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GU > Lecture 4: CKD Part 1 > Flashcards

Lecture 4: CKD Part 1 Flashcards

1
Q

Define CKD.

A
  • Markers of kidney damage for 3+ months.
    OR
  • GFR < 60ml/min/1.73m2 for 3+ months w or w/o kidney damage.

Kidney damage markers: Blood, Urine, or Imaging abnormalities

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2
Q

What two things characterize CKD?

A
  • Abnormal kidney function
    OR
  • Progressive decline in GFR

Can be either or.

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3
Q

What happens to our nephrons as we lose nephrons?

A
  • Increased hyperfiltration (no noticeable change in GFR)
  • Increased hypertrophy

Prolonged hypertrophy => inflammation and fibrosis.

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4
Q

If a patient starts to see improvement in kidney markers but has had kidney damage, what does this mean?

A

Removal of disease burden on existing nephrons. You cannot restore renal tissue that has been scarred or necrosed.

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5
Q

What are the 2 primary causes of late stage (5+) CKD?

A
  • DM
  • HTN/vascular disease

70% of all cases.

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6
Q

What kind of CKD is a risk factor for CV mortality?

A

Proteinuric CKD

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7
Q

What is cardiorenal syndrome?

A

Deterioration of one of the organs resulting in deterioration of the other.

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8
Q

What are the 5 types of CRS and RCS?

A
  • Type 1: Acute CRS: Cardiac causes AKI (C then R)
  • Type 2: Chronic CRS: Cardiac causes CKD (C then R)
  • Type 3: Acute RCS: AKI causes cardiac (R then C)
  • Type 4: Chronic RCS: CKD causes cardiac (R then C)
  • Type 5: Secondary CRS: both caused by something else.

You have 1 heart, so type 1 begins with the heart.

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9
Q

What two factors are used to stage CKD?

A
  • GFR
  • Albuminuria
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10
Q

Describe KDIGO criteria for CKD.

A
  • G1-5 based on GFR: 90-15.
  • A1-A3 based on albuminuria: 30-300.

Good is G1-2 + A1.

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11
Q

Stage these 4 patients:

● A patient with a GFR of 38 mL/min and urine albumin of 100 mg/g =
● A patient with a GFR of 96 mL/min and urine albumin of 38 mg/g =
● A patient with a GFR of 10 mL/min and urine albumin of 350 mg/g =
● A patient with a GFR of 110 mL/min and urine albumin of 12 mg/g

A
  • Stage 3b (G3b, A2)
  • Stage 1 (G1, A2)
  • Stage 5 (G5, A3)
  • Normal (G1, A1)
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12
Q

How do patients present symptomatically in early-mid CKD usually?

A

Asymptomatic.

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13
Q

What is the most common vital finding in CKD?

A

HTN

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14
Q

With late stage CKD, what term refers to the general symptoms that begin occurring?

A

Uremia.

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15
Q

In CKD, what serum labs tend to be low?

A
  • RBCs, H&H
  • Calcium and Sodium
  • GFR
  • Vit D, HDL
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16
Q

In CKD, what serum labs tend to be elevated?

A
  • Potassium
  • BUN, Cr
  • Phosphate, PTH, triglycerides, uric acid
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17
Q

What UA findings are typical in CKD?

A
  • Broad, waxy casts (Dilated nephrons)
  • Proteinuria
  • Glucosuria
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18
Q

At what stage of CKD do most S/S begin appearing?

A

Stage 3-4.

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19
Q

What kidney imaging findings would suggest CKD?

A
  • Polycystic kidneys
  • Small kidneys < 9cm
  • Asymmetry (vascular disease)
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20
Q

What is the overall treatment goal of CKD?

A

Slowing its progression.

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21
Q

What is the most common complication of CKD?

A

HTN

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22
Q

What is the primary dietary change suggested to treat HTN from CKD?

A

Sodium reduction. (< 2300mg)

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23
Q

For HTN 2/2 CKD, what is the first-line treatment? What do we need to monitor for it?

A
  • ACE/ARB
  • Increases in serum Cr and K+.

>30% Cr increase or hyperkalemia requires stoppage or adjustment.

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24
Q

When are thiazides preferred over loops in CKD?

A

Thiazides are preferred in early CKD.

Loops are better in GFR < 30.

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25
Q

What is the primary lipid abnormality found in CKD?

A

Hypertriglyceridemia.

