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sem 2 year 2 > Kidney conditions > Flashcards

Kidney conditions Flashcards

1
Q

What are the total body water volumes of men and women?

A

Men= 60% water, 42 litres
Women= 55% water, 38 litres

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2
Q

How much water a day is lost via sweat and evaporation?

A

Around 500ml a day- if unwell with a fever can lose upto 1L

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3
Q

How is water pushed in and out of cells?

A

Drawn due to osmotic pressure, pushed out to hydrostatic pressure

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4
Q

What are the names for patients who are volume deplete, volume overloaded or normal volume?

A

Volume deplete= hypovolaemic
Volume overloaded= Hypervolaemic
Normal= euvolaemic or normovolaemic

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5
Q

What are the 3 states of hyponatraemia that can occur?

A

Norvolaemic hyponatraemia
Hypovolaemic hyponatraemia
Hypervolaemic hyponatraemia

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6
Q

What happens when there is a increase of water in all compartments?

A

No clinical signs- is harder to spot

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7
Q

In what clinical scenarios does fluid loss occur?

A

Haemorrhage
Burns, water can evaporate
Vomiting- can lose a lot of salt. Same as diarrhoea
Diuretic states e.g. diabetes
Sequestration= pleural space in body is inflammaned and holds water in it
Iatrogenic- diuretics, stroma’s/fistulae and gastric aspiration

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8
Q

In what clinical scenarios does fluid gain occur?

A

Heart and liver failure
Renal failure- pass a reduced amount of urine
Hypothyroidism; unknown why. Oedema common
Psychogenic polydipsia
ADH excess
Iatrogenic= IV fluids, supplemental nutrition

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9
Q

What are the different ways hyponatraemia can occur?

A

Pure water gain
When water gain > Na+ gain
When Na+ loss > water loss
Or pure Na+ loss (not possible)

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10
Q

What conditions cause pure water gain?

A

SIADH, hypothyroidism and iatrogenic causes
Appears as normovolaemic as all compartments swell so hard to detect

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11
Q

What is hypovolaemia and hypervolaemia caused by?

A

Hypo= when Na+ loss > water loss
Hyper= When water gain > Na+ gain

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12
Q

What are the clinical symptoms of hypovolaemia?

A

Postural hypotension
Tachycardia
Reduced skin turgor
Organ failure

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13
Q

What are the clinical symptoms of hypervolaemia?

A

Hypertension
Tachycardia
Peripheral and pulmonary oedema
Organ failure

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14
Q

What type of hyponaetraemia is caused by diahorrea?

A

Hypovolaemic hyponatraemia
Excessive sodium losses; water losses are insufficient to concentrate sodium back up

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15
Q

What happens in euvolaemic hyponatraemia?

A

Water is distributed across all compartments

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16
Q

What happens in heart failure?

A

The pump stops working, and there is a reduced circulatating pressure and reduced organ perfusion.
The coresponding blood pressure mechanisms switch on, even though there is enough volume
There is renin/angiotensin/aldosterone/ADH stimulation, causing more water retetion

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17
Q

What is the vicious cycle of heart failure?

A

Retaining more water so there is more blood volume
However the weakened left ventricle cannot pump all that volume of water and the blood is very dilute
This causes the osmolaric pressure to pull water into the extracellular space
This leaves the blood volume low- cycle starts again

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18
Q

What is SIADH?

A

Syndrome of inappropriate ADH secretion- where the body makes too much ADH and there is water retention

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19
Q

What are the causes of SIADH?

A

Intracranial lesions, infection or inflammation of brain, antipsychotics, sedatives, pain and nausea

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20
Q

What is the treatment of SIADH?

A

Restrict fluids
Vasopressin antagonists- vaptans

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21
Q

What can cause hypervolaemic hyponatraemia?

A
  • Heart failure
  • Liver failure
  • Nephrotic syndrome
    Where water gains exceed sodium gains
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22
Q

What is the common treatment of hypovolaemia and hypervolaemia?

A

Hypo= restoration of volume state, blood and saline solution. Cessation of diuretics
Hyper= Diuretics, fluid restriction and treatment of underlying cause

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23
Q

What is the treatment for euvolaemia hyponatraemia?

A

Treat underlying cause
Stop IV fluids
Fluid restriction
Rarely= demeclocycline

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24
Q

What is the commonest form of malignancy that causes SIADH?

A

Small cell lung cancer

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25
Q

What are the different ways that hypernatraemia can occur?

A

Pure water loss
Water gain < water loss
Na loss < water loss
Pure Na gain

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26
Q

What state of volaemia is usually the case in hypernatraemia?

A

Hypovolaemia

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27
Q

Why can hypernatraemia occur with a stoma?

A

Salt is absorbed in the small bowel, left in colon is water and fibre. If there is a stoma you will lose alot of water but the salt has already been reabsorbed

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28
Q

Why does hypovolaemia occur in hypernatraemia?

A

There is water loss and thus a high conetration of salt in the blood. Osmotic pressure pulls water out from the cells

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29
Q

What are specific causes of hypernatraemia?

