Nephrology

Question 1

How does minimal change disease present?

Answer 1

Tetrad:
Hypercholesterolaemia
Hypoalbuminaema
Proteinuria
Oedema

Question 1

Give causes of minimal change disease

Answer 1

drugs: NSAIDs, rifampicin
Hodgkin’s lymphoma, thymoma
infectious mononucleosis

Question 2

What is the pathophysiology of minimal change disease

Answer 2

T-cell and cytokine-mediated damage to the glomerular basement membrane → polyanion loss
increased glomerular permeability to serum albumin

Question 3

What does renal biopsy show in minimal change disease?

Answer 3

Normal glomeruli on light microscopy
electron microscopy shows fusion of podocytes and effacement of foot processes

Question 4

What is the management of minimal change disease?

Answer 4

Management
oral corticosteroids: majority of cases (80%) are steroid-responsive
cyclophosphamide is the next step for steroid-resistant cases

Question 5

How do we manage ascites in liver cirrhosis?

Answer 5

Spironolactone is a potassium-sparing diuretic that is the recommended first-line therapy for managing ascites in patients with liver cirrhosis.

Question 6

How does transitional cell carcinoma of the bladder present?

Answer 6

Painless haematuria

Question 7

Would you expect hypo or hypercalcaemia in CKD?

Answer 7

Hypo

Question 8

How does HSP present?

Answer 8

Henoch-Schonlein purpura classically presents with abdominal pain, arthritis, haematuria and a palpable purpuric rash over the buttocks and extensor surfaces of arms and legs

Question 9

What is spironolactone?

Answer 9

Aldosterone antagonist

Question 10

How does HUS present?

Answer 10

Haemolytic uraemic syndrome is generally seen in young children and produces a triad of:
acute kidney injury
microangiopathic haemolytic anaemia
thrombocytopenia

Question 11

How do we manage HUS?

Answer 11

treatment is supportive e.g. Fluids, blood transfusion and dialysis if required
there is no role for antibiotics, despite the preceding diarrhoeal illness in many patients

Question 12

What normally causes HUS?@

Answer 12

Haemolytic uraemic syndrome - classically caused by E coli 0157:H7

Question 13

How does Post-streptococcal glomerulonephritis present?

Answer 13

A 21-year-old woman presents to the emergency department with visible haematuria. On further questioning, she states that 10 days ago she had ‘tonsillitis’ which has resolved but she continues to feel very tired.

Her blood pressure is 182/72mmHg. Other observations are normal. Urine dip is positive for blood and protein.

Question 14

What do we use to confirm recent streptococcal infection in post-streptococcal glomerulonephritis?

Answer 14

raised anti-streptolysin O titres are used to confirm the diagnosis of a recent streptococcal infection

Question 15

How do we determine if kidney disease is chronic or acute?

Answer 15

Hypocalcaemia is an indication that kidney disease is chronic and not acute

Question 16

How does minimal change disease present?

Answer 16

Minimal change disease is the most likely diagnosis. This child has clinical signs of nephrotic syndrome: oedema with proteinuria. The bi-basal lung crackles are suggestive of pulmonary oedema. The most common cause of glomerulonephritis in children is minimal change disease, making this the best answer

Question 17

How does renal cell carcinoma present?

Answer 17

Features of renal cell carcinoma:
classical triad: haematuria, loin pain, abdominal mass
pyrexia of unknown origin
left varicocele (due to occlusion of left testicular vein)
endocrine effects: may secrete erythropoietin (polycythaemia), parathyroid hormone (hypercalcaemia), renin, ACTH
25% have metastases at presentation

Question 18

What is Berger’s disease?

Answer 18

IgA Nephropathy

Question 19

How does acute tubular necrosis and pre-renal uraemia differ?

Answer 19

ATN = AllTheNa = high Na everything else low
Pre renal urine = low Na everything else high

Question 20

Give the most common presentation of HUS in exams

Answer 20

Normocytic anaemia, thrombocytopaenia and AKI following diarrhoeal illness - consider HUS

Question 21

What is a common complication of significant NaCl fluid therapy?

