Lecture 4: CKD Part 1 Flashcards

(73 cards)

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
What is the primary lipid abnormality found in CKD?
Hypertriglyceridemia.
26
What is recommended for CAD risk factor modification for those with CKD?
* Statins. * Adjunct therapy: PCSK9 inhibitors and/or ezetimibe | Do not use fibrates: increased rhabdo w/ statin. ## Footnote Accelerated atherosclerosis is common in ESRD.
27
Why does HF tend to occur in CKD and how do we prevent it?
* 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.
28
At stage 5 of CKD, why is anticoagulation used in caution for AFib?
Higher bleeding risk
29
What are the S/S of pericarditis?
* Retrosternal chest pain * Friction rub * Uremic pericardial effusions (need admission) | Usually due to uremia. Hospitalize asap
30
What is the main treatment goal of CRS/RCS?
Maintain euvolemia.
31
What is the typical pattern of mineral metabolism abnormalities in CKD?
1. Hyperphosphatemia 2. Hypovitaminosis D 3. Hypocalcemia 4. Secondary Hyperparathyroidism
32
What are the 3 types of renal osteodystrophy?
* Osteitis fibrosa cystica (MC) * Adynamic bone turnover * Osteomalacia ## Footnote Requires bone biopsy to definitively diagnose.
33
What is osteitis fibrosa cystica?
* Hyperparathyroidism leading to osteoclast stimulation and HIGH rates of bone turnover.
34
What is adynamic bone disease?
Low bone turnover due to suppression of PTH.
35
What is osteomalacia?
Lack of bone mineralization, usually due to hypovitaminosis D or bisphosphonates.
36
What is a common finding of osteitis fibrosa cystica on XRAY?
Brown tumors.
37
What is the first step in treating mineral metabolism abnormalities in CKD?
* Controlling hyperphosphatemia. * Requires dietary phosphorus restriction and binders.
38
What are the first-line phosphate binders?
Non-calcium based: Sevelamer or Lanthanum. | Can also be combined with calcium-based binder after.
39
When is aluminum hydroxide used for phosphate binding?
Only in severe cases like osteomalacia or neurologic complications. | Has a lot of SE.
40
Once hyperphosphatemia is controlled, what needs to be managed next in CKD in regards to mineral metabolism?
Manage PTH via D3 (Calcitriol) and cinacalcet. ## Footnote D3 will increase serum calcium and phosphorus. Cinacalcet targets CaSRs and can be used if serum calcium/phosphorus are too high.
41
Why are goal PTH levels in ESRD higher?
Prevention of adynamic bone disease.
42
What must be ruled out before using EPO to treat anemia due to CKD?
Make sure it is not a different anemia, such as iron deficiency.
43
What two iron studies correspond to iron deficiency?
* Ferritin < 100 ng/mL * Iron saturation < 20% | Either
44
What is the iron treatment for CKD anemia?
Auryxia (Ferric citrate)
45
What ferritin level contraindicates iron supplementation?
> 500 ng/mL
46
What Hb level is goal for EPO treatment for CKD anemia?
10-11 g/dL
47
What are the 2 EPO agents used in treating anemia due to CKD?
* Epoetin (Recombinant): 1-2x/week * Darbepoetin: every 2-4 weeks.
48
Why does hypocoagulability occur in CKD and how do we treat it?
Occurs due to platelet dysfunction. We can use short term desmopressin, dialysis, and conjugated estrogens. | Only used if symptomatic and short-term.
49
How can hypercoagulability also occur in CKD?
Severe proteinuria can lead to a protein C & S deficiency.
50
At what stage does hyperkalemia tend to manifest?
Stages 4-5.
51
What drugs can contribute to hyperkalemia in CKD?
* Decreased K+ secretion: Triamterene, spironolactone, ACE/ARB, NSAIDs. * Decreased K+ uptake by cells: BBs
52
What is recommended for chronic hyperkalemia treatment?
* Dietary potassium restriction * Loop diuretics
53
Why does metabolic acidosis tend to occur in CKD and what are the associated complications?
* Inability to excrete acid due to loss of renal mass. * Can result in renal osteodystrophy. (Ca pulled to buffer)
54
How is metabolic acidosis treated in CKD?
Oral sodium bicarb to maintain bicarb > 21 mEq/L.
55
What is uremic encephalopathy and the suggested treatment?
Aggregration of uremic toxins, resulting in neurologic dysfunction. Requires dialysis to get rid of the toxins.
56
How does uremic neuropathy typically present?
* Sensory before motor * Loss of position and vibration in toes. * Paresthesias, burning, pain * Muscle atrophy => paralysis
57
How is uremic neuropathy diagnosed and what is the treatment?
Requires EP studies to determine nerve changes. Usually treated with dialysis. Can give TCAs or anticonvulsants to help with symptoms.
58
What kind of glucose abnormality can occur in CKD and why?
Increased risk of hypoglycemia due to decreased renal clearance of insulin.
59
What common DM medication needs to be used in caution in CKD and why?
Metformin cannot be used in patients with a serum Cr < 1.4 or GFR < 30 due to the increased risk of lactic acidosis.
60
What reproductive abnormalities can occur in CKD?
* Decreased libido * ED * Pregnancy preemies
61
What diet restrictions are recommended for people with CKD?
* 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. ## Footnote Too much sodium will lead to HTN and edema. (3-4g) Too little leads to hypotension. (1g)
62
What drug classes should be avoided in CKD patients?
* Renally excreted drugs (Monitor) * Mg-containing: antacids or laxatives. * Phosphorus-containing * Nephrotoxic: NSAIDs, IV contrast * Morphine: accumulates with late stage CKD
63
When is dialysis generally indicated in terms of CKD?
GFR of 5-10 mL/min/1.73m2.
64
Differentiate hemodialysis (HD) vs peritoneal dialysis (PD).
* HD is a few hours at a dialysis center. * PD is for 30 minutes, 4 times a day at home. ## Footnote PD requires abdominal access. HD requires arm access or central port access.
65
What are the indications for dialysis for a CKD patient?
* GFR < 10 * Uremic symptmos * Metabolic disturbances refractory to therapy * Fluid overload unresponsive to diuretics
66
What is the ideal renal replacement therapy? (RRT)
Transplantation
67
How does HD work?
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
What are the 3 ways to get access for HD?
* 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
How does PD work?
* 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
What are the two types of PD?
* Continuous ambulatory peritoneal dialysis (CAPD): 4-6x a day manually. * Continuous cyclic peritoneal dialysis (CCPD): Runs at night
71
What are the biggest pros and cons of PD?
Pros: * Autonomy * Less diet restrictions * No travel Cons: * Removes a lot of albumin * Peritonitis risk * Patient needs to manage the machine.
72
What is peritonitis?
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
What is the most common cause of death for patients on dialysis?
Cardiac disease ):