LPCing through the nephron accelerates diabetic kidney disease

Lipid dysmetabolism is emerging as an important contributor to diabetic kidney disease, suggesting that intrarenal lipid accumulation is detrimental to kidney function. This commentary discusses the finding by Yoshioka et al., connecting tubular lipotoxicity induced by an increase in locally produced lysophosphatidylcholine in patients with a fast progression of diabetic kidney disease, known as “fast decliner.” Insight into the lipid species in the kidney may prove beneficial for the diagnosis and stratification of patients with diabetic kidney disease. Lipid dysmetabolism is emerging as an important contributor to diabetic kidney disease, suggesting that intrarenal lipid accumulation is detrimental to kidney function. This commentary discusses the finding by Yoshioka et al., connecting tubular lipotoxicity induced by an increase in locally produced lysophosphatidylcholine in patients with a fast progression of diabetic kidney disease, known as “fast decliner.” Insight into the lipid species in the kidney may prove beneficial for the diagnosis and stratification of patients with diabetic kidney disease. Lysophosphatidylcholine mediates fast decline in kidney function in diabetic kidney diseaseKidney InternationalVol. 101Issue 3PreviewSome patients with diabetic kidney disease (DKD) show a fast progression of kidney dysfunction and are known as a "fast decliner" (FD). Therefore, it is critical to understand pathomechanisms specific for fast decline. Here, we performed a comprehensive metabolomic analysis of patients with stage G3 DKD and identified increased urinary lysophosphatidylcholine (LPC) in fast decline. This was confirmed by quantification of urinary LPC using mass spectrometry and identified urinary LPC containing saturated fatty acids palmitic (16:0) and stearic (18:0) acids was increased in FDs. Full-Text PDF Open Access