NephrologyTier 2Topic

Laboratory tests - arterial blood gases (ABGs)

Focus in nephrology

ABG interpretation in nephrology focuses on metabolic acid-base derangement from renal disease - the kidney's role in acid excretion and bicarbonate regeneration
CKD -> normal anion gap (hyperchloraemic) acidosis early, high anion gap acidosis in advanced CKD as uraemic acids (sulfates, phosphates) accumulate
Metabolic acidosis is near-universal in advanced CKD (eGFR <20-30) and worsens with disease progression

Reduced nephron mass -> reduced ammoniagenesis and reduced net acid excretion -> retained hydrogen ions -> metabolic acidosis
Renal tubular acidosis (RTA) - a distinct entity from CKD-related acidosis: a normal-anion-gap acidosis from a specific tubular transport defect despite normal or near-normal GFR - Type 1 (distal, impaired H+ secretion, urine pH cannot fall, hypokalaemia), Type 2 (proximal, impaired bicarbonate reabsorption, self-limited as filtered load falls, hypokalaemia), Type 4 (hypoaldosteronism/resistance, hyperkalaemia - the type usually seen in diabetic nephropathy)

Calculate the anion gap [(Na+K) - (Cl+HCO3)] to distinguish the mechanism; a urine anion gap helps localise the RTA subtype when the picture is ambiguous
Correlate with potassium - hypokalaemic (Type 1/2 RTA) vs hyperkalaemic (Type 4 RTA, or simply reduced GFR with reduced potassium excretion)

Oral sodium bicarbonate - guidelines recommend treating to keep serum bicarbonate >=22 mmol/L, which may slow CKD progression
RTA-specific: Type 1/2 - bicarbonate/citrate replacement (higher doses needed in Type 2 given ongoing losses); Type 4 - treat the underlying hyperkalaemia (fludrocortisone in true hypoaldosteronism, dietary potassium restriction)

Diabetic nephropathy (Type 4 RTA), Sjogren's syndrome and other autoimmune disease (Type 1 RTA), Fanconi syndrome (Type 2 RTA)

Untreated chronic metabolic acidosis contributes to muscle wasting, bone demineralisation, and accelerated CKD progression

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