Chronic Renal Disease Flashcards

1
Q

What is the definition of chronic kidney disease?

What is the hallmark of CKD?

A
  • a permanent reduction in glomerular filtration rate. Permanent is anything that last longer than 3 months. So an AKI that lasts 3 months becomes CKD.
  • a loss of flexibility in responding to changes in external balance of solutes and water (have trouble adapting to eating a salty big mac etc).
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2
Q

describe the stages in the classification system of CKD.

A
  • stage 1 (Normal GFR with kidney damage): GFR >/=90. There is evidence of kidney damage.
  • stage 2 (Normal GFR with kidney damage): GFR= 60-89. There is evidence of kidney damage.
  • stage 3 (mild): GFR= 30-59
  • stage 4 (moderate): GFR= 15-29
  • stage 5 (severe): GFR
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3
Q

What are the two most common causes of CKD? which one is the most common?

A
  • diabetic nephropathy (most common)

- hypertensive nephrosclerosis & Renal vascular disease

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4
Q

What does it mean to say that CKD is ‘silent’. Why is CKD ‘silent’?

A

patients are often asymptomatic until the kidneys are super bad. Can feel good when only at around 10% of kidney fxn sometimes.

  1. intact nephron hypothesis: Many nephrons are damaged and non-functional. The extra ones work in overdrive to keep the filtration and net excretion coordinated.
  2. magnification phenomenon: Because they are over worked they must alter the handling of certain solutes to maintain external balance of that solute. They to do this until kidney disease gets real bad (stage 4ish).
  3. individual solute control systems: there are individual control systems (like hormones) to help control electrolytes when needed.
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5
Q

Small shrunken kidneys are indicative of ______(acute/chronic) kidney disease.

A

chronic.

takes a little while to develop.

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6
Q

what happens to creatinine over time with a slow loss of GFR?

A

always in creatinine balance.

When GFR drops we get back to a steady state at the expense of increased serum creatinine. In CKD we are in a steady state, unlike in AKI (this is why can’t use GFR equations in AKI).

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7
Q

T or F. water handling is passive in the kidney.

A

F. It is an active process.

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8
Q

What is the normal range of urine dilution for the Kidney? What is the range for a failing kidney?

A

Normal:

  • maximum dilution: 50 mosm/L
  • maximum concentration: 1200 mosm/L

Failing Kidney:

  • maximum concentration: 300 mosm/L
  • maximum dilution: 200 mosm/L
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9
Q

what is the normal idea behind sodium handling in the kidney? How does this change in CKD?

A

-kidney excretes sodium you eat. fraction of sodium reabsorbed and excreted are changed to stay in balance.

  • kidneys is unable to rapidly respond to changes in sodium intake or extra renal losses.
    Inc. Na intake –> edema
    Major decreases in Na–> volume depletion.

so we see that flexibility in handling substances gets greatly diminished in failing kidney (CKD).

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10
Q

what adaptive processes does the kidney have to overcome the effects of CKD with respect to K balance?

A
  1. inc. tubular flow
  2. inc. solute load per nephron
  3. inc. Na delivery (exchange more Na distally allows you to excrete K).
  4. inc. aldosterone (increases secretion and excretion of K).

This works until CKD is severe and then patient gets inc. fecal excretion of k (50%).

Patients can become hyperkalemic with CKD.

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11
Q

How does acid balance work in a normal kidney?

A

acid is generated during the normal metabolic process (about 1meq/kg per day).

It is then excreted via:

  • NaH2PO4-
  • free hydrogen ion (H+)
  • NH4+
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12
Q

How does acid balance work in a CKD kidney?

What condition does this cause

A

nephrona are lost and the remaining nephrons compensate by increasing their net acid excretion by producing more NH3 (acid leaves as NH4+).

in CKD we start to see metabolic acidosis if the kidney fxn falls below 25% of normal. Bc the kidney is not secreting enough NH3 to clear H+.

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13
Q

Explain what happens to Calcium, Phosphorus, and PTH in CKD?

A

In CKD, the phosphate usually increases. high phosphate starts everything in the cascade.

Early on, high phosphate causes an increase in FGF-23 and PTH (these work to excrete phosphate in the urine).

Also, high phosphate causes the FGF-23 to rise which leads to low 1,25 vitamin D. This leads to low calcium which in turn increases PTH.

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14
Q
  1. what is uremia (as defined by this lecturer)?
  2. how do we measure it?
  3. What things are overproduced in a uremic state?
  4. underproduced?
A
  1. systemic intoxication
  2. Urea (other solutes accumulate but this is the easiest to measure.
  3. counter-regulatory hormones- PTH
  4. kidney hormones- erythropoietin and 1,25 vit. D
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15
Q

almost every CKD patient has _____ when GFR is

A

anemia.

erthyropoiesis is marekedly decreased bc of reduced production from kidney. Toxins in blood shorten RBC life. Uremia decreases iron absorption so can get anemia that way also.

Dialysis patients can get blood loss and marrow space fibrosis from secondary parathyroidism which causes anemia.

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16
Q

what are the most common systemic problems related to CKD?

A
  • hypertension- very common. occurs bc of expansion of ECF.

- bone and marrow disorders- fractures and pain

17
Q

According to the intact nephron hypothesis, surviving nephrons take on a bigger workload to make up for dead nephrons. What compensatory changes occur to allow them to do this?

A
  • glomeruli hypertrophy
  • blood flow per nephron increases
  • intra-glomerular pressure increases
  • solute flow per tubule increases.
18
Q

net acid excretion falls in stage ___. renal replacement therapy is needed in stage __.
Most other symptoms (HTN, anemia, volume overload, etc.) occur around stage ____.

A
  • 4
  • 5
  • 3
19
Q

CKD leads to a huge ___ risk.

A

cardiovascular disease. patients with CKD should be considered in the highest risk group for CVD.

20
Q
  1. What are most important principles for management of CKD?

What is the most important factor in decreasing the progression of kidney disease? is the goal level to get it to?

A
    • delay CKD progression
      - treat complications of CKD
      - screen for and treat CVD risk
      - prepare for dialysis
  1. BP control (reduces CVD risk and proteinuria). 130/80
21
Q

How do we control BP in CK (what drugs, what do we treat)?

A

patients need at least 3 different drugs including an ACEi or an ARB. These help to slow progression but don’t completely stop progression.

we should also try to treat the metabolic acidosis

22
Q
  1. At what stage do we select a site for dialysis access and preserve veins?
  2. place an AVF?
  3. graft or catheter?
  4. restrict dietary phosphorus?
  5. give an ACEi or an ARB?
A
  1. stage 3
  2. stage 4
  3. stage 5
  4. stage 3 (GFR around 60)
  5. stage 1 all the way through the disease process (trying to slow progression of co-morbid conditions