Despite reduction of stroke and coronary mortality rates, progression of renal disease to end stage continues to occur with increasing frequency. Recent studies emphasize common pathways of elevated arterial pressures that produce increased glomerular capillary pressures and increase filtered proteins in the urinary space. Such proteinuria, along with activation of the intrarenal renin-angiotensin system, endothelin, and inflammatory cytokines, magnifies progressive renal injury and fibrosis. Malignant forms of hypertension with severe arteriolar injury and proteinuria can be treated effectively with current antihypertensive regimens with improved patient survival. Several recent studies indicate improved renal outcomes in proteinuric diseases, generally regardless of the specific antihypertensive agent. Recent trials of hypertensive subjects with minimal proteinuria demonstrate slower rates of disease progression than that seen in subjects with proteinuria above 1 gram per day. Reduction of arterial pressures, particularly when it leads to reduced proteinuria, can slow the progression of many renal diseases.