Question Bank

NICE NG203 recommends an ACE inhibitor (such as ramipril) or ARB as first-line antihypertensive therapy for patients with CKD who also have diabetes, when the urine albumin:creatinine ratio (ACR) is ≥3 mg/mmol. For patients with CKD without diabetes, an ACE inhibitor or ARB is recommended when ACR is ≥30 mg/mmol. This patient has diabetes and an ACR of 15 mg/mmol — well above the 3 mg/mmol threshold — making ramipril the correct first-line choice. ACE inhibitors and ARBs are nephroprotective in diabetic CKD by reducing intraglomerular pressure and proteinuria. Amlodipine and thiazides do not have the same renoprotective benefit; spironolactone requires caution in CKD due to hyperkalaemia risk.

The clinical picture of fluid loss (vomiting/diarrhoea) combined with hypotension and tachycardia suggests dehydration. The high urea-to-creatinine ratio and negative urinalysis further support a pre-renal cause rather than intrinsic or post-renal damage.

In severe hyperkalaemia (>6.5 mmol/L) or with ECG changes, the priority is to stabilise the cardiac membrane using 10% IV calcium gluconate. Insulin/dextrose and salbutamol shift potassium into cells but do not stabilise the myocardium.

This patient presents with the nephrotic triad (proteinuria >3.5g/day, hypoalbuminaemia, and oedema). In adults, membranous nephropathy is the most common primary cause, whereas minimal change disease is most common in children.

IgA nephropathy typically presents with 'synpharyngitic' haematuria (occurring during or shortly after an upper respiratory tract infection). Post-streptococcal glomerulonephritis usually has a longer lag period (1-3 weeks) between infection and renal symptoms.

A significant rise in creatinine (usually >20-30%) after starting an ACE inhibitor is a classic indicator of bilateral renal artery stenosis. ACE inhibitors reduce efferent arteriolar pressure, which in the presence of stenosis, leads to a drop in glomerular filtration pressure.

In Minimal Change Disease (MCD), light microscopy typically appears normal. The diagnosis is confirmed via electron microscopy showing effacement of podocyte foot processes. MCD is the most common cause of nephrotic syndrome in children and is highly steroid-responsive.

The patient likely has Autosomal Dominant Polycystic Kidney Disease (ADPKD). There is a significant association between ADPKD and intracranial berry aneurysms, which can lead to subarachnoid haemorrhage (explaining her father's early death).

Goodpasture's syndrome (Anti-GBM disease) presents with the combination of pulmonary haemorrhage and rapidly progressive glomerulonephritis. It is characterised by anti-GBM antibodies and a linear pattern of IgG deposition.

Acute Tubular Necrosis (ATN) is often caused by prolonged ischaemia (e.g., hypotension/shock during surgery). The presence of 'muddy brown' casts in the urine is highly pathognomonic for ATN compared to simple pre-renal azotaemia.