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26
Q

What is recommended for CAD risk factor modification for those with CKD?

A
  • Statins.
  • Adjunct therapy: PCSK9 inhibitors and/or ezetimibe

Do not use fibrates: increased rhabdo w/ statin.

Accelerated atherosclerosis is common in ESRD.

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27
Q

Why does HF tend to occur in CKD and how do we prevent it?

A
  • Increased cardiac workload due to the HTN which leads to LVH and diastolic dysfunction.
  • Treatment typically consists of Diuretics, ACE/ARBs, and fluid/salt restriction.

Avoid digoxin due to toxicity in CKD patients.

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28
Q

At stage 5 of CKD, why is anticoagulation used in caution for AFib?

A

Higher bleeding risk

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29
Q

What are the S/S of pericarditis?

A
  • Retrosternal chest pain
  • Friction rub
  • Uremic pericardial effusions (need admission)

Usually due to uremia. Hospitalize asap

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30
Q

What is the main treatment goal of CRS/RCS?

A

Maintain euvolemia.

31
Q

What is the typical pattern of mineral metabolism abnormalities in CKD?

A
  1. Hyperphosphatemia
  2. Hypovitaminosis D
  3. Hypocalcemia
  4. Secondary Hyperparathyroidism
32
Q

What are the 3 types of renal osteodystrophy?

A
  • Osteitis fibrosa cystica (MC)
  • Adynamic bone turnover
  • Osteomalacia

Requires bone biopsy to definitively diagnose.

33
Q

What is osteitis fibrosa cystica?

A
  • Hyperparathyroidism leading to osteoclast stimulation and HIGH rates of bone turnover.
34
Q

What is adynamic bone disease?

A

Low bone turnover due to suppression of PTH.

35
Q

What is osteomalacia?

A

Lack of bone mineralization, usually due to hypovitaminosis D or bisphosphonates.

36
Q

What is a common finding of osteitis fibrosa cystica on XRAY?

A

Brown tumors.

37
Q

What is the first step in treating mineral metabolism abnormalities in CKD?

A
  • Controlling hyperphosphatemia.
  • Requires dietary phosphorus restriction and binders.
38
Q

What are the first-line phosphate binders?

A

Non-calcium based: Sevelamer or Lanthanum.

Can also be combined with calcium-based binder after.

39
Q

When is aluminum hydroxide used for phosphate binding?

A

Only in severe cases like osteomalacia or neurologic complications.

Has a lot of SE.

40
Q

Once hyperphosphatemia is controlled, what needs to be managed next in CKD in regards to mineral metabolism?

A

Manage PTH via D3 (Calcitriol) and cinacalcet.

D3 will increase serum calcium and phosphorus.
Cinacalcet targets CaSRs and can be used if serum calcium/phosphorus are too high.

41
Q

Why are goal PTH levels in ESRD higher?

A

Prevention of adynamic bone disease.

42
Q

What must be ruled out before using EPO to treat anemia due to CKD?

A

Make sure it is not a different anemia, such as iron deficiency.

43
Q

What two iron studies correspond to iron deficiency?

A
  • Ferritin < 100 ng/mL
  • Iron saturation < 20%

Either

44
Q

What is the iron treatment for CKD anemia?

A

Auryxia (Ferric citrate)

45
Q

What ferritin level contraindicates iron supplementation?

A

> 500 ng/mL

46
Q

What Hb level is goal for EPO treatment for CKD anemia?

A

10-11 g/dL

47
Q

What are the 2 EPO agents used in treating anemia due to CKD?

A
  • Epoetin (Recombinant): 1-2x/week
  • Darbepoetin: every 2-4 weeks.
48
Q

Why does hypocoagulability occur in CKD and how do we treat it?

A

Occurs due to platelet dysfunction.

We can use short term desmopressin, dialysis, and conjugated estrogens.

Only used if symptomatic and short-term.

49
Q

How can hypercoagulability also occur in CKD?

A

Severe proteinuria can lead to a protein C & S deficiency.

50
Q

At what stage does hyperkalemia tend to manifest?

A

Stages 4-5.

51
Q

What drugs can contribute to hyperkalemia in CKD?

A
  • Decreased K+ secretion: Triamterene, spironolactone, ACE/ARB, NSAIDs.
  • Decreased K+ uptake by cells: BBs
52
Q

What is recommended for chronic hyperkalemia treatment?