A

Water loss= fever, hyperventilation, diabetes insipidus
Reduced water intake= iatrogenic, psychosocial, stroke, coma, confusion
High sodium intake= IV fluids high in salt, emetics

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30
Q

What are emetics?

A

fluids with high conc of sodium that makes you vomit. Used to be given as treatment for people who had taken an overdose. Largely not used

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31
Q

What is the main cause of patients becoming dehydrated whilst in hospital?

A

Due to lack of access to water or no supplemental water given whilst they were in hospital

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32
Q

What is diabetes insipidus?

A

Failure of production of ADH (cranial) or inactivity of receptors (nephrogenic). Free water loss occurs, sodium becomes concentrated and hypernatraemia occurs
There is a failed feedback mechanism

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33
Q

What are the causes of cranial diabetes insipidus?

A

Pituitary tumour, head injury, meningitis, genetic and idiopathic

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34
Q

What are the causes of nephrogenic diabetes insipidus?

A

Reduced tubular response- inherited or drugs such as lithium

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35
Q

What is the treatment of diabetes insipidus?

A

Hydration= tends to cause polyuria
Desmopressin= for cranial. Synthetic ADH
NSAIDs and diuretics may help for nephrogenic but results are unsatisfactory

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36
Q

What are the different plasma and urine osmolarities for DI and SIADH?

A
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37
Q

What is given instead of water via an IV?

A

Dextrose 5%.
It is isotonic to plasma. Due to sugar, insulin is produced which will drive glucose into cells and water will follow

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38
Q

What can occur with rapid correction of hyponatraemia?

A

Central ponine myelinosis.
Symptoms= confusion, slurred speech, sensory problems and paralysis

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39
Q

What are the clinical symptoms and signs of volume depletion?

A

Volume depletion= thirst, dizziness, dysphagia, weakness, confusion, aggression and coma
Signs- postural hypotension, tachycardia, absence of JVP, reduced skin turgor, supine hypotension, oliguria and organ failure
Skin turgor= will be increased in elderly

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40
Q

What are the clinical symptoms and signs of volume excess?

A

Volume excess= localized discomfort, dyspnoea, confusion, aggression, coma, nausea
Signs= hypertension, tachycardia, raised JVP, oedema and organ failure
Odema can be commonly in ankles or in back whilst lying down. To be odema needs to be able to be displaced

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41
Q

What are the clinical manifestations of hypercalcaemia?

A

‘Stones, bones, aldominal moans and pyschic groans’
Muscle weakness, renal stone formation, abdominal pain, ECG changes, impaired water concentration in the urine, and central effects such as anorexia, nausea, mood changes.

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42
Q

Why is there muscle weakness in hypercalcaemia?

A

Competition betweem Na and Ca entering muscles

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43
Q

What are the ECG changes that occur in hypercalcaemia?

A

Shortened QT interval, risk of arrythmias

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44
Q

What is factitious hypercalcaemia?

A

Raised calcium due to high plasma albumin (venous stasis, dehydration and IV albumin can cause this)
Therefore it is important to interpret calcium and albumin levels together

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45
Q

What is hyperparathyroidism?

A

Causes hypercalcaemia
Can be due to solitary ademona, hyperplasia, carcinoma. Causes high levels of PTH to be produced and more calcium retained

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46
Q

What are the different types of hyperparathyroidism?

A

Primary= adenoma or hyperplasia of glands. Oversecretion of PTH despite normal Ca levels
Secondary= oversecretion of PTH in result to low Ca levels (due to chronic kidney disease or Vit D deficiency)
Tertiary= may occur following a prolonged period of secondary hyperparathyroidism. In response to chronic PTH secretion, the glands may become hyperplastic and begin to secrete PTH autonomously.

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47
Q

What are the blood tests for the 3 types of hyperparathyroidism?

A

Primary= increased PTH, increased Ca
Secondary= increased PTH, low Ca
Tertiary=increased PTH, increased Ca

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48
Q

What happens to the body in hyperparathyroidism?

A

Renal stones full of calcium precipitate can form
Loss of normal bone structure- osteopenia as bone becomes more reabsorbed and is weak

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49
Q

What is the diagnosis of primary hyperparathyroidism?

A

Raised Ca with raised PTH
Phosphate and bicarbonate tend to be low due to increased renal excretion
Alkaline phosphate normal or moderatly increased (bone marker)

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50
Q

What investigations can be done to prove primary hyperparathyroidism?

A

Parathyroid imaging scans using radio-isotopes
Use technicium

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51
Q

What is the treatment for primary hyperparathyroidism?

A

Re hydration and drugs such as bisphosphonates, furosemide, calcitonin and glucocorticoids
Surgery to remove adenoma

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52
Q

Why do 20-30% of cancer patients develop hypercalcaemia?

A

Endocrine factors secreted by malignant cells act on bone
Metastatic tumour deposits in bone, stimulating bone resoption via osteaclast activation

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53
Q

What endocrine factors are released from malignancies that cause hypercalcaemia?

