key concepts

• SSRIs e.g. Citalopram are a cause of SIADH. Raised levels of ADH causes increased reabsorption of water from the collection ducts in the nephrons leading to a dilutional hyponatraemia.
• KDIGO AKI stage 3

  • ↑ creatinine >3.0 times, or
  • ↓ urine output <0.3 mL/kg/hr for ≥ 24 hours

  Important
• Diarrhoea can cause a normal anion gap acidosis whereas vomiting causes alkalosis
• ACE inhibitors should be stopped in AKI as may worsen renal function
• Eplerenone can be used in patients with troublesome gynaecomastia on spironolactone
• Diarrhoea can cause a normal anion gap acidosis whereas vomiting causes alkalosis
• The time taken for an arteriovenous fistula to develop is 6 to 8 weeks
• Alfacalcidol is used as a vitamin D supplement in end-stage renal disease because it does not require activation in the kidneys
• Patients with active Henoch-Schonlein purpura: blood pressure and urinanalysis should be monitored to detect progressive renal involvement
• IgA nephropathy classically presents as visible haematuria following a recent URTI
• Diarrhoea - normal anion gap metabolic acidosis
• High phosphate levels in CKD 'drags' calcium from the bones, resulting in osteomalacia
• Diuretics should usually be stopped in AKI as they may worsen renal function
• If a patient has a urine output of < 0.5ml/kg/hr postoperatively the first step is to consider a fluid challenge, if there are no contraindications or signs of haemorrhage etc
• In a patient with suspected anaemia of chronic disease secondary to CKD, iron status should be checked prior to commencing EPO
• Fluid restriction should be used in euvolemic and hypervolemic hyponatraemic patients who don't have severe symptoms
• Acute tubular necrosis - poor response to fluid challenge
• An ECG should be done in all new cases of hyperkalaemia
• Patients who are high-risk for contrast-induced nephropathy should have metformin withheld for a minimum of 48 hours and until the renal function has been shown to be normal
• Low total thyroxine levels may be seen in nephrotic syndrome
• NSAIDs should be stopped in AKI except aspirin at cardio-protective dose
• Acute tubular necrosis - urine sodium > 40 mmol/L
• IgA nephropathy classically presents as visible haematuria following a recent URTI
• Hypertonic saline is usually indicated in patients with acute, severe, symptomatic hyponatraemia (< 120 mmol/L)
• Minimal change glomerulonephritis - prednisolone
• HIV infection is a cause of focal segmental glomerulosclerosis
• Think of Alport syndrome when renal failure, sensorineural hearing loss and ocular abnormalities develop in a child
• When prescribing maintenance fluids, 25-30 ml/kg/day of water is typically required
• A differential for AKI is dehydration - the latter is characterised by a urea that is proportionally higher than the rise in creatinine
• Calcium resonium results in removal of potassium from the body, rather than shifting potassium between fluid compartments in the short-term
• PSGN develops 1-2 weeks after URTI. IgA nephropathy develops 1-2 days after URTI
• Henoch-Schonlein purpura classically presents with abdominal pain, arthritis, haematuria and a purpuric rash over the buttocks and extensor surfaces of arms and legs
• No treatment is possible for hyperacute transplant rejection - the graft must be removed
• An ultrasound is required in the investigation of all patients presenting with an AKI of unknown aetiology
• ADPKD is associated with mitral valve prolaspe
• The early stages of diabetic nephropathy are associated with enlarged kidneys, in contrast to most other causes of CKD
• Trousseau's sign is a carpopedal spasm caused byinflating the blood-pressure cuff to a level above the systolic blood pressure in patients with hypocalcaemia
• Thiazide duiretics can lead to hypokalaemia
• Acute tubular necrosis - urine osmolality < 350 mOsm/kg
• A common endocrine complication of small cell lung cancer is SIADH