There are renal implications when employing intensive blood pressure control strategies. While this approach provides cardiovascular benefit in patients with and without chronic kidney disease, the impact on renal disease progression differs according to the pattern of underlying renal injury. In the setting of proteinuria, stringent blood pressure control has generally conferred a protective effect on renal disease progression, but in the absence of proteinuria, this benefit tends to be much less impressive. Thiazide diuretics are frequently part of the regimen to achieve intensive blood pressure control. These drugs can cause hyponatremia and present with biochemical evidence mimicking the syndrome of inappropriate antidiuretic hormone secretion. Altered prostaglandin transport may explain the unique susceptibility to this complication observed in some patients. Hyperkalemia is also a complication of intensive blood pressure lowering particularly in the setting of renin-angiotensin-aldosterone blockade. There are strategies and new drugs now available that can allow use of these blockers and at the same time ensure a normal plasma potassium concentration.