A

Solid tumours may secrete PTH-related peptide (PTHrP) which are structuarally similar to PTH and shares simlar actions

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54
Q

What is ig called when PTHrP is the cause of hypercalcaemia?

A

Humoral hypercalcaemia of malignancy

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55
Q

What is malignant hypercalcaemia associated with and why?

A

Bony metastases
Secretion of osteoclast activating cytokines

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56
Q

What is multiple myeloma?

A

A type of bone cancer- cancer of the plasma cell

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57
Q

What happens to bone in multiple myeloma?

A

Hypercalcaemia is produced in patients with multiple myeloma due to the increased bone resorption caused by osteoclast activation, especially due to the hyperactivity of the RANK/RANK-L receptor.
Causes breakdown of bone- weakens the bones

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58
Q

What can happen specifically to the skull in multiple myeloma?

A

Pepperpot skull-

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59
Q

What do blood tests show when a patient has hypercalcaemia due to malignancy?

A

Raised Ca with supressed PTH
Phosphate tends to be high, alkaline phosphate may be very high

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60
Q

What is sarcoidosis?

A

A disease that causes granulomas (full of immune cells). Increases calcium levels leading to hypercalcaemia

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61
Q

What is familial hypocalciuric hypercalcaemia?

A

The calcium sensor on the parathyroid gland is less sensitive to Ca supression of PTH
PTH levels tend to be high normal or slightly raised.

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62
Q

What are the clinical neuromuscular affects of hypocalcaemia?

A

Numbness, tingling in fingertips and toes
Fatigue
Muscle cramps, bronchial or laryngeal spasm
Seizures

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63
Q

What are the mental state symptoms of hypocalcaemia?

A

Personality change
Mental confusion
Anxiety
Impaired intellectual ability

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64
Q

What can happen to the eye in hypocalcaemia?

A

Cloudiness of the lense

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65
Q

What happens to the ECG in hypocalcaemia?

A

Prolongation of the QT interval

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66
Q

Why do the main clinical symptoms of hypocalcaemia occur?

A

Predominantly due to an increase in neuromuscular excitability- when Ca are absent, there is a decrease in the threshold needed for the activation of neurons

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67
Q

What tests can be done to check for hypocalcaemia?

A

Chvostek’s sign= tap along facial nerve, will see contraction of the muscles of the eye
Trousseau’s sign= Brachial artery is occulded by a blood pressure monitor and will see spasm

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68
Q

What causes factitious hypocalcaemia?

A

Consequence of low plasma albumin from malnutrician, liver disease, nephrotic syndrome or malabsorbsion

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69
Q

What are the common causes of deficient Vit D or inaction of vit D?

A

Lack of sunlight
Inadequate dietary source
Malabsorpsion
Chronic renal disease

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70
Q

What are the effects of vit D deficiency on calcium metabolism?

A

Low vit D= low absorsion of calcium
Low blood calcium is detected by parathyroid; releases PTH which causes increased bone resorption and increased phosphate wasting
This can lead to problems with bones- osteomalacia/rickets

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71
Q

Where is vit D activated to its active form?

A

Vitamin D is metabolized sequentially in the liver and kidneys into 25-hydroxyvitamin D which is a major circulating form and 1,25-dihydroxyvitamin D or calcitriol

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72
Q

What is osteomalacia?

A

Pathological bone problem clssically associated with vit D deficiency
Osteoid laid down by osteoblasts is not adequately calcified
Bones are softened, weake and susceptible to fracture
Known as rickets in children

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73
Q

What are the symptoms of rickets?

A

Boney deformity- bowing of legs and widening of cartilage at growth plates e.g. wrists
Bone pain and weakness

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74
Q

What are the inherited causes of osteomalacia or rickets?

A

Deficient 1-hydroxylase
Defective receptor for calcitriol
Hypophosphataemic

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75
Q

What is the biochemistry of hypoparathyroidism?

A

Low Ca
Innappropriately low PTH
Phosphate may be raised

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76
Q

What are the causes opf hypoparathyroidism?

A

Surgical damage to PT
Drugs
Developmental parathyroid problems or genetic conditions e.g. DiGeorge syndrome

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77
Q

What are the principles of treating hypocalcaemia?

A

In acute situations, IV calcium can be given to stop arrythmias
Normally oral calcium and vit D are given

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78
Q

What is osteoporosis?

A

Weakening of bone- reduced bone mineral density and disruption of the microarchitecture
Increased risk of fracture
Routine biochemistry unaffected

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79
Q

What is the differences between osteoporosis and osteomalacia?

A
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80
Q

What is used to assess bone mineral density and diagnose osteoporosis?

A

Dual-energy X-ray absorptiometry (DEXA)
Scoring system measures bone loss against that of a healthy adult- number of SDs between these
-1 or above are normal, -1.1 – 2.4 is osteopenia and -2.5 and below is OP

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81
Q

What are the different forms of Vit D?

A

Cholecalciferol, calcidiol and calcitriol

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82
Q

What happens when plasma calcium falls?

