs: fecal load and lumbosacral/hip joints
  3. treatment:
    -hydration
    -correct electrolyte abnormalities
    -adjunctive management of OA

then, depending on severity/chronicity:
-added fiber
-oral laxatives
-prokinetics
-enemas

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14
Q

what are all the things to consider in CKD? NEPHRONS and shit

A

Nutrition
Electrolytes
Ph of blood (acid-base status); proteinuria
Hydration
Retention of wastes (uremia)
Other renal insults-avoid
Neuroendocrine function: hyperparathyroidism, hyproproliferative anemia, and hyeprtension
Serial monitoring: CKD is irreversible and progressive

SHIT: defecation/constipation

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15
Q

what are 4 general recommendations for any stage of CKD?

A
  1. discontinue all potentially nephrotixic drugs if possible
  2. ID and treat and prerenal and postrenal abnormalities
  3. rule out any treatable conditions like pyelonephritis and renal urolithiasis
  4. measure blood pressure and UPC
    -treat proteinuria/SAH if present
  5. ensure hydration, document that care is needed with blood pressure under anesthesia, increase monitoring frequency (frequent rechecks)
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16
Q

describe how the animal generally presents in stage 1 and stage 2

A

stage 1: usually “well”; may see PU/PD and some beginnings of mild weight loss
-hypertension and proteinuria are possible and can have associated clinical signs so def screen all affected animals

CKD in stage 1 and 2 usually NOT a cause for:
-GI imbalances, lethargy
-acid-base and electrolyte imbalances
-anemia

so search for an underlying reason if an stage 1 or 2 animal presents unwell

17
Q

what are general CKD recommendations in stage 2?

A
  1. discontinue all potentially nephrotoxic drugs if possible
  2. ID and treat and prerenal and postrenal abnormalities
  3. rule out any treatable conditions like pyelonephritis and renal urolithiasis
  4. measure blood pressure and UPC
    -treat proteinuria/SAH if present
  5. (new) consider feeding a clinical renal diet
    -recommended for stages 3-4 and for aniamls with renal proteinuria or evidence of phosphate regardless of stage
    -considered in stage 2: animals may accept the diet better at this stage
18
Q

describe CKD stages 3 and 4

A
  1. less than 25% of renal function remaining
  2. progressive renal dysfunction leads to worsening metabolic derangements: phosphate retention, electrolyte disturbances, acid-base disturbances, non-regenerative anemia, uremia
  3. is now a challenge to maintain nutritional support and hydration
19
Q

describe general recommendations for CKD stage 3 and 4

A
  1. discontinue all potentially nephrotoxic drugs if possible
  2. ID and treat and prerenal and postrenal abnormalities
  3. rule out any treatable conditions like pyelonephritis and renal urolithiasis
  4. measure blood pressure and UPC
    -treat proteinuria/SAH if present
  5. FEED a renal diet (reduce phosphate intake)
  6. intensify efforts to prevent protein/calorie malnutrition
  7. intensify efforts to prevent dehydration
  8. consider dialysis (dogs and cats) or renal transplant (cats)
  9. manage dehydrations
  10. treat anything you can treat to improve QOL
20
Q

describe renal transplants

A
  1. viable option for cats
  2. considered for stage 3 (creatinine >4)
  3. life-long immunosuppression
  4. renal donation not found to affect lifespan of donor
21
Q

describe extracorporeal renal replacement therapy

A
  1. intermittent hemodialysis for CKD available in select centers
  2. treatments 3x/week
  3. improves uremia/QOL
  4. not for all owners/pets