Abstract
High protein intake can increase renal plasma flow and glomerular filtration rate (GFR) in response to excretory overload, which may exacerbate kidney disease progression. Glomerular hypertrophy has been shown to be closely associated with sclerosis at the level of a single nephron in experimental models. However, the mechanisms by which an excessive protein diet causes glomerular hyperfiltration and increases single-nephron GFR (SNGFR) have not been fully elucidated in humans. The present study aimed to calculate SNGFR by estimating the number of nephrons in living kidney donors and to evaluate the clinicopathological findings associated with SNGFR.
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