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Urogenital 2 > Chronic Kidney Disease > Flashcards

Chronic Kidney Disease Flashcards

1
Q

How id CKD defined?

A

CKD is defined by the presence of markers of kidney damage or decreased kidney function.
eGFR < 60
Persistent for 3 or more months.

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2
Q

What are markers of kidney damage?

A 
Albuminuria
Urinary sediment abnormality
Electrolyte abnormality due to tubular disorder
Abnormality of histology
Structural abnormality
History of kidney transplantation
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3
Q

What are the stages of CKD?

A

G1, G2 - markers of kidney dysfuntion
G3a, G3b
G4
G5

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4
Q

What is the eGFR of end stage kidney disease? (kidney failure)

A

GFR < 15ml/min

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5
Q

What are the treatment options for a patient with end stage kidney disease?

A

Transplant
Dialysis
Conservative care

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6
Q

What hormones are synthesised by the kidneys?

A

EPO
Vitamin D activation
Renin

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7
Q

Kidney failure is a risk factor for what?

A

Cardiovascular mortality

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8
Q

Pallor

A

Unhealthy pale like appearance

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9
Q

Who should be tested for CKD?

A

Patients with diabetes, hypertension, Haematuria, patients taking nephrotoxic medication e.g NSAIDs, lithium.

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10
Q

Why is early diagnosis of CKD important?

A

Enables slow down of the progression of CKD.

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11
Q

What investigations are carried out in cases of suspected CKD?

A

Tests determining filtration
Urine testing
Scanning of kidneys
Kidney biopsy

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12
Q

Markers of kidney dysfunction are:

A 
Reduction inf GFR
Blood and protein in the urine - albuminuria
Scan of kidneys showing: 
     small kidneys
     polycystic kidneys
     hydronephrosis
Kidney transplant
Histological abnormalities
ACR >3mg/mmol
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13
Q

What are the main tests for kidney dysfunction?

A 
Creatinine 
eGFR
Creatinine clearance
GFR measurement
Cystatin C measurement and Cystatin C eGFR
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14
Q

What is ACR?

A

Albumin : Creatinine ratio

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15
Q

What is a normal to high GFR?

A

> 90ml/min

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16
Q

What is the GFR of someone with G2 CKD?

A

60-89ml/min

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17
Q

What is the GFR of someone with G3a CKD?

A

45-59ml/min

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18
Q

What is the GFR of someone with G3b CKD?

A

30-44ml/min

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19
Q

What is the GFR of someone with G4 CKD?

A

15-29ml/min (severe)

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20
Q

What is the GFR of someone with G5 CKD?

A

<15ml/min (kidney failure)

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21
Q

What is an A1 ACR?

A

<3mg/mmol

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22
Q

What is an A2 ACR?

A

3-30mg/mmol

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23
Q

What is an A3 ACR?

A

> 30mg/mmol

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24
Q

Azotemia

A

Abnormally high levels of urea in the blood.

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25
Q

What are the two most common causes of CKD?

A

Hypertension

Diabetes

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26
Q

How does hypertension cause CKD?

A

Causes the walls of the renal artery to thicken leading to a narrower lumen so less blood is supplied to the kidney. This leads to ischaemic injury to the neprhons glomerulus.

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27
Q

How does ischaemic injury to the nephron result in glomerulosclerosis?

A

Macrophages migrate to the damaged nephron and secrete growth factors such as TGFbeta.
TGFbeta causes mesangial cells to regress back into mesangioblasts.

Mesangioblasts secrete excess extracellular matrix leading to glomerulosclerosis.

28
Q

How does diabetes cause narrowing of the efferent arteriole?

A

The excess glucose sticks to proteins on the efferent arteriole wall in non-enzymatic glycation. This causes the efferent arteriole to become stiff and more narrow.
This process is known as hyaline arteriosclerosis.

29
Q

How does hyaline arteriosclerosis lead to CKD?

A

The narrowing of the efferent arteriole makes it harder for blood to leave the glomerulus, and increases pressure within the glomerulus leading to hyperfiltration.

Mesangial cells then secrete more ECM causing glumerulosclerosis diminishing the kidneys ability to filter the blood and causing CKD.

