Male transgenic mice expressing methylmalonyl–coenzyme A–mutase (Mut) in the liver under the control of an albumin promoter on a knockout background Mut−/−;TgINS-Alb-Mut, designated as Mut−/− (n = 8), or littermate controls, Mut+/− (n = 5), were used. The mice were further subdivided by placing half on a regular mouse chow diet (RD) and the remainder on an HP diet, containing 70% (w/w) casein (HP), as described previously (TD.06723; Harlan Laboratories). HP mice lost weight (P < 0.0001) and had elevated plasma MMA (1330 μM; P = 0.017 compared to controls), associated with increased Lcn2 mRNA expression in their kidneys (P = 0.002), similar to previous findings in this model. Notably, no significant renal histological changes were evident on hematoxylin and eosin staining at this stage of renal disease in these mice. Exposure to an HP diet for 6 months was necessary to induce tubulointerstitial nephritis, as has been previously described (1). GFR measurements, on the other hand, were abnormal even on RD, when measured by 125I-iothalamate clearance in single-nephron microperfusion studies, and significantly decreased on an HP diet after 2 months, as assessed by the FITC inulin plasma decay method at the whole-animal level (1).

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