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Chronic kidney disease = chronic renal insufficiency = progressive kidney disease = nephropathy
progressive loss of renal function over several months to years
Criteria for CKD
1. Kidney damage for > 3 months, as defined by structural or functional abnormalities of the kidney, with or without decreased GFR, manifest by either: a) pathological abnormalities b) markers of kidney damage, including abnormalities in the composition of the blood or urin, or abnormalities in imaging tests
2. GFR < 60 ml/min/1.73 m2 for > 3 months, with or without kidney damage
Susceptibility risk factors for CKD
- 1. older age
- 2. decreased kidney mass
- 3. low birth weight
- 4. family history of CKD
- 5. US ethnic minority status
- 6. low income or eduction
Initiation risk factors for CKD (causing direct damage to kidney)
- 1. diabetes mellitus
- 2. hyeprtension
- 3. glomerulonephritis
progression risk factors for CKD
- 1. proteinuria
- 2. poor glycemic cotnrol in diabetes
- 3. elevated blood pressure
- 4. smoking
- 5. hyperlipidemia
- 6. obesity
What is the main structural marker for kidney damage?
List the amounts of protein present in a urine dipstick test.
- Trace: 15-30 mg/dL
- 1+: 30-100 mg/dL
- 2+: 100-300 mg/dL
- 3+: 300-1000 mg/dL
- 4+: > 1000 mg/dL
What is the albumin:creatinine ratios for spot urin collection?
- Normal: <30
- Microalbuminuria: 30-299
- Clinical proteinuria or albuminuria: > 300
What things should be screened annually (at minimum) for high risk patients?
DESCRIPTION: Kidney damage with normal or increased GFR
GFR: > 90
STAGE: 1 CKD
DESCRIPTION: kidney damage with mild decreased GFR
DESCRIPTION: moderate decreased GFR
SYMPTOMS: generally asymptomatic, HTN, anemia
DESCRIPTION: severe decreased GFR
SYMPTOMS: nocturia, fatigue, cold intolerance, anorexia, hyperphosphatemia, hypocalcemia, metabolic acidosis
DESCRIPTION: kidney failure
GFR: < 15 (or dialysis)
SYMPTOMS: malaise, lack of energy, pruritis, N/V, myoclonus, asterixis, seizures
What are the desired outcomes of modifying the progression of renal disease?
- 1. Reverse or delay progression of renal injury
- 2. Reduce incidence of Stage 5 CKD
What is the nutritional management for modifying the progression of renal disease?
- 1. Dietary protein restriction
- 2. 0.6 g/kg/day of protein
- 3. Only for patients with GFR < 25 ml/min/1.73 m2
What are the 4 pharmacologic therapies for CKD?
- 1. Intensive glucose control - intensive insulin therapy (ITT)
- 2. Hypertension
- 3. Hyperlipidemia
- 4. Smoking cessation
What are the goals for intensive insulin therapy (ITT)?
- Preprandial goal: 70-130 mg/dL
- Postprandial goal: < 180 mg/dL
What are the goals for hypertension for CKD?
- Goal: < 130/80 mmHg
- Drugs of choice:
- a) Diabetes mellitus: ACE inhibitor or ARB
- b) Proteinuria: ACE inhibitor or ARB
- c) No diabetes, no proteinuria: Diuretic
What are the goals for hyperlipidemia for CKD?
- Goal LDL: < 100 mg/dL
- May limit progression of disease
What are the 3 main complications of decreased renal function?
- 1. decreased filtration, secretion, reabsorption
- 2. decreased endocrine function
- 3. decreased metabolic function
What occurs when there is decreased filtration, secretion, reabsorption?
- 1. build up of toxins
- 2. fluid & electrolyte disturbances
- 3. metabolic acidosis
What occurs when endocrine function is decreased due to a decrease in renal function?
Erythropoeitin is decreased causing anemia
What occurs when metabolic function is decreased due to a decrease in renal function?
Vitamin D decreases causing secondary hyperparathyroidism and renal osteodystrophy
Do people with CKD have an increased or decreased ability to concentrate or dilute urine?
Fill in the blanks:
_____total renal Na excretion --> ___ body fluid --> volume _______
decreased total renal Na excretion --> increased body fluid --> volume overload
What is the goal serum Na for CKD?
between 135 and 145 without volume overload or depletion
What is the treatment for sodium and fluid balance for CKD?
- 1. No-added-salt diet
- 2. Fluids restriction
- a) not necessary if Na intake controlled
- b) reserve for dialysis patients between sessions
- 3. Diuretics
- a) loop diuretics
- b) loop + thiazide diuretics
What monitoring should be done for sodium and fluid balance for CKD patients?
blood pressure, volume status, and serum electrolytes (frequency depends on institution)
How is potassium homeostasis regulated?
Regulated by renal excretion, shifting in and out of cell, GI excretion
What happens to potassium homeostasis in stages 4 and 5 of CKD?
The body can no longer adapt to decreased renal excretion of potassium and hyperkalemia is unavoidable.
What are the goals for potassium homeostasis in CKD?
- 1. Prevent hyperkalemia and adverse consequences
- 2. Stage 2-3: maintain serum K in normal range (3.5-5)
- 3. Stage 4-5: maintain serum K between 4.5 and 6
What is the treatment for Acute hyperkalemia?
- 1. calcium gluconate
- 2. insulin (plus glucose)
- 3. beta-adrenergic agonists
- 4. sodium polystyrene sulfonate (kayexalate)
What is the treatment for Chronic hyperkalemia?
- 1. dietary restrictions
- 2. prevent constipation
- 3. eliminate medications likely to cause hyperkalemia
- 4. sodium polystyrene sulfonate (kayexelate)
Define metabolic acidosis.
