**Core Concept**
Late metabolic acidosis in infants is primarily due to impaired renal function and delayed maturation of acid-base regulatory mechanisms. Cow’s milk, when consumed by preterm infants, is high in protein and phosphorus and low in buffer capacity, leading to increased metabolic acid load that the immature kidneys cannot adequately handle.

**Why the Correct Answer is Right**
Preterm babies have underdeveloped renal tubules that poorly excrete hydrogen ions and regenerate bicarbonate. When fed cow’s milk, which is high in protein and low in phosphate, it generates more acidic byproducts (e.g., sulfuric and organic acids). The immature kidneys fail to compensate, leading to persistent metabolic acidosis. This is especially relevant in long-term cow milk feeding due to the lack of buffering capacity and high protein load.

**Why Each Wrong Option is Incorrect**
Option A: Term infants on formula feed have mature renal function and are less prone to acidosis; formula is designed to match maternal milk in buffering.
Option C: Breast milk has a natural buffering capacity and is low in protein, so long-term breastfeeding protects against metabolic acidosis.
Option D: The condition *is* seen in preterm babies on cow milk, so "none of the above" is incorrect.

**Clinical Pearl / High-Yield Fact**
Cow’s milk should never be given to infants under 12 months, especially preterms. Breast milk or fortified infant formulas are preferred due to their optimal pH and buffer capacity. Delayed acid-base correction in preterms on cow milk is a classic sign of malnutrition or renal immaturity.

✓ Correct Answer: B. Preterm baby getting cow milk