We have previously shown that salt excess has adverse cardiac effects in the SHR, independent of its increased arterial pressure; however, the renal effects have not been reported. In the present study we evaluated the role of three levels of salt-loading in SHR on renal function, systemic and renal hemodynamics, and glomerular dynamics. At 8-wk of age, rats were given a 4 (n = 11), 6 (n = 9), or 8% (n = 11) salt-load diet for the ensuing 8 weeks; controls (n = 11) received standard chow (0.6% NaCl). Rats had weekly 24-h proteinuria and albuminuria quantified. At the end of salt-loading, all rats had systemic and renal hemodynamics measured; glomerular dynamics were specially studied by renal micropuncture in the 4 and 6% salt-loaded rats. Proteinuria and albuminuria progressively increased by the second week of salt-loading in the 6 and 8% salt-loaded rats. Mean arterial pressure increased minimally and glomerular filtration rate decreased in all salt-loaded rats. The 6 and 8% salt-loaded rats demonstrated decreased renal plasma flow and increased renal vascular resistance and serum creatinine concentration. Furthermore, 4 and 6% salt-loaded rats had diminished single nephron plasma flow and increased afferent and efferent arteriolar resistances; glomerular hydrostatic pressure also increased in the 6% salt-loaded rats. In conclusion, dietary salt-loading as low as 4% dramatically deteriorated renal function, renal hemodynamics, and glomerular dynamics in SHR independent of a minimal further increase in arterial pressure. These findings support the concept of a strong independent causal relationship between salt-excess and cardiovascular and renal injury.