Caloric restriction protects from acute and chronic kidney injury by inhibiting monocyte recruitment

Researchers compared Fasting Mimicking Diet (FMD) cycles with unrestricted feeding in mice with acute kidney injury and chronic kidney disease induced by aristolochic acid or folic acid. They also tested cycles of caloric restriction, started the diet at the peak of acute injury in one experiment, and blocked the CCR2 receptor in another. Serum creatinine, kidney injury and repair markers, renal cytokines, pro-fibrotic genes, CCL2 levels and monocyte recruitment were measured.

The authors reported that the diet reduced serum creatinine, kidney injury and maladaptive repair marker expression in these models and promoted faster recovery. They reported lower renal cytokines and pro-fibrotic genes, reduced CCL2 and decreased monocyte recruitment, with a shift toward monocyte phenotypes they describe as protective. They reported that caloric restriction cycles produced similar kidney protection, that starting the diet at the peak of injury enhanced repair, and that blocking CCR2 abolished the protective effect. They note that broader anti-inflammatory actions may also contribute and that the reduced CCL2 may be a downstream effect.

This is an animal study in chemically induced mouse models of kidney injury, not a study in people and not a study of Prolon. Caloric restriction cycles produced similar protection, so the findings are not specific to a fasting-mimicking diet. The authors frame their own conclusion as a potential rather than an established effect and offer an alternative explanation for part of the proposed mechanism.