27 - Chronic Kidney Disease Flashcards

1
Q

What is done to identify chronic kidney disease in px w/ diabetes?

A

Screening for proteinuria & assessment of sCr converted into eGFR

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2
Q

All px w/ CKD considered high risk for _____

A

CV events

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3
Q

How can progression of CKD in diabetes be slowed?

A

Use of medications that disrupt RAAS

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4
Q

Earliest stage of diabetic nephropathy = ____

A

Hyperfiltration (GFR significantly higher than normal)

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5
Q

Earliest clinical sign of diabetic nephropathy is _____

A

Persistent albuminuria

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6
Q

What should be done for prevention of diabetic nephropathy?

A
  • Optimal glycemic control ASAP after diagnosis will reduce risk of developing diabetic kidney disease
  • Optimal BP control
  • Blockade of RAAS w/ ACEi or ARB can reduce risk of developing CKD independent of their effect on BP (protective effect demonstrated in px w/ diabetes & HTN, but not normotensive px w/ diabetes)
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7
Q

What does albumin/creatinine ratio (ACR) describe?

A
  • How much protein is in the urine and if there is renal dysfunction
  • Need the ratio b/c don’t know if urine is dilute (drinking lots of water) or concentrated
  • Creatinine shows how concentrated urine is
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8
Q

What do the values of ACR mean?

A
  • ACR 2-20 = microalbuminuria

- ACR 20-66.7 = over nephropathy (macroalbuminuria)

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9
Q

What are some potential causes of transient albuminuria?

A
  • Recent major exercise
  • UTI
  • Febrile illness
  • Decompensated CHF
  • Menstruation
  • Acute severe elevation in blood glucose or BP
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10
Q

How can you decrease albuminuria?

A

Decrease amount of pressure on glomerulus

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11
Q

Which drug should be given to adults w/ diabetes & CKD w/ either HTN or albuminuria? What should be monitored?

A
  • ACE inhibitor/ ARB and started at very low dose to slow progression of diabetic nephropathy
  • Check sCr and K+ in first 2 weeks
  • ACEi or ARB can cause dramatic increase in sCr in short period of time; this is caused by renal artery stenosis or on a sick day
  • ACE inhibitor in type 1 w/ macroalbuminuria reduces renal outcomes
  • Don’t use ACE & ARB together b/c increased risk of AKI & hyperkalemia
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12
Q

How long can ACEi or ARBs be safely continued in px w/ declining renal function over time?

A

Based on Lexicomp

  • ACE inhibitors require dosage changes for renal dysfunction (decreased dose or frequency < 30 mL/min)
  • ARBs don’t require dosage changes
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13
Q

What normally accompanies hyperphosphatemia?

A

Hypocalcemia and low serum levels of vitamin D

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14
Q

When are oral phosphate binders used?

A

Majority (over 90%) of px w/ kidney failure b/c dietary restriction isn’t enough to control hyperphosphatemia

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15
Q

Renagel - MOA, dose, SE, advantage, disadvantage

A
  • Binds to phosphate w/o calcium (polysaccharide complex) so doesn’t cause hypercalcemia
  • Usually 800 mg TID w/ meals
  • GI effects (N/V, abdominal pain, bloating, diarrhea), hypercalcemia, metabolic acidosis
  • Advantage = effective & doesn’t contain calcium & reduces LDL
  • Disadvantage = GI effects & higher cost
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16
Q

Calcium carbonate - SE, advantage, disadvantage

A
  • Interferes w/ absorption of aspirin, digoxin, isoniazid, quinolone, tetracycline
  • AE = GI effects (N/V, diarrhea, constipation), hypercalcemia, xerostomia
  • Advantage = effective & inexpensive
  • Disadvantage = may contribute to hypercalcemia, promote vascular calcification, or both
17
Q

What is the target phosphate serum level?

A

1.8 mmol/L

18
Q

What is the relationship between the kidneys and vitamin D?

A

Kidneys are the final activation of vitamin D in the body, so when kidneys aren’t working then vitamin D doesn’t get activated

19
Q

What is calcitriol?

A
  • Activated vitamin D

- Has inhibitory effect on parathyroid gland

20
Q

Which px can’t receive calcitriol?

A

Px w/ hypercalcemia (> 2.6) or hyperphosphatemia (> 1.8) b/c calcitriol will make phosphate & calcium higher (must control phosphates first)

21
Q

What happens to phosphate in end stage renal disease?

A

Phosphate builds up in blood b/c can’t be filtered out by kidneys

22
Q

What is the relationship between calcium and phosphate? Is this good?

A

Calcium & phosphate bind together, but don’t want calcium-phosphate to stay around in the body b/c will calcify in the arteries (called calcium phosphate deposition); also deposits in subcutaneous fat under skin (causes you to become very itchy; this can break the skin & cause infection)

23
Q

Why don’t you want phosphate to be increased?

A
  • Will bind to calcium and deposit in heart or subcutaneous fat
  • Increased phosphate stimulates parathyroid gland (controls calcium levels) to release PTH (parathyroid hormone) that goes looking for calcium that needs to be replaced b/c phosphate is binding it all
    • Will go to the bones to find the calcium => can lead to osteitis fibrosa cystica
24
Q

How can phosphate be decreased?

A

Remove intake (processed meats, dairy products, can of soda)

25
Q

Where do phosphate and calcium normally bind and where do we want them to bind?

A
  • Normally phosphate & calcium bind in the blood

- Want it to happen in stomach so you can poop them out (that’s why you give calcium supplementation w/ meals)

26
Q

What is the goal for PTH levels?

A

PTH (parathyroid hormone) should be < 200 ng/L in adults w/ chronic kidney disease (don’t know the exact amount for best protection)

27
Q

What causes renal osteodystrophy? What is the tx?

A
  • Caused by hyperphosphatemia b/c too much phosphate binds all the calcium, so body takes calcium from bones
  • Tx would be treatment of high phosphate, which is phosphate binders (ex: Renagel)