There is a sex difference in hypertensive renal injury with males experiencing greater severity and a more rapid progression of renal disease compared to females, however the molecular mechanisms protecting against renal injury in females are unknown. The goal of this study was to determine if sex hormones modulate blood pressure and the progression of albuminuria during the developmental phase of hypertension in male and female spontaneously hypertensive rats (SHR). Studies were also performed to examine how sex and sex hormones influence two major risk factors for albuminuria, over activation of the renin-angiotensin system and oxidative stress. Blood pressure was measured by telemetry in gonad-intact and gonadectomized male and female SHR. Microalbumin excretion, measured over time, and macrophage infiltration were used to assess renal health. Male SHR had significantly higher blood pressures compared to females and gonadectomy decreased blood pressures in males with no effect in females. Male SHR displayed a gonad-sensitive increase in albuminuria over time and females had a gonad-sensitive-suppression in macrophage infiltration. Female SHR had greater plasma Ang II levels and similar levels of renal cortical Ang II compared to males, yet less AT₁ receptor protein expression in the renal cortex. Female SHR also had a gonad-sensitive decrease in renal oxidative stress. Therefore, the renal protection afforded female SHR is associated with lower blood pressure, decreased macrophage infiltration, and decreased levels of oxidative stress.