Introduction: Primary aldosteronism (PA) is an increasingly recognized secondary cause of hypertension characterized by higher cardiovascular, renal, and metabolic disease rates than blood pressure-matched essential hypertensives. Current literature suggests expanding screening for PA to include the majority, if not all, hypertensive patients. This expansive screening would place considerable burden on patients and the healthcare system. A simple clinical risk prediction model that identifies patients with low risk for PA could reduce this testing burden. Methods: We evaluated 111 hypertensive patients in the Southern Illinois University Hypertension Clinic who underwent a screening test and, if positive, had subsequent confirmatory testing for PA. We characterized patients based on routine clinical measