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NEPHROLOGY Flashcards

Interstitial Kidney Disease Acute Tubular Necrosis Renal Tubular Acidosis

1
Q

Define interstitial nephritis

A

Interstitial nephritis is a term used to describe a situation where there is inflammation of the space between cells and tubules (the interstitium) within the kidney.

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2
Q

How many types of interstitial nephritis is there and what are they?

A
  1. Acute interstitial nephritis
  2. Chronic tubulointerstitial nephritis
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3
Q

What is acute interstitial nephritis?

A

There is acute inflammation of the tubules and interstitium

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4
Q

What is usually the cause of acute interstitial nephritis?

A

Acute interstitial nephritis is usually caused by a hypersensitivity reaction to drugs (NSAIDs or antibiotics) or infection

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5
Q

How does acute interstitial nephritis usually present?

A

Usually presents with an AKI and hypertension.

Features of a generalised hypersensitivity reaction can accompany the AKI:

  • rash
  • fever
  • eosinophilia
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6
Q

How is acute interstitial nephritis usually managed?

A

Treating the underlying cause

Steroids have a role in reducing inflammation and improving the recovery

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7
Q

How does chronic tubulointerstitial nephritis usually present?

A

With CKD

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8
Q

What are the possible causes of chronic tubulointerstitial nephritis?

A
  • autoimmune
  • infectious
  • iatrogenic
  • granulomatous
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9
Q

How should chronic tubulointerstital nephritis be managed?

A

Treat the underlying cause

Steroids have a role when guided by a specialist

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10
Q

Where is the inflammation in acute interstitial nephritis?

Where is the inflammation in chronic tubulointerstitial nephritis?

A

BOTH have inflammation in the

tubules AND interstitium

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11
Q

What is acute tubular necrosis?

A

necrosis of the epithelial cells of the renal tubules due to ischeamia or toxins

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12
Q

Discuss the recovery in acute tubular necrosis

A

The epithelial cells have the ability to regenerate making acute tubular necrosis reversible.

It usually takes between 7 and 21 days to recover.

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13
Q

What are the two causes of necrosis in acute tubular necrosis?

What can cause these?

A

Ischaemia can occur secondary to hypoperfusion in:

  • shock
  • sepsis
  • dehydration

Direct damage from toxins can occur due to:

  • radiology contrast dye
  • Gentamicin
  • NSAIDs
  • Lithium
  • Heroin
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14
Q

What investigations would you carry out for acute tubular necrosis?

A

Urinalysis

‘muddy brown casts’ = pathognomonic

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15
Q

What investigation finding is pathognomonic of acute tubular necrosis?

A

‘muddy brown casts’ on urinalysis

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16
Q

How do you manage acute tubular necrosis?

A

Same as other causes of AKI:

  • Supportive management
  • IV fluids
  • Stop nephrotoxic medications
  • Treat complications
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17
Q

What are the different types of renal tubular acidosis?

Which is the most common?

A

Types 1-4

Types 4 is the most common

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18
Q

What is renal tubular acidosis?

A

where there is a metabolic acidosis due to pathology in the tubules of the kidney

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19
Q

What are the tubules responsible for in the kidney?

A

The tubules are responsible for balancing the hydrogen and bicarbonate ions between the blood and ruine and maintaining a normal pH.

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20
Q

What is the pathophysiology in Type 1 Renal Tubular Acidosis?

A

Renal tubular acidosis type 1 is due to pathology in the distal tubule.

The distal tubule is unable to excrete hydrogen ions.

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21
Q

What are the different possible causes of renal tubular acidosis type 1?

A
  1. genetic. there are both autosomal dominant and recessive forms
  2. SLE
  3. Sjogrens syndrome
  4. primary biliary cirrhosis
  5. hyperthyroidism
  6. sickle cell anaemia
  7. Marfan’s syndrome
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22
Q

How might renal tubular acidosis type 1 present?

A
  • failure to thrive in children
  • hyperventilation (to compensate for the metabolic acidosis)
  • CKD
  • bone disease (osteomalacia)
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23
Q

What blood and urinalysis results would you expect in someone with type 1 renal tubular acidosis?

A
  • hypokalaemia
  • metabolic acidosis
  • high urinary pH (above 6)
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24
Q

What is the management of someone with type 1 renal tubular acidosis?

A

Treatment is with oral bicarbonate

This corrects the other electrolyte imbalances as well as the acidosis

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25
Q

What is the pathophysiology of type 2 renal tubular acidosis?

A

Type 2 renal tubular acidosis is due to pathology in the proximal tubule.

The proximal tubule is unable to resorb bicarbonate from the urine to the blood. Excessive bicarbonate is excreted in the urine.

(type 2… b is the second letter of the alphabet)

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26
Q

What is the main cause of type 2 renal tubular acidosis?

Discuss.

A

Fanconi’s syndrome

A genetic condition commonly associated with Ashkenazi Jews

Causes bone marrow failure, acute myeloid leukaemia and other cancers.

Features such as cafe au lait spots, certain facial features and an absence of the radius bone bilaterally.

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27
Q

Discuss Fanconi’s syndome

A

Fanconi’s syndrome is the main cause of type 2 renal tubular acidosis.

Associated with Ashkenazi Jews

Causes bone marrow failure, acute myeloid leukaemia and other cancers.

Features include cafe au lait spots, certain facial features and an absence of radius bone bilaterally.

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28
Q

What bloood and urinalysis results would you expect for a patient with Type 2 renal tubular acidosis?

A
  • hypokalaemia
  • metabolic acidosis
  • high urinary pH (above 6)
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29
Q

How is type 2 renal tubular acidosis managed?

A

Treatment is with oral bicarbonate

30
Q

What is type 3 renal tubular acidosis?

A

A combination of type 1 and type 2 with pathology in the proximal and distal tubule

31
Q

What is the pathophysiology of type 4 renal tubular acidosis?

A

Reduced aldosterone

32
Q

Discuss the role of aldosterone and the effects when it’s low

A

Aldosterone is responsible for stimulating sodium reabsorption and potassium and hydrogen ion exretion in the distal tubules.

Therefore, low aldosterone leads to insufficient potassium and hydrogen ion excretion, causing a hyperkalaemic renal tubular acidosis.

Normally, ammonia is produced in the distal tubules to balance the excretion of hydrogen and prevent the urine from becoming too acidotic.

Hyperkalaemia suppresses the production of ammonia, so the urine is acidotic in type renal tubular acidosis.

33
Q

What can cause a low aldosterone?

A
  • adrenal insufficiency
  • medications such as ACEI or spironolactone
  • systemic conditions that affect kidneys such as SLE, diabetes or HIV
34
Q

What blood and urinalysis results would you expect in type 4 renal tubular acidosis?

A
  • hyperkalaemia
  • high chloride
  • metabolic acidosis
  • low urinary pH (due to reduced ammonia production)
35
Q

How would you manage someone with type 4 renal tubular acidosis?

A
  1. Fludrocortisone (a mineralocorticoid steroid medication)

Sodium bicarbonate and treatment of the hyperkalaemia may also be required

36
Q

What is haemolytic uraemic syndrome?

A

HUS occurs when there is thrombosis in small blood vessels throughout the body.

It is usually due to the shiga toxin.

37
Q

What is the classic triad seen in haemolytic uraemic syndrome?

A
  1. Haemolytic anaemia
  2. AKI
  3. Low platelet count (thrombocytopenia)
38
Q

What bacteria produces the shiga toxin?

A

e.coli 0157

also Shigella

39
Q

How would haemolytic uraemic syndrome present?

A

E.coli 0157 causes a brief gastroenteritis, often with bloody diarrhoea.

Around 5 days after the diarrhoea the person will start displaying symptoms of HUS:

  1. Reduced urine output
  2. Haematuria or dark brown urine
  3. Abdominal pain
  4. Lethargy and irritability
  5. Confusion
  6. Hypertension
  7. Bruising
40
Q

How is haemolytic uraemic syndrome managed?

A

HUS is a medical emergency and has a 10% mortality.

The condition is self-limiting and SUPPORTIVE MANAGEMENT is the mainstay of Tx with:

  • Antihypertensives
  • Blood transfusion
  • Dialysis

70-80% of patients make a full recovery

41
Q

What is rhabdomyolysis?

A

Muscle cells (myocytes) undergo cell death (apoptosis). The cell death results in muscle cells releasing:

  • myoglobin (causing myoglobinurea)
  • potassium
  • phosphate
  • creatine kinase
42
Q

What are the breakdown products of rhabdomylosis?

Which one is particularly toxic to the kidneys?

A
  • myoglobin
  • potassium
  • phosphate
  • creatine kinase

The myoglobin is particularly toxic to the kidneys and causes an AKI.

The AKI results in further breakdown products accumulating further in the blood.

43
Q

What are the possible causes to rhabdomyolysis?

A

Anything that causes significant damage to muscle cells can cause rhabdomyolysis:

  • prolonged immobility
  • extremely rigorous exercise
  • crush injuries
  • seizures
44
Q

What are the signs and symptoms of rhabdomyolysis?

A
  • muscle aches and pain
  • oedema
  • fatigue
  • confusion (esp in elderly frail patients)
  • red-brown urine
45
Q

What investigations would you request in someone with suspected rhabdomyolysis?

A
  1. Creatine kinase
  2. Myoglobinurea
  3. U&Es
  4. ECG
46
Q

What result would you expect in a creatine kinase of someone with rhabdomyolysis?

Describe the pattern

A

in the thousands to hundreds of thousands of units/L

CK typically rises in the first 12 hours, then remains elevated for 1-3 days, then falls gradually.

47
Q

What is the relation between creatine kinase and kidney injury?

A

A higher CK increases the risk of kidney injury

48
Q

How would you test for myoglobin?

A

Urine dispstick is positive for blood

(myoglin is in the urine- gives urine red-brown colour)

49
Q

What are you looking for in U&Es in a patient with rhabdomyolysis?

A

AKI

and

Hyperkalaemia

50
Q

What are you looking for in the ECG of someone with a rhabdomyolysis?

A

Hyperkalaemia

  • tall tented t waves
  • loss of p waves
  • broad QRS
  • sinusoidal wave pattern
  • ventricular fibrillation
51
Q

How would you manage rhabdomyolysis?

A
  1. IV Fluids
    • main stay
    • aim= rehydrate the patient and encourage filtration of the breakdown products
  2. Consider IV Sodium Bicarbonate
    • aim= make urine more alkaline reducing the toxicity of the myoglobin on the kidneys
    • the evidence is not clear and there is some debate about it
  3. IV mannitol
    • aim= increase the GFR to flush out the breakdown products and reduce oedema surrounding the muscles and nerves
    • hypovolaemia must be corrected before giving mannitol
    • evidence not clear and debate about it
  4. Treat complications
    • e.g. hyperkalaemia
52
Q

What conditions can cause hyperkalaemia?

A
  • AKI
  • CKD
  • Rhabdomyolysis
  • Adrenal insufficiency
  • Tumour lysis syndrome
53
Q

What medications can cause hyperkalaemia?

A
  • Aldosterone antagonists (spironolactone and eplerenone)
  • ACEI
  • ARBs
  • NSAIDs
  • Potassium supplements
54
Q

What ECG changes are seen in someone with hyperkalaemia?

A
  • tall tented t-waves
  • flattening or absence of P waves
  • broad QRS complexes
55
Q

What is polycystic kidney disease?

A

PKD is a genetic condition where the kidneys develop multiple fluid filled cysts.

Kidney function is also significantly impaired.

56
Q

What are the different types of PKD?

Which type is more common?

A

autosomal dominant type (more common)

autosomal recessive type

57
Q

How is polycystic kidney disease diagnosed?

A

kidney ultrasound scan

genetic testing

58
Q

What are the autosomal dominant genes involved in PKD?

How common is each?

A

PKD-1: Chromosome 16 (85%)

PKD-2: Chromosome 4 (15%)

59
Q

What extra-renal manifestations are seen with PKD?

A
  • cerebral aneurysms
  • hepatic, splenic, pancreatic, ovarian and prostatic cysts
  • cardiac valve disease (mitral regurgitation)
  • colonic diverticula
  • aortic root dilatation
60
Q

What diagnosis could account for all of these conditions?

  • cerebral aneurysms
  • hepatic, splenic, pancreatic, ovarian and prostatic cysts
  • cardiac valve disease (mitral regurgitation)
  • colonic diverticula
  • aortic root dilatation
A

PKD autosomal dominant type

61
Q

What are the possible complications of PKD autosomal dominant type?

A
  • chronic loin pain
  • hypertension
  • cardiovascular disease
  • gross haematuria can occur with cyst rupture. This usually resolves within a few days.
  • renal stones are more common in patients with PKD
  • end stage renal failure occurs at a mean age of 50 years
62
Q

Which type of PKD is more common?

Which type of PKD is more severe?

A

autosomal dominant is more common

autosomal recessive is more severe

63
Q

How does polycystic kidney disease recessive type normally present?

A

It often presents in pregnancy with oligohydramnios as the fetus does not produce enough urine

64
Q

What is the timeline of PKD autosomal recessive type?

A

It often presents in pregnancy with oligohydramnios as the fetus does not produce enough urine.

The oligohydramnios leads to underdevelopment of the lungs, resulting in respiratory failure shortly after birth.

Patients may require dialysis within the first few days of life.

They usually have end stage renal failure before reaching adulthood.

65
Q

What features may be seen in someone with PKD recessive type?

A

underdeveloped ear cartilage

low set ears

flat nasal bridge

66
Q

Is there any specific management for PKD recessive or dominant?

A

Tolvaptan (a vasopressin receptor antagonist) can slow the development of cysts and the progression of renal failure in autosomal dominant polycystic kidney disease.

(initiated and monitored by a specialist)

67
Q

What complications may arise in PKD and how are they managed?

A
  1. Anti-hypertensives for HTN
  2. Analgesia for renal colic related to stones or cysts
  3. ABX for infection. Drainage of infected cysts may be required.
  4. Dialysis for end stage renal failure
  5. Renal transplant for end stage renal failure
68
Q

What general management steps can be taken for someone with PKD?

A
  1. Genetic counselling
  2. Avoid contact sports due to risk of cyst rupture
  3. Avoid anti-inflammatory medications and anticoagulations
  4. Regular ultrasound to monitor the cysts
  5. Regular bloods to monitor renal function
  6. Regular blood pressure to monitor for hypertension
  7. MR angiogram can be used to diagnose intracranial anaeurysms in symptomatic patients or those with a family history
69
Q

What are the indications for acute dialysis?

A

AEIOU

  • Acidosis (severe and not responding to treatment)
  • Electrolyte abnormalities (severe and unresponsive hyperkalaemia)
  • Intoxication (overdose on certain medications)
  • Oedema (severe and unresponsive pulmonary oedema)
  • Uraemia (symptoms such as seizures or reduced consciousness)
70
Q
A

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