30
Q

Glumerulosclerosis

A

Glomerulosclerosis is hardening of the glomeruli in the kidney. It is a general term to describe scarring of the kidneys’ tiny blood vessels, the glomeruli. This leads to decreased GFR’s (CKD).

31
Q

How does CKD lead to azotemia?

A

Decreased GFR means less urea gets filtered out the blood.

32
Q

Build up of urea in the blood is

A

Azotemia

33
Q

Excessive azotemia leads to what?

A

Encephalopathy
~ asterixis
Pericarditis
Uremic frost

34
Q

Asterixis

A

Tremor of the hand best seen when extending the hand

35
Q

Uremic frost

A

Deposition of urea in the skin appears like crystals

36
Q

In CKD how do levels of potassium and calcium change?

A

You get high potassium levels and low calcium.

37
Q

How does CKD lead to hyperkalaemia?

A

Decreased GFR means less potassium is excreted and so more potassium builds up in the blood.

38
Q

How does CKD lead to hypocalcemia?

A

In CKD less active vitamin D is produced. Vitamin D helps with calcium uptake in the diet, therefore less calcium is absorbed into the blood.

39
Q

Explain the effect CKD has on bones.

A

Hypocalcemia causes more parathyroid hormone to be released this causes the bones to lose calcium resulting in renal osteodystrophy (the bones become weak and brittle).

40
Q

How does low GFR affect blood pressure?

A

When the kidneys sense a low GFR they respond by releasing renin. Renin results in increased blood pressure. This leads to hypertension which in turn worsens CKD.

41
Q

How does CKD cause anaemia?

A

CKD leads to a decrease in EPO produced by the kidneys leading to less red blood cells being produced.

42
Q

Enuresis

A

Involuntary urination

43
Q

What is high pressure urinary retention characterised by?

A

High pressure chronic retention is characterised by late onset enuresis, a tense, palpable bladder, hypertension, and progressive renal impairment associated with bilateral hydronephrosis and hydroureter commonly leading to uraemia and death.

44
Q

In urinary retention what do the terms high and low pressure refer to?

A

The terms “high” and “low” refer to the bladder pressure at the end of voiding.

45
Q

How does high pressure urinary retention affect the upper renal tract?

A

HPUR leads to a back up through the ureters into the upper renal tract.

46
Q

What can HPUR lead to?

A

Hydroureter and hydronephrosis

47
Q

Hydroureter

A

Dilation of the ureter

48
Q

Hydronephrosis

A

Swelling of the kidney due to a build up of urine. Occurs when urine cannot drain out from the kidney to the bladder.

49
Q

Hyperphosphataemia causes what?

A

Arrythmyias

50
Q

Build up of lactate results in what?

A

Shortness of breath

51
Q

What is the first step of Diabetic neuropathy causing CKD.

A

Non-enzymatic glycation of the efferent arteriole.

52
Q

The loss of Nephrons in CKD is irreversible.

A

The loss of Nephrons in CKD is irreversible.

53
Q

What is CKD a major risk factor for?

A

Cardiovascular disease and mortality.

54
Q

Read how CKD can cause normochromic and normocytic anaemia:

A
  • Erythropoietin deficiency – this is the most significant mechanism.
  • Increased blood loss – there may be occult gastrointestinal bleeding, repeated blood sampling, blood loss during haemodialysis, or platelet dysfunction.
  • Bone marrow toxins – these are retained in CKD, or there is fibrosis secondary to hyperparathyroidism.
  • Haematinic deficiency – there may be decreased iron, vitamin B12 or folate.
  • Increased red-cell destruction – red cells have a shortened lifespan in uraemia, and haemodialysis itself may cause a degree of haemolysis.
  • ACE inhibitors – these may cause anaemia in CKD, probably by interfering with the control of endogenous erythropoietin release.
55
Q

CKD mineral and bone disorder

A

Mineral and bone disorder in CKD occurs when damaged kidneys and abnormal hormone levels cause calcium and phosphorus levels in a person’s blood to be out of balance - ultimately this leads to osteopenia.

56
Q

Explain the pathology of how CKD leads to osteopenia.

(Read and understand).