A

PTH released- causes Ca reabsorption in the loop of henle, DCT and collecting duct
Vit D3 activation in kidney which stimulates Ca2+ intestinal absorption
Bone reabsorption by OCs and releases free Ca

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83
Q

How is calcium present in the plasma?

A

Three compartments-

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84
Q

How do you account for albumin bound calcium when calculating corrected calcium?

A

Albumin is in g/L

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85
Q

What are symptoms related to hypercalcaemia?

A

Anorexia, nausea and vomiting- all central effects of hypercalcaemia
Constipation, muscle weakness- reduced peripheral neuromuscular excitability

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86
Q

What is serum electrophoresis?

A

Shows the number and weight of proteins in the blood serum

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87
Q

What is the acute management of hypercalcaemia?

A
  1. Make sure patient is properly hydrated
  2. Calcium excretion can be promoted by using loop diuretics
  3. Bisphosphonates
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88
Q

How do bisphosponates work?

A

Bind to bone matrix and inhibit bone breakdown by preventing OC attachment and action

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89
Q

Why can raised PTH activity cause low serum phosphate and low total CO2?

A

PTH inhibits proximal tubule reabsorpsion of phosphate
PTH also inhibits the renal re-absorption of bicarbonate

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90
Q

What are the main functions affected in acute kidney injury?

A

Salt and water balance
Potassium excretion
Acid base balance

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91
Q

What happens to nephrons once they are destoryed by inflammation?

A

They are irreversibly damaged

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92
Q

What can inflammation in the kidney cause?

A

Proteinuria and haematuria

93
Q

What is acute kidney injury definied by?

A

Increase in serum creatinine by > 26.5 µmol/l in 48 hours OR
Increase in serum creatinine by > 1.5x baseline creatinine in the last 7 days OR
Urine volume < 0.5ml/kg/hr for 6 hours

94
Q

What are the 3 stages for acute kidney injury?

A
95
Q

As acute kidney stages rise, what also rises?

A

Mortality rate and length of stay in hospital
Also increased incidence of chronic kidney disease

96
Q

What can happen to creatinine levels in someone who has an acute kidney injury?

A

Never return to baseline levels again- changes life trajectory

97
Q

Is acute kidney injury a diagnosis?

A

No, it is a syndrome rather than a diagnosis
Need to think of underlying cause

98
Q

What are the 3 broad categories of acute renal injury?

A

Pre renal- reduced blood supply
Renal- affecting the glomerulus, tubules and interstitium
Post renal- obstruction

99
Q

What are pre-renal causes of acute kidney injury?

A

Hypovolaemia e.g. haemorrhage or too high diuretic dose
Hypotension in shock
Reduced renal blood supply- dissection, stenosis

100
Q

What are post renal causes of acute kidney injury?

A

Bilateral obstruction is needed for AKI (unless only got one)
Prostate hypertrophy, cancer, bladder lesions, extrinsic compression of the ureter or kidney stones

101
Q

How can myeloma cause obstruction in the kidney?

A

Cancer of B cells, antibodies get into urine and form a ‘cast’ or build up that causes an obstruction in the kidneys

102
Q

What is hydronephrosis and how can it be diagnosed?

A

One or both kidneys become stretched and swollen as the result of a build-up of urine inside them.
Detected in ultrasounds or in CT scans

103
Q

Why do all patients with acute kidney injury need to have an ultrasound scan?

A

To exclude or demonstrate obstruction to the renal tract
Also to check how many kidneys they have

104
Q

What can cause acute tubular injury?

A

Tubular toxins- NSAIDs and gentamicin
Severe prolonged hypotension
Renal hypofusion (due to diuretics, diahorrea, vomiting and ACEi)

105
Q

What causes 50% of acute kidney injuries?

A

Ischaemia

106
Q

What does a kidney with acute kidney injury look like?

A
107
Q

What is an allergic response that can cause AKI and how can this be treated?

A

Acute allergic interstitial nephritis
Can be drug related e.g. proton pump inhibitors, antibiotics, diuretics or NSAIDS
May have eosinophilia (high number) and no rash
Often responds well to steroids

108
Q

What are some causes of rapidly progressive glomerulonephritis?

A

Goodpastures syndrome, Wegener granulmatosis, microscopic polyarteritis

109
Q

What may suggest an immune cause to AKI?

A

Anyone with renal impairment, proteinuria, haematuria, anaemia, rash and red eyes

110
Q

What is haemolytic uraemic syndrome and what can cause it?

A

Hemolytic uremic syndrome (HUS) is a condition that can occur when the small blood vessels in your kidneys become damaged and inflamed
Causes include genetic aetiology and E coli related

111
Q

What do you do when a patient with AKI presents to you?

A
  1. Take a clinical history
  2. Perform a clinical examination
  3. Request appropriate investigations
112
Q

What is important to gather in a history for an AKI patient?

A

Renal history- pre-existing renal disease, diabetes, family history
Urine volume status
Drug history- nephrotoxic drugs such as NSAIDs, ACEi and antibiotics
Systemic symptoms- diarrhoea, rashes

113
Q

What should be done in a clinical examination in AKI?

