Nephrology Flashcards

1
Q

What are the three aspects of nephrotic syndrome in terms of presentation?

A

Proteinuria
Hypoalbuminemia
Oedema

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2
Q

What is minimal change disease?

A

Minimal change disease (MCD) is the most common form of nephrotic syndrome (a clinical condition characterised by heavy proteinuria, oedema, hypoalbuminaemia, and hyperlipidaemia) affecting children. 90% of children with nephrotic syndrome have minimal histological changes in the kidney. MCD is typically primary (idiopathic) but may also be secondary to another condition.

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3
Q

What is the presentation of minimal change disease?

A

Facial or generalised oedema
History of viral illness (gastroenteritis)
Can be associated with lymphoma or leukaemia
Dyspnoea from resp complications
Normal blood pressure
No Frank haematuria
Normal renal function

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4
Q

In what circumstances of nephrotic syndrome would you consider a renal biopsy?

A

Suggestions of autoimmune disease
Abnormal renal function
Steroid resistance

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5
Q

What is the management of nephrotic syndrome?

A

8 weeks prednisolone
Low salt diet and fluid restriction
Albumin and furosemide

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6
Q

What is the management of steroid resistant nephrotic syndrome?

A

Secondary immunosuppression

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7
Q

Name a steroid resistant nephrotic syndrome?

A

Focal Segmental Glomerulosclerosis (FSGS)

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8
Q

What is the presentation of nephritic syndrome?

A
Haematuria and proteinuria
Reduced GFR
Oliguria 
Fluid overload
Raised JVP
oedema
Hypertension
Worsening renal failure = Rapidly Progressive GN
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9
Q

What investigations should be done in glomerulonephritis?

A

Urinalysis-exclude UTI
Comprehensive metabolic profile-may see hyperkalaemia, hyponatraemia
Glomerular filtration rate (GFR)
Full blood count-raised creatinine, anaemia
Lipid profile
Spot urine albumin:creatinine ratio (ACR)
Ultrasound of kidneys
Investigations to consider
Erythrocyte sedimentation rate (ESR) or C-reactive protein (CRP)
Renal biopsy
Complement levels, bacterial culture and ASOT (to look for acute post infectious GN)

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10
Q

What is the management of post infectious GN?

A

Antibiotic
Support the 5 renal functions
Electrolyte / acid base
Diuretics

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11
Q

What is the presentation of Henoch Schonlein Purpura/IgA related vasculitis?

A
Mandatory palpable purpura
One of 4
1. Abdominal pain
2. Renal involvement
3. Arthritis or arthralgia
4. Biopsy - IgA depostition
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12
Q

What is the management of IgA vasculitis?

A

Immunosuppression - Prednisolone / cyclophosphamide

Use ACE inhibitors to reduce proteinuria

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13
Q

What is IgA nephropathy?

A
Most common glomerulonephritis
IgA nephropathy (IgAN) is defined by the presence of dominant or co-dominant mesangial IgA immune deposits, often accompanied by C3 and IgG in association with a mesangial proliferative glomerulonephritis of varying severity.
1-2 days after  URTI
Non streptococcal post infectious GN
Usually older children and adults
Clinically
Recurrent macroscopic haematuria
Chronic microscopic haematuria
Varying degree of proteinuria
Clinical diagnosis and biopsy
Treat with Ace inhibitor and immunosuppression
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14
Q

What is an acute kidney injury?

A

Abrupt loss of kidney function, resulting in the retention of urea and other nitrogenous waste products and in the dysregulation of extracellular volume and electrolytes
Serum creatinine: > 1.5x age specific reference creatinine (or previous baseline if known)
Urine output<0.5 ml/kg for > 8hours

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15
Q

What are the criteria for acute renal failure?

A

Anuria/oliguria (<0.5ml/kg/hr)
Hypertension with fluid overload
Rapid rise in plasma creatinine

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16
Q

What is the treatment of AKI?

A
3 Ms
Monitor
Paediatric Early Warning Scores(BP), Urine Output, weight
Maintain
good hydration
Minimise 
Drugs
17
Q

What is haemolytic uraemic syndrome?

A

Haemolytic uraemic syndrome (HUS) is characterised by microangiopathic haemolytic anaemia, thrombocytopenia, and acute kidney injury. Ninety percent of HUS cases occur in the paediatric population, due to Shiga toxin-producing Escherichia coli. Atypical HUS occurs due to abnormalities in the alternative complement regulatory pathway, resulting in endothelial cell damage and causing microvascular thrombosis.

18
Q

What is the presentation of HUS?

A

Bloody diarrhoea
Abdominal pain
Fever
Vomiting

19
Q

What is the management of HUS?

A
Monitor 
5 kidney functions
Fluid balance - hypertension
Electrolytes
Acidosis
Waste
Hormones - hypertension
Aware of other organs
Maintain
IV normal saline and fluid
Renal replacement therapy
Minimise
No antibiotics / NSAIDS
Red cell transfusion if anaemic
20
Q

What are the stages of CKD?

A
Normal function- 90-120
CKD2-60-89
CKD3- 30-59
CKD4- 15-29
CKD5- end stage renal disease
21
Q

What is the presentation of CKD?

A

Uraemic – loss of appetite, weight loss, itch
Water – polyuria
Salt / acid base – lethargy
Endocrine – lethargy, reduced effort tolerance
Bladder - UTIs

22
Q

What is the management of CKD?

A
Low phosphate diet
Oral phosphate binders
Calcium containing
Active Vitamin D
If ongoing poor growth
Growth hormone