To test the hypothesis that increments in protein intake increase the capacity of the kidney to excrete ammonium (NH4+), two strictly controlled diet studies (both repeated-measures design with n = 6 healthy adult subjects) were performed. In study I, comprising two 5-day diet periods (A and B, protein intake: 120 and 95 g/day, respectively), the urine pH was adjusted to a low pH level by administration of L-methionine (20 mmol/day) along with diet B. In study II, comprising three 4-day diet periods (C1–C3: C1, basic diet containing 50 g protein/day; C2, basic diet + 32 g of egg white protein/day; C3, basic diet + 10 mmol L-methionine/day), the urine pH was adjusted to a high pH level by sodium citrate (6.67 mmol/day) administered with diets C2 and C3. Urine pH constancy, which guarantees a constant tubular NH4+ transfer, was achieved for either study (diets A, B: 5.5 ± 0.2, 5.4 ± 0.2; diets C1, C2, C3: 6.7 ± 0.1, 6.8 ± 0.1, 6.7 ± 0.1), thus allowing assessment of urinary NH4+ excretion rates as an index of the renal NH4+ production capacity. With the higher protein intake on diet A compared with diet B, a significantly elevated NH4+ excretion (82.8 ± 11.4 vs. 73.6 ± 7.2 mmol/day; P < 0.01) was observed. NH4+ excretion also increased from 29.4 ± 5.5 mmollday (C1) to 34.8 ± 5.1 mmollday (C2) in study II (P < 0.05) after the protein intake was raised with egg protein. When methionine was administered instead of egg protein as a different source of sulfur (C3), no effect on renal NH4+ output occurred, thus demonstrating that protein as a whole has a specific impact. It is concluded that the renal capacity to excrete excess acidity as NH4+ is modulated (independently of the underlying level of the respective renal acid load) by the amount of protein ingested.