A

Fluid status- JVP and postural BP
Check for evidence of infection, rash, arterial bruits
Try and palpate the bladder (indicative of obstruction)
Check drug chart

114
Q

What investigations should be done in AKI?

A

Urine dipstick- blood protein ect
Urine culture
Renal ultrasound
Renal biopsy (done if there is no apparent reason for AKI)
Angiography (x-ray that checks blood vessels)
Blood tests

115
Q

What is creatinine kinase a sign of?

A

Rhabdomyolysis
Good biomarker of muscle mass. When the body gets squashed or trauma occurs muscles release myoglobin and hemoglobin which are renal toxic
Turns urine black

116
Q

What should you do if you think an immune cause is possible in AKI?

A

Immunological tests such as IgGs and serum electrophoresis

117
Q

What is the general treatment of AKI?

A

Supportive treatment
Optimise fluid balance and circulation
Stop exacerbating factors such as nephrotoxic drugs
Appropriate prescribing to not make situation worse
Supportive treatment- dialysis or nutrician

118
Q

What is the treatment for AKI when you know the specific cause?

A

Obstruction= drain renal tract
Sepsis= effective antibiotics
Acute allergic interstitial nephritis= immunosupression
Goodpastures syndrome= plasma exchange
Compartment syndrome= fasciotomy

119
Q

When is dialysis initiated in AKI?

A

Severe uraemia (build up of toxins in blood)
Uraemic encephalopathy or seizures
Uraemic pericarditis
Hyperkalaemia unresposive to medical treatment
Severe acidosis
Fluid overload- especially pulmonary oedema resistant to treatment

120
Q

What are some of the possible consequences of haemodialysis for AKI?

A

Pneumothorax, infection, bleeding
Anticoagulation required- problem in patients with bleeding

121
Q

What are the different components of the immune system?

A

Innate= macrophages, neutrophils, complement and natural antibodies
Adaptive= Dendritic, T cells, Natural killers and B cell cells

122
Q

What is the role of dendritic cells?

A

Patrol and sample cells
Present antigens to T cells

123
Q

What are HLA genes and how do they relate to transplantation?

A

HLA (histocompatibility locus antigen) create the blueprint for the major histocompatibility complex part of immune cells that antigens bind to when they are presented
Can be expressed by most somatic cells or antigen presenting cells
For transplant, need to have similar HLA profiles

124
Q

What are the differences between class I and class II HLA molecules?

A

Class I molecules- HLA -A, -B and -C are expressed by most somatic cells and are used to present peptides from internally processed proteins. Infected cells then killed by cytotoxic T cells
Class II molecules -DP, -DQ and -DR are expressed by antigen presenting cells and are used to present exogenous peptides. T cell response then initiated

125
Q

What causes a T cell response?

A

Need co-stimulation- yes have a pathogen and yes it is significant

126
Q

How do cytotoxic T cells kill pathogens?

A

Eiether by fas ligand (causes apoptosis), TNF, Gz B or perforin (punching holes in cell)

127
Q

What is the cycle of T cell activation?

A
128
Q

How does transplantation exibit memory?

A

A second similar transplant is rejected more rapidly due to more rapid generation of cytotoxic antibodies

129
Q

What is HLA profiling?

A

Every donor and transplant patient is profiled to find their molecular makeup
This is stored on a database and the ‘best match’ is chosen when kidneys become available
If HLA -A, -B and -DR loci are the same then it is a 0-0-0 mismatch, if they are all different then it is a 2-2-2 mismatch

130
Q

What different drugs are given to boost immunosupression?

A

Corticosteroids- kill lymphocytes and interfere with T cell activation
Calcineurin inhibitors- Tacrolimua, inhibits T cell activation
Anti-proliferative agents- MMF, inhibits clonal expansion of T cells

131
Q

What is important in assessing when deciding transplant?

A

Age
Primary cause of renal failure- will it occur again
Comorbid disease e.g. CVD
History of infection
History of tumours
Urological disease e.g. bladder dysfunction

132
Q

What are the different types of transplantation and which has a better outcome?

A

Cadaveric- DCD, donated after cardiac death and DBD after brain death
Living donor- better outcome

133
Q

What is the criteria for a kidney transplant to go ahead?

A

Blood group compatible and immunological cross match negative

134
Q

How are immunological cross matches done?

A
135
Q

When can HLA antibodies be produced and why is this a problem?

A

If a person is exposed to foreign HLA material, e.g. paternal through pregnancy or blood transfusion or previous transplantation
Can produce HLA antibodies which could attack transplanted organ

136
Q

What test is done to detect HLA antibodies?

A

Luminex HLA antibody detection- using beads

137
Q

What are the types of transplant rejection?

A

Hyperacute- immediate
Acute (first few months) and chronic

138
Q

What happens in hyperacute rejection?

A

Due to error
Cytotoxic antibodies bind endothelial cells and induce complement activation, platelet aggregation and intravascular thrombus formation

139
Q

What are the features of acute rejection?

