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An elevated pulmonary pressure (PASP >35 mm Hg) is a highly prevalent finding in patients with chronic kidney disease (CKD) – approaching over 30% of patients with CKD in some studies. This is often first detected on an echocardiogram, which is a very common test performed in patients with kidney failure, as the volume overload consistent with CKD can often be confused for congestive heart failure at times. In addition, some national guidelines have recommended a screening echocardiogram at the start of dialysis to rule out possible cardiac contribution to poor kidney function. Often, the high pulmonary pressure is a reflection of chronic volume overload and diastolic dysfunction (WHO group 2 pulmonary HTN), but patients with chronic kidney disease may have other unique factors that make them more susceptible to pulmonary hypertension, including elevated levels of endothelin, decreased levels of nitric oxide, metabolic abnormalities of calcium handling, anemia, and high-flow states associated with an AV fistula. Whether as a marker of underlying disease or as a contributing factor, significant pulmonary hypertension has been associated with worse outcomes in patients with CKD as well as kidney transplant recipients. An invasive hemodynamic study can be used to further classify pulmonary hypertension into sub-groups and help generate targets for optimal treatment. Further work is needed to determine whether some of the advances in the treatment of pulmonary hypertension can help improve clinical outcomes in this challenging group of patients.