Goal: We describe the relationship between mean arterial pressure (MAP) and glomerular filtration rate (GFR) since therapies affecting MAP can have large effects on kidney function. Methods: We developed a closed-loop, steady-state mechanistic model of the human kidney with a reduced parameter set estimated from measurements. Results: The model was first validated against literature models. Further, GFR was validated against intensive care patient data (root mean squared error (RMSE) 13.5 mL/min) and against hypertensive patients receiving sodium nitroprusside (SNP) (RMSE less than 5 mL/min). A sensitivity analysis of the model reinforced the fact that vascular resistance is inversely related to GFR and showed that changes to either vascular resistance or renal autoregulation cause a significant change in sodium concentration in the descending limb of Henle. Conclusions: This model can be used to determine the impact of MAP on GFR and overall kidney health. The modeling framework lends itself to personalization of the model to a specific human.