Increased ketone utilization by the kidney reduces renal lactate uptake but does not affect tubular sodium reabsorption.
Level 5 - mechanism / opinion, no new human data
Animal physiological experiment without human clinical data.
PubMed 8389961 · doi:10.1016/0026-0495(93)90247-l
What was done
Thirty anesthetized dogs were divided into three groups of 10 to evaluate if moderate hyperketonemia alters renal substrate uptake or induces natriuresis: 1) sodium D(-)3-hydroxybutyrate (3OHB) infused at 20 µmol/kg·min⁻¹ for 135 minutes; 2) sodium bicarbonate infused with equivalent sodium to match alkalinization; and 3) equimolar NaCl infusion as a reference. Renal uptake of 3OHB, lactate, free fatty acids (FFA), and glucose was measured.
What was found
Before infusion, lactate was the main renal fuel taken up (average 28 ± 3 µmol/100 g kidney·min⁻¹), baseline 3OHB uptake was low (0.7 ± 0.1 µmol/100 g·min⁻¹; P < .05), and FFA or glucose uptake was not significant. 3OHB infusion raised plasma 3OHB to 1.7 mmol/L and increased renal 3OHB uptake to 25 ± 3 µmol/100 g·min⁻¹ (correlation with availability: r = .73, P < .001). Despite higher arterial lactate levels, renal lactate uptake and extraction ratio decreased (P < .001). Numerical data for sodium reabsorption and control groups were omitted due to abstract truncation.
Why it matters
This demonstrates that moderate ketonemia prompts the kidney to shift its primary energy substrate uptake from lactate to ketone bodies without altering tubular sodium reabsorption.
Limits
The study was conducted in anesthetized dogs, limiting translation to human starvation physiology. The abstract is truncated at 250 words, leaving out quantitative results for tubular sodium handling and the comparator groups.
Cited by
- contradicts The kidney nephron uses ketones as its primary fuel rather than glucose.