A
  • Dietary potassium restriction
  • Loop diuretics
53
Q

Why does metabolic acidosis tend to occur in CKD and what are the associated complications?

A
  • Inability to excrete acid due to loss of renal mass.
  • Can result in renal osteodystrophy. (Ca pulled to buffer)
54
Q

How is metabolic acidosis treated in CKD?

A

Oral sodium bicarb to maintain bicarb > 21 mEq/L.

55
Q

What is uremic encephalopathy and the suggested treatment?

A

Aggregration of uremic toxins, resulting in neurologic dysfunction.

Requires dialysis to get rid of the toxins.

56
Q

How does uremic neuropathy typically present?

A
  • Sensory before motor
  • Loss of position and vibration in toes.
  • Paresthesias, burning, pain
  • Muscle atrophy => paralysis
57
Q

How is uremic neuropathy diagnosed and what is the treatment?

A

Requires EP studies to determine nerve changes.

Usually treated with dialysis. Can give TCAs or anticonvulsants to help with symptoms.

58
Q

What kind of glucose abnormality can occur in CKD and why?

A

Increased risk of hypoglycemia due to decreased renal clearance of insulin.

59
Q

What common DM medication needs to be used in caution in CKD and why?

A

Metformin cannot be used in patients with a serum Cr < 1.4 or GFR < 30 due to the increased risk of lactic acidosis.

60
Q

What reproductive abnormalities can occur in CKD?

A
  • Decreased libido
  • ED
  • Pregnancy preemies
61
Q

What diet restrictions are recommended for people with CKD?

A
  • Protein restriction if no cachexia or low albumin.
  • Sodium restriction of 2g/d.
  • Water restriction of 2L/d if volume overloaded.
  • K restriction of 2g/d for GFR < 20 or hyperkalemia.
  • Phosphorus restriction.

Too much sodium will lead to HTN and edema. (3-4g)
Too little leads to hypotension. (1g)

62
Q

What drug classes should be avoided in CKD patients?

A
  • Renally excreted drugs (Monitor)
  • Mg-containing: antacids or laxatives.
  • Phosphorus-containing
  • Nephrotoxic: NSAIDs, IV contrast
  • Morphine: accumulates with late stage CKD
63
Q

When is dialysis generally indicated in terms of CKD?

A

GFR of 5-10 mL/min/1.73m2.

64
Q

Differentiate hemodialysis (HD) vs peritoneal dialysis (PD).

A
  • HD is a few hours at a dialysis center.
  • PD is for 30 minutes, 4 times a day at home.

PD requires abdominal access.
HD requires arm access or central port access.

65
Q

What are the indications for dialysis for a CKD patient?

A
  • GFR < 10
  • Uremic symptmos
  • Metabolic disturbances refractory to therapy
  • Fluid overload unresponsive to diuretics
66
Q

What is the ideal renal replacement therapy? (RRT)

A

Transplantation

67
Q

How does HD work?

A
  1. Blood is poured into a container containing a semipermeable membrane with dialysate.
  2. The dialysate will draw the unwanted substances out of the blood.
  3. The clean blood is then returned to the person.
68
Q

What are the 3 ways to get access for HD?

A
  • AV fistula (longest lasting, 6-8 week to prep)
  • Prosthetic graft (short lasting, 2 weeks to prep, prone to infection)
  • Indwelling vascular catheter (Temporary, high infection risk)

AV fistula formation is the preferred method.

69
Q

How does PD work?

A
  • Dialysate is poured into peritoneal cavity via indwelling catheter, which functions as the semipermeable membrane.
  • Same process as HD but the peritoneal cavity is where the blood and dialysate meet.
70
Q

What are the two types of PD?

A
  • Continuous ambulatory peritoneal dialysis (CAPD): 4-6x a day manually.
  • Continuous cyclic peritoneal dialysis (CCPD): Runs at night
71
Q

What are the biggest pros and cons of PD?

A

Pros:

  • Autonomy
  • Less diet restrictions
  • No travel

Cons:

  • Removes a lot of albumin
  • Peritonitis risk
  • Patient needs to manage the machine.
72
Q

What is peritonitis?

A

The MC complication of doing PD.

Diagnosed with peritoneal fluid > 100 WBCs/mL and 50%+ neutrophils. (usually staph aureus)

Standard ABX therapy for causative organism.

73
Q

What is the most common cause of death for patients on dialysis?

A

Cardiac disease ):

GU (14 decks)

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