Urinary prostaglandin E and kallikrein activity in glomerular hyperfiltration induced by a meat meal in man

Because renal vasodilator systems may be involved in the physiologic response to a protein meal, we studied the relationship of prostaglandin E (PGE) and kallikrein (KE) activity to the renal hemodynamic changes induced by a meat meal. Ten normal subjects on a maintenance diet providing 1 g protein per kg and 100 mmol Na daily were studied before and after a meal of 86 g of meat protein, once without medication, and again after treatment with indomethacin (150 mg daily for 3 days before and 50 mg the morning of the test). A carbohydrate meal of similar caloric, Na and K content was used in control studies. Glomerular filtration rate (GFR, inulin clearance), renal blood flow (RBF, para-aminohippurate [PAH] clearance), PGE and kallikrein urinary excretion were determined. All studies were performed during water diuresis to avoid bladder catheterization. The protein load induced an increase in GFR (ml/min, mean ± s.e.m.: baseline 107.2 ± 6.05, peak postmeal 146.4 ± 6.79, p < 0.01) and RBF (baseline 529.7 ± 42.9, postmeal 678.9 ± 61.9, p < 0.05). Renal hemodynamic changes were unrelated to changes in urinaryy PGE and KE excretion. Indomethacin treatment inhibited PGE excretion by 73% during the test meal but did not modify the protein-induced hyperfiltration. Our results suggest that these renal vasodilator systems are not primary responsible for the hyperfiltration response. In addition, the data show that inhibition of prostaglandin synthesis is not a practical approach to prevent glomerular hyperfiltration in clinical practice.