A

Rise in creatinine
Reduced urine output
Tender transplant
Fever

140
Q

What needs to be ruled out before transplant rejection is considered?

A

Dehydration
Renal obstruction
Vasular catastrophe
Drug toxicity

141
Q

What does C4d staining do?

A

Cd4 staining indicates where antibodies are bound

142
Q

What is tubulitis?

A

Tubulitis in the kidney is defined as the presence of inflammatory cells in the tubular wall
Key marker of rejection

143
Q

What is the treatment for acute rejection?

A

High dose methy prednisolone
Increase dose of immunosupressive drugs or switch to a more potent one

144
Q

What conditions can occur in the renal patient’s original kidney and the transplanted one?

A

Crescentric nephritis also known as rapidly progressive glomerulonephritis or lupus or diabetic nephropathy

145
Q

What are the causes of chronic rejection?

A

Increased HLA mismatch
Previous acute rejection
Poor drug compliance in patient
Prolonged cold ischaemia time of kidney prior to surgery

146
Q

What are some factors that promote kidney transplantation failure?

A

Delayed graft function- need to re connect it multiple times
Cytomegalovirus infection
Age of donor and ‘donor disease’
Poor blood pressure control
Proteinuria

147
Q

What is the management of chronic rejection?

A

No specific treatment
Most patients require dialysis and a further transplant
Optimise immunosupression
Proactive treatment of BP, lipids, proteinuria ect

148
Q

What are some of the infective risks that accompany immunosupression?

A

Bacteria- UTIs, chest infection
Viral- Cytomegalovirus, herpes, virus, BK virus

149
Q

What is BK virus?

A

BK virus is a virus that most people get in childhood. Symptoms can feel like a common cold. But it does not cause a problem for most people except those immunosupressed due to transplant
50% of people infected with it

150
Q

What are the tumour risks of immunosupression?

A

Incidence of all cancers increased- skin cancer common
Post transplant lymphoproliferative disorder is secondary to EBV infecion

151
Q

What are the side effects of immunosupressive drugs (other than decreased immune function)

A

Calcineurin inhibitors are nephrotoxic
Increased risk of diabetes (steroids and tacrolimus)
Hypertension and OP (steroids)

152
Q

What is the future for transplantation?

A

Xenotransplantation using genetically modified pigs
Tolerance induction
Artifically engineered kidneys using stem cells, organoids and biological scaffolds

153
Q

What is the definition of chronic kidney disease?

A

GFR of less than 60ml/min for > 3 months or 90 days

154
Q

What are the causes of chronic kidney disease?

A

Diabetes, hypertension, glomerulonephritis, cystic kidney disease and renovascular disease

155
Q

What is a normal GFR?

A

Around 125/ml/min/1.73^2

156
Q

What are the different ways to estimate renal function?

A

Serum creatinine- can be misleading
Creatinine clearance- need 24 hour urine collection
Isotope GFRs- expensive
Formulae for estimated GFR

157
Q

What are the different equasions used to estimate creatinine clearance?

A

MDRD and CKD-EPI more recent

158
Q

What are the different stages of CKD?

A

Based on GFR. For stage 4 and 5 also need abnormal ultrasound, biopsy or hypertension to be classed in these

159
Q

At what GFR is dialysis usually started?

A

Around 15 ml/min/1.73^2

160
Q

At what GFR is dialysis usually started?

A

Around 15 ml/min/1.73^2

161
Q

What are the strategies used to prevent progression of CKD?

A

Control blood pressure and reduce proteinuria via RAS inhibition (ACEi and ARBs)
If there is diabetes, optimise glycaemic control
SGLT2 inhibitors increasingly used

162
Q

What factors are important to consider when working out risk of CKD?

A
163
Q

How does fibrosis occur in the glomerulus in CKD?

A

In health, the protein will be absorbed, but if there is large amounts of protein excreted this overloads the system and it gets damaged. Causes fibrosis

164
Q

What does chronic interstitial fibrosis look like?

A

Tubules should be nicely stacked but instead they are surrounded by fibrosis

165
Q

What toxins should be avoided in those with CKD?

A

NSAIDs
Contrast
Gentamicin
Phosphate enemas

166
Q

What can hypertension caused by CKD cause?

A

Left ventricular hypertrophy, stroke, retinopathy and further damage to the kidneys

167
Q

Why do patients with CKD need to watch their dietary intake of potassium?

A

Hyperkalaemia is common as GFR declines

168
Q

What foods are high in potassium?

A

Orange juice, bananas, beer, wine, coffee, chocolate, crisps, nuts, baked potatoes, chips and beans

169
Q

What causes acidosis in CKD and what is the treatment option?

A

Due to animal protein in food. Use sodium bicarbonate to raise the pH

170
Q

Why can anaemia occur in CKD patients?

A

There is less EPO produced
Also blood loss due to dialysis and blood samples, albumin deficiency, iron deficiency and decreased red cell survival

171
Q

What CKD patients should be erthyropoiten replacement therapy?