A

Osteopenia mainly results from secondary hyperparathyroidism which occurs as follows:

  • Decreased renal production of 1α-hydroxylase results in reduced conversion of 25-(OH)2D3 to the more metabolically active 1,25-(OH)2D3 (1,25-dihydroxycholecalciferol).
  • 1,25-(OH)2D3 deficiency results in reduced gut calcium absorption and a fall in calcium.
  • Reduced activation of vitamin D receptors in the parathyroid glands by 1,25-(OH)2D3 increases the release of PTH.
  • Calcium-sensing receptors, expressed in the parathyroid glands, react rapidly to acute changes in extracellular calcium concentrations, and a low calcium triggers increased PTH release.
  • Retained phosphate also indirectly lowers ionized calcium (and probably directly via a putative but unrecognized phosphate receptor), resulting in increased PTH synthesis and release.
  • PTH promotes reabsorption of calcium from bone and increased proximal renal tubular reabsorption of calcium. This mechanism attempts to reverse the hypocalcaemia caused by 1,25-(OH)2D3 deficiency and phosphate retention.
57
Q

In what ways does CKD affect the cardiovascular system?

A

Hypertension, sudden cardiac death, myocardial infarction, cardiac failure, stroke and peripheral vascular disease all occur in excess as GFR declines.

58
Q

How can pericarditis be caused by CKD?

A
  • Uraemic pericarditis is a feature of severe, pre-terminal uraemia or of under-dialysis. Haemorrhagic pericardial effusion and atrial arrhythmias are often associated. There is a danger of pericardial tamponade, and anticoagulants should be used with caution. Pericarditis usually resolves with intensive dialysis.
  • Dialysis pericarditis occurs as a result of an intercurrent illness or surgery in a patient receiving apparently adequate dialysis.
59
Q

What are the general managements of CKD?

A
  • As always, make a diagnosis, and treat any modifiable underlying cause.
  • Address cardiovascular risk factors – in particular, smoking cessation, exercise and weight loss.
  • Avoid nephrotoxic drugs (see below).
  • Arrange systematic follow-up, depending on the stage of CKD, to identify those most likely to progress early.
60
Q

Summarise Glomerulonephritis

A

Caused by: a pathology in the glomerulus.
Symptoms: Haematuria and proteinuria
Causes: CKD can progress to kidney failure.

61
Q

Complications of CKD:

A

Anaemia
Renal bone disease
Cardiovascular disease

62
Q

How are CKD complications treated?
Anaemia
Bone disease

A

Oral sodium bicarbonate to treat metabolic acidosis
Iron supplementation and erythropoietin to treat anaemia
Vitamin D to treat renal bone disease
Dialysis in end stage renal failure
Renal transplant in end stage renal failure

63
Q

What medication is first line for CKD?

A 
ACE inhibitors are the first line in patients with chronic kidney disease. These are offered to all patients with:
Diabetes plus ACR > 3mg/mmol
Hypertension plus ACR > 30mg/mmol
All patients with ACR > 70mg/mmol
Aim to keep blood pressure <140/90
64
Q

What needs to be monitored in CKD patients on an ACE inhibitor?

A

Hyperkalemia

65
Q

Read summary of bone disease in CKD:

A

High serum phosphate occurs due to reduced phosphate excretion. Low active vitamin D because the kidney is essential in metabolising vitamin D to its active form. Active vitamin D is essential in calcium absorption from the intestines and kidneys. Vitamin D also regulates bone turnover.

Secondary hyperparathyroidism occurs because the parathyroid glands react to the low serum calcium and high serum phosphate by excreting more parathyroid hormone. This leads to increased osteoclast activity. Osteoclast activity lead to the absorption of calcium from bone.

Osteomalacia occurs due to increased turnover of bones without adequate calcium supply.

Osteosclerosis occurs when the osteoblasts respond by increasing their activity to match the osteoclasts by creating new tissue in the bone, however due to the low calcium level this new tissue is not properly mineralised.

Osteoporosis can exist alongside the renal bone disease due to other risk factors such as age and use of steroids.

66
Q

How is bone disease in CKD managed?

A

Active forms of vitamin D (alfacalcidol and calcitriol)
Low phosphate diet
Bisphosphonates can be used to treat osteoporosis

Urogenital 2 (22 decks)

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