The Acute Dialysis Quality Initiative has recently published a consensus on the pathophysiology of type I CRS [12]. This syndrome has established risk predictors including hypertension, elevated jugular venous pressure, pulmonary congestion, and reduced renal filtration function at baseline (Fig. 18.1). A proposed approach to subset patients according to hemodynamic and pathophysiologic mechanisms is shown in Fig. 18.2. Because it is believed that a very narrow therapeutic window of intravascular volume management exists for the kidney in the setting of ADHF (Fig. 18.3), it follows that some attempt based on clinical exam, chest-x-ray, noninvasive hemodynamic measures, and even invasive pressure measures are needed to adequate select a patient for a specific therapy. For patients who have intact perfusion and little or no congestion, then minimal diuresis and adjustment to baseline medications is a reasonable strategy. For those with impaired perfusion but still little or no congestion, in the absence of ischemic cardiomyopathy, use of a renal-dose adjusted inotropic agent such as milrinone or levosimendan could be a reasonable pathway. If there is intact perfusion but considerable congestion, then use of vasodilator agents such as nitroglycerin or nesiritide could be entertained. Finally, those with impaired perfusion and pulmonary/systemic congestion and the highest risk for type 1 CRS and inpatient mortality, combined use of diuretics and inodilators, and possibly early continuous renal replacement therapy could be considered. It is important to understand in each of these four scenarios, none of the therapies above have been specifically tested in that subset in an adequately powered, randomized, placebo controlled randomized trial. Hence, novel agents should have the advantage of collective hindsight and be tested in specific phenotypic patients at risk for type 1 CRS in order to give the most valid treatment inferences and help move the field forward.