Answer 21

Use of 0.9% Sodium Chloride for fluid therapy in patients requiring large volumes = risk of hyperchloraemic metabolic acidosis

Question 22

What is the glucose requirement of a person?

Answer 22

50-100g - not influenced by weight

Question 23

Which electrolyte abnormality do you see in rhabdomyolysis, and why?

Answer 23

Patients with rhabdomyolysis should have a bone profile taken to measure calcium and phosphate. Calcium typically binds to myoglobin released from damaged muscle tissue causing serum hypocalcaemia.

Question 24

How do we diagnose AKI in adults?

Answer 24

NICE recognise any of the following criteria to diagnose AKI in adults:
↑ creatinine > 26µmol/L in 48 hours
↑ creatinine > 50% in 7 days
↓ urine output < 0.5ml/kg/hr for more than 6 hours

Question 25

Which acid-base disorder is seen in diarrhoea on ABG?

Answer 25

Vomiting = normal anion gap metabolic alkalosis

Diarrhoea= normal anion gap metabolic acidosis

Question 26

What causes hyperacute transplant rejection?

Answer 26

Signs of rejection within the immediate (24-48h) post-transplant period should always raise suspicions of hyperacute rejection, the rapidity of which is caused by pre-existing of antibodies against a donor’s ABO/HLA antigens.

Question 27

Where do you see Cell-mediated (cytotoxic T-cell) mediated rejection?

Answer 27

Cell-mediated (cytotoxic T-cell) mediated transplant rejection is a cause of acute rejection but usually manifests within the first 6 months as oppose to the first 24h.

Question 28

What can change the eGFR?

Answer 28

Creatinine, Age, Gender, Ethnicity

Question 29

What is the most likely cause of death with CKD on haemodialysis?

Answer 29

CKD on haemodialysis - most likely cause of death is IHD

Question 30

How do we measure AKI staging with creatinine?

Answer 30

Basically if creatinine doubles (2x), its stage 2. If it triples (3x), its stage 3
(copied from another Q)

Question 31

How do we determine AKI staging with urine production?

Answer 31

1. < 0.5ml/kg/h for >6 consecutive hours
   2 < 0.5ml/kg/h for >12 consecutive hours
   3 >354 µmol/L < 0.3ml/kg/h for > 24h or anuric for 12h

Question 32

How do we classify CKD stage?

Answer 32

CKD stage GFR range
1 Greater than 90 ml/min, with some sign of kidney damage on other tests (if all the kidney tests* are normal, there is no CKD)
2 60-90 ml/min with some sign of kidney damage (if kidney tests* are normal, there is no CKD)
3a 45-59 ml/min, a moderate reduction in kidney function
3b 30-44 ml/min, a moderate reduction in kidney function
4 15-29 ml/min, a severe reduction in kidney function
5 Less than 15 ml/min, established kidney failure - dialysis or a kidney transplant may be needed

*i.e. normal U&Es and no proteinuria

Question 33

What is the most common cause of peritonitis secondary to peritoneal dialysis

Answer 33

Staphylococcus epidermidis

Question 34

What causes raised anion gap acidosis?

Answer 34

The only listed cause of raised anion gap metabolic acidosis is septic shock, which results in acidosis due to the production of lactic acid due to inadequate tissue perfusion.

Question 35

How do we calculate anion gap?

Answer 35

To determine the cause of metabolic acidosis, the anion gap can be calculated. The anion gap is calculated by calculating the difference between positively charged ions (sodium and potassium) and negatively charged ions (bicarbonate and chloride)

Question 36

What is a normal anion gap?

Answer 36

A normal anion gap is 8-14 mmol/L

Question 37

How does IgA nephropathy present?

Answer 37

IgA nephropathy classically presents as visible haematuria following a recent URTI

Question 38

What is the most common cause of haematuria worldwide?

Answer 38

Berger’s disease

IgA nephropathy

Question 39

How do we treat hyperacute transplant rejection?

Answer 39

Removal of transplant