- pH < 7.35
- pCO2 < 35 mmHg
- serum HCO3- < 24mEq/L
Describe the pathophysiology of metabolic acidosis.
- 1. decreased ammonia synthesis
- 2. decreased urinary buffer
- 3. decreased net H+ excretion
- 4. positive H+ balance
- 5. decreased pH
Presentation of metabolic acidosis.
- 1. fatigue
- 2. decreased exercise tolerance
- 3. hyperkalemia
What are the goals for metabolic acidosis?
- 1. normalize pH
- 2. maintain serum HCO3- within normal range of 22-28 mEq/L
- 3. prevent complications of severe acidosis (bone disease, decreased cardiac contractility)
What are the treatment "guidelines" for metabolic acidosis?
- 1. asymptomatic patients with mild acidosis generally do not need emergent treatment
- 2. severe acidosis: pH < 7.2; serum HCO3- < 15 mEq/L
- 3. initial dosing depends on the calculated base deficit
- 4. maintenance doses usually 12-20 mEq/day
- 5. dialysis patients: adjust dialysate fluid
What are the treatment options for metabolic acidosis and what are the mechanisms of action?
- 1. sodium bicarbonate
- 2. sodium citrate
- 3. potassium citrate
- MOA: alkalinizing agents
What are the side effects of sodium bicarbonate in the treatment of metabolic acidosis?
- GI distress
What are the side effects of sodium citrate (Bicitra) in the treatment of metabolic acidosis?
What are the side effects of potassium citrate (Polycitra) in the treatment of metabolic acidosis?
- cardiac arrhythmias
What are the contributing factors of anemia of CKD?
- decreased EPO production
- uremic toxins decrease the life span of RBC
- iron deficiency
- blood loss from HD and lab testing
- poor nutrition (dec. folic acid and B vitamins)
What should be evaluated in a CKD patient suspected of having anemia?
- RBC indices
- Iron indices
- Serum ferritin
- Serum iron
- Folic acid and vitamin B12
What are the RBC indices that need to be evaluated in a CKD patient with anemia?
Why is hematocrit not a good indicator for anemia?
- Because hematocrit fluctuates with volume status
- dehydration = elevated hematocrit
What is iron indices?
- Transferrin saturation (Tsat)
- Tsat = serum iron/TIBC x 100
- how much iron is immediately available
What is serum ferritin?
- acute phase reactant
- can be elevated in inflammation processes
- not always the best indicator
What are the goals for a CKD patient with anemia?
- Increase oxygenation
- Improve QOL
- Prevent complications
What is the target hemoglobin for CKD patient?
What are the target iron indices for hemodialysis dependent patients?
- Serum ferritin >200 ng/mL AND
- Tsat >20% or content of hemoglobin in reticulocytes (CHr) >29 pg/cell
What are the target iron indices for non-hemodialysis or peritoneal dialysis dependent patients?
- Serum ferritin >100 ng/mL AND
- Tsat >20%
What is the oral treatment for anemia in CKD patients?
200mg of elemental iron per day
How much iron is absorbed in the body and where is it absorbed?
~10% is absorbed in the duodenum and upper jejunum
How should oral iron supplements be taken?
- Take on an empty stomach
- Decreased absorption with food
How much elemental iron is found in ferrous sulfate?
How much elemental iron is found in ferrous sulfate exsiccated? What does exsiccated mean?
- Exsiccated = moisture has been removed
How much elemental iron is found in ferrous fumarate?
How much elemental iron is found in ferrous gluconate?
How much elemental iron is found in iron polysaccharide complex (capsule) (a/k/a Niferex -150)?
How much elemental iron is found in Heme iron polypeptide (a/k/a Proferrin-ES 12mg)?
What are the adverse effects of oral iron supplementation?
- abdominal cramping
What drug interactions are common with oral iron supplementation?
- Vitamin C (ascorbic acid): increases acidity in the stomach which increases the absorption of iron
- Fluoroquinolones: separate from FQ
What is the typical IV iron supplementation dose?
Generally give 1 gram in divided doses via dialysis or slow IV infusion
Which IV iron supplement has a black box warning and requires a test dose?
Iron dextran (anaphylaxis)
What are some common adverse reactions of IV iron supplementation?
Infusion reactions: hypotension, arthralgias, myalgias, fever, flushing, headache, risk of iron overload
What is the MOA of erythropoiesis stimulating agents (ESA)?
same biologic activity as endogenous erythropoietin
When should erythropoiesis stimulating agents be initated in HD-CKD patients?
- Hgb < 10 g/dL
- Reduce or interrupt dose of ESA if Hgb approaches or exceeds 11g/dL
When should erythropoiesis stimulating agents be initated in non-HD-CKD patients?
- Consider when Hgb < 10 g/dL AND the following considerations apply:
- - Rate of Hgb decrease indicated likely need for transfusion AND
- - Reducing risk of alloimmunization and/or other transfusion related risks is a goal
- Reduce or interrupt dose of ESA if Hgb exceeds 10 g/dL
What are the boxed warnings of ESA products such as Epogen, Procrit, Aranesp and Omontys?
Which ESA drug is only approved for patients receiving dialysis?
How should dose adjustments of ESA's be addressed?
- 1. Individualized for each patient
- 2. Dose increases = once every 4 weeks only
- - if Hgb has not increased by >1 g/dL after 4 weeks of therapy then increase by 25%
- 3. Dose reductions = can be more frequent
- - with rapid Hgb rise (>1 g/dL in any 2-wk period) then decrease by 25%
- 4. Inadequate response over 12-week escalation period
- - higher doses not likely to elicit response
- - use lowest dose possible to reduce need for transfusions
- 5. Monitor Hgb at least weekly until stable, then monthly
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