A

All patients with Hb < 105 and adequate iron stores should be on Epo

172
Q

What abnormal changes to bone (osteodystrophy) can occur in CKD?

A

Osteomalacia
Adynamic bone disease
Aluminum bone disease
Secondary hyperparathyroidism- high turn over

173
Q

How can you treat renal osteodystrophy?

A

Restrict phosphate in diet or take phosphate binder to inhibit absorpsion
Vit D therapy with alfacalcidol
Parathyroidectomy may be required

174
Q

What are some consequences of hyperphosphataemia?

A

Vessel calcification- non compliant vessels
Systolic hypertension- leads to left ventricular hypertrophy
Diastolic hypotension- myocardial ischaemia
Calciphylaxis- calcium accumulates in small blood vessels of the fat and skin tissues. In serious cases can lead to ulceration

175
Q

The increase of what increases as stages of CKD increase?

A

Death from any cause, any cardiovascular event and any hospitalisation

176
Q

Why can malnutrition occur in CKD?

A

Decreased protein intake due to dietary restrictions
Decreased appetite

177
Q

Who should you refer to the renal clinic?

A

Any patient with rapid increase in creatinine or hypertension
Stage 3 CKD with hypertension/ proteinuria/ haematuria or rising creatinine
Any stage 4/5 CKD who is suitable for treatment

178
Q

What is a fistula?

A

Joining of artery and vein

179
Q

What is renal clearance?

A

The rate at which a substance is removed from the bloodstream

180
Q

What is GFR?

A

Volume filtered by glomeruli, per unit time

181
Q

What substances can be used to measure GFR?

A

Exogenous= Insulin, radioisotope tracers and iohexol
Endogenous= creatinine and cystatin C

182
Q

Why is creatinine clearance not usually used for GFR?

A

Need plasma creatinine measurement
And 24 hour urine collection- inconvienient and may be inaccurate

183
Q

Why is plasma creatinine not used as a measure of GFR?

A

The same creatinine level in two patients can reflect very different GFR rates
E.g. muscle mass, age, sex affects it

184
Q

Why are equasions for estimating GFR used?

A

Take into account age, sex, ethnicity, body mass
Only requires a plasma creatinine measurement

185
Q

Where do estimated GFR equasions lose applicability?

A

Children, pregnancy, very elderly
Extreme muscle masses either direction
Very low GFR
Rapidly changing renal function

186
Q

What is chronic kidney disease?

A

Progressive and irreversible loss of kidney function caused by damage to increasing numbers of nephrons

187
Q

What is used to classify CKD categories?

A

GFR and albumin creatinine ratios

188
Q

What is acute kidney injury characterised by?

A

Acute oliguria and increases in plasma urea and creatinine
Often accompanied by a loss in ability to regulate water, electrolyte and acid-base balance

189
Q

What is the diagnosis of acute kidney injury?

A

Plasma creatinine and urine output levels
Estimated GFR is not accurate for rapidly changing renal function

190
Q

What is more acidic, plasma or urine?

A

Urine is significantly more acidic than plasma
pH of urine= 5.5, pH of plasma= 7.35-7.45

191
Q

What is renal tubular acidosis and what causes it?

A

Distal tubular cells become unable to secrete H+ and pH in urine rises
Causes= autoimmune, paraproteinaemia and nephrocalcinosis

192
Q

What test is used to confirm suspected renal tubular acidosis?

A

Ammonium chloride loading test

193
Q

How do you calculate the fractional excretion of phosphate?

A
194
Q

What does urine sodium tell us?

A

Urine Na+ < 30mmol/L= tubules appropriately re-absorbing Na+ e.g. pre-renal failure caused by hypotension
Urine Na+ > 30 mmol/L= innappropriate loss due to tubular dysfunction, damage or inadeuate aldosterone action

195
Q

What will urine concentrating ability look like in chronic renal failure, acute tubular necrosis, diabetes, diabetes inspidis?

A
196
Q

How can renal disease lead to proteinuria?

A

Via increased glomerular permability- increasing urinary albumin, detectable levels of large MW proteins not normally found in urine
Decreased tubular protein reabsorption- increased concentration of low molecular weight proteins

197
Q

What is proteinuria and albuminuria?

A

The presence of protein in the urine
The presence of albumin in the urine- most important protein to look out for

198
Q

What is proteinuria a cardinal sign of?

A

Renal disease

199
Q

What is the presentation of proteinuria?

A

Usually no symptoms
Can accompanied by oedema, rash or painful joints

200
Q

How is proteinuria tested for and categorised?

A

Dipstick test
Trace, 1+, 2+, 3+, 4+ based on the colour change of the test

201
Q

When should proteinuria be tested for?

A

Any form of oedema, unexplained ascites or pleural effusions
Patients with hypertension, diabetes mellitus
Patients with suspected systemic disease

202
Q

What was the traditional method of detecting proteinuria?

A

Old method of detecting proteinuria= shaking it. If there is protein present, bubbles which do not disperse will appear. Also, boiling urine with protein present leaves a white deposit

203
Q

What does a proteinuria score of 2+ or more suggest?

