Renal Medicine
Core concepts
KDIGO defines AKI as a creatinine rise ≥26 µmol/L in 48 hours, ≥1.5× baseline within 7 days, or urine output <0.5 mL/kg/h for 6 hours. Divide into prerenal (responds to fluid; bland urine; fractional excretion of sodium <1%), intrinsic (acute tubular necrosis, glomerulonephritis, interstitial nephritis, myoglobin, contrast) and postrenal (obstruction - image the tract). Glomerular disease: nephritic (haematuria, hypertension, oliguria, red cell casts) versus nephrotic (proteinuria >3.5 g/day, hypoalbuminaemia, oedema). IgA nephropathy follows a sore throat within days; post-streptococcal glomerulonephritis follows 1–3 weeks; anti-GBM disease causes pulmonary haemorrhage; ANCA vasculitis causes a pulmonary-renal syndrome; minimal change disease is the commonest childhood nephrotic syndrome and responds to steroids. Hyperkalaemia with ECG changes (peaked T waves, broad QRS, sine wave) is treated first with intravenous calcium gluconate, then insulin-dextrose, salbutamol and definitive removal. Hyponatraemia: assess volume status, urine osmolality and urine sodium; correct chronic hyponatraemia by less than 10 mmol/L in 24 hours to avoid osmotic demyelination. Metabolic acidosis: calculate the anion gap; a normal gap suggests bicarbonate loss (diarrhoea, renal tubular acidosis). Dialysis indications: AEIOU.
Traps
Missing obstruction as a cause of AKI. Giving insulin for hyperkalaemia without rechecking glucose. Assuming a raised urea means renal failure when it may reflect dehydration or gastrointestinal bleeding. Using eGFR in AKI - use creatinine trend and urine output.
Rule of thumb
A rising creatinine and falling urine output after starting a new drug suggests acute interstitial nephritis (NSAIDs, proton pump inhibitors, antibiotics): look for eosinophilia and sterile pyuria.