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Flashcards in Complications of CKD Deck (27):
1

What are the complications of CKD?

Accumulation of waste products

Salt and water retention

High blood pressure

Metabolic acidosis

Hormone disturbaces

2

Examples of hormonal disturbances triggered by CKD

Secondary hyperparathyroidism

Bone disease

3

Why does fluid accumulate in CKD?

The ability for the tubule to filter water and sodium breaks down

Water and salt retention leads to fluid accumulation

4

What are clinical ways to pick up fluid accumulation?

Press on skin - leaves dent due to presence of water

Pulmonary oedema - can hear crackles via stethoscope

5

How does CKD affect blood pressure?

CKD leads to secondary hypertension

Secondary hypertension causes more kidney injury

6

What causes secondary hypertension in CKD?

Fluid retention

Activation of the renin-angiotensin system

Excess renin production

Increased sympathetic activity

7

What are the consequences of hypertension?

Left ventricular hypertrophy

Heart failure - many patients with CKD die from heart failure rather than kidney failure

8

What is metabolic acidosis?

When kidney are not removing enough acids from the body, so there is a build up of acid in the blood

9

Why does CKD lead to metabolic acidosis?

There is diminished excretion of non-volatile acids

Increased loss of bicarbonate ions

10

What do patients with metabolic acidosis present wit clinically?

Hyperventilation

To remove the carbon dioxide from the system - pushes to form less carbonic acid

11

Which hormones do kidneys control?

EPO

Vitamin D

12

What stimulates EPO production from the kidney?

Decreased blood oxygen

13

What is the role of EPO?

Acts in the bone marrrow to increase numbers of RBC precursors

14

What happens to EPO production during CKD?

EPO concentration decreases

There is less RBC precursor production

Less RBC in the blood

15

What condition stems from the decreased EPO synthesis?

Normochromic normocytic anaemia

16

What does normochromic normocytic anaemia mean?

Normochromic - normal shape

Normocytic - normal size

The RBC are normal, there are just less produced than what is needed

17

How is vitamin D metabolised in the body?

Vitamin D is obtained from the gut or skin

FIrst it is hydroxylated in the liver to form 25(OH)D

Then it passes to the kidneys and is hydroxylated to 1,25(OH)2D - active form

18

What does PTH do?

Maintains bone turnover

19

What do patients with CKD have in context to PTH?

Secondary/ tertiary hyperthyroidism

20

What is the pathogenesis of secondary/ tertiary hyperthyroidism?

Kidneys diseases and becomes smaller

Therefore it releases less active form of vitamin D -> 1,25(OH)2D

Parathyroid gland has receptor for this molecule -> negative feedback loop

There is a compensatory increase in the PTH released

The parathyroid gland becomes hypertrophied and autonomous -> releases PTH regardless of stimulus

21

What is the condition called when the parathyroid gland releases PTH regardless of the stimulus?

Tertiary hyperthyroidism

22

What are the clinical presentations of hyperthyroidism?

Bone erosion

Bone fracturing

Hypercalcemia

23

What other hormone does the parathyroid release?

FGF23

24

What is FGF23?

A fibroblast growth factor

25

How does FGF23 affect 1,25-vitD levels?

Decreases the release of the vitamin D intermediate

26

What stimulus causes FGF23 to be released?

An increase in blood concentration of vitamin D active intermediate

An increase in phosphate concentration in the blood

27

How does CKD affect FGF23 release?

Inhibits reabsorption of phosphate from the urinary tract

Blood concentration of phosphate decreases

FGF decreases 1,25-vitD release - there is an increase in PTH release (negative feedback loop)

Phosphate also binds directly to receptors on the parathyroid - increases PTH release