A

2+ or more implies intrinsic renal disease and is very unlikely to be explained by asymptomatic infection

204
Q

What should you do if proteinuria is found?

A
  • If there is proteinuria, test kidney renal function and consider systemic disease but NEVER ignore it
  • The correct response to a finding of proteinuria is NOT to send an MSU (midstream urine sample) ‘to exclude infection”
  • If there is symptoms of UTI, treat it and then re rest the urine to check that was the cause of the proteinuria.
205
Q

How can you quantify the amount of protein in the urine?

A

Use the albumin/creatinine ratio to quantify it.
A/C ratio (mg/mmol) can be performed on small urine sample taken at any time of day
ACR x 10 approximates to mg/24 hours as the average adult will excrete around 10 mmol of a creatinine a day

206
Q

What are normal and abnormal albumin creatinine ratios?

A

Normal ACR is less than 3.5, 3.5-30 is microalbuminuria and > 30 is macroalbuminia. In renal disease can have ACR of upto 1000. More than 10 is definitely abnormal

207
Q

Does creatinine directly related to glomerular filtration rate?

A

No
People can have the same levels of creatinine in their body but have very different estimated GFR due to muscle mass

208
Q

What are ways to measure excretory renal function?

A

Plasma/serum creatinine (either works)
Estimated glomerular filtration rate
Creatinine clearance
Isotope glomerular filtration rate

209
Q

What is the structure of the glomerular blood vessels?

A

Outside blood vessels= complicated cells known as podocytes or glomerular epithelaial cells. They have a body and primary/secondary processes which branch down. The ‘zippers’ are the processes that are coming together to form slits- where the filtration occurs

210
Q

How much liquid is filtered and how much is passed as urine per day?

A

180L filtered, 1.5L passed

211
Q

How many nephrons do adults have?

A
  • Healthy young adults have approx 1 million nephrons
  • Black and Asian people may have fewer nephrons, although the evidence is not completely robust
  • Number of functioning nephrons decreases with age
212
Q

What is congenital nephrotic syndrome?

A
  • Due to mutation in podocyte specific gene e.g. nephrin
  • Causes massive leakage of protein in the urine
  • Causes swelling,
213
Q

Does a high albumin creatinine ratio mean there is kidney failure?

A

You can have high A/C but no kidney failure and vice versa so important to test kidney renal function

214
Q

What investigations can be done for those who have proteinuria?

A

These include BP, testing for diabetes, quantifying proteinuria, checking kidney function, doing a renal ultrasound and a renal biopsy

215
Q

What does the presence of blood and protein in the urine imply?

A

Glomerular disease
There is an urgent need to test excretory kidney function and consider systemic diseases such as vasculitis and lupus

216
Q

What is an early clinical feature of diabetes mellitus?

A

Microalbuminuria (may be intermittent or constant)

217
Q

What does albuminuria in patients with hypertension indicate?

A

A primary renal cause

218
Q

What increases are albuminuria level rises?

A

Cardiovascular mortality and incidence

219
Q

How do proteins leak out into the urine?

A

When podocytes are broken and the kidney becomes ‘leaky’

220
Q

What is the differences in albumin and creatinine?

A
  • Albumin produced by liver and normally not lost in urine (or in very small amounts)
  • Creatinine is produced by muscles and is normally is excreted in the urine
221
Q

What are causes of glomerular damage (and thus may cause protein or blood in the urine)?

A
  • Rare genetic disorders
  • Diabetes mellitus, most common
  • Vascular disease/ischaemia/age
  • Inflammation of blood vessels isolated or part of systemic disease
  • Inflammation of glomerulus itself (glomerulonephritis)
  • Deposition diseases such as amyloid, myeloma
222
Q

What is nephrotic syndrome?

A

Compromises oedema, heavy proteinuria, hypoalbuminaemia in the blood.

223
Q

What are causes of nephrotic syndrome?

A

glomerulonephritis (infection of glomerulous), diabetes, infections (Hep B/C, malaria, HIV), amyloid depositions

224
Q

What is increased in patients with nephrotic syndrome?

A

Thrombotic risk, infection risk and hyperlipideamia

225
Q

What are the symptoms of nephrotic syndrome?

A

Severe lethargy, reduced exercise tolerance, nausea, loss of appetite. May or may not be associated with impairment of excretory kidney function

226
Q

What does more blood than protein in the urine indicate?

A

Inflammatory causes- inflammation of the glomerulous

227
Q

What marker is systemic vaculitis associated with?

A

ANCA (anti-neutrophil cytoplasm antibody)

228
Q

What can haematuria be a sign of and haematuria with proteinuria?

A
  • Haematuria, whether visible (macroscopic) or non-visible (microscopic) can be a sign of a serious systemic disease for which diagnosis and treatment is very urgent, whether or not there is also albuminuria
  • Could have blood disease, could have UTI, kidney stones or gallbladder stones if there is blood in the urine
  • However if there is proteinuria, indicative of a problem with the kidney

sem 2 year 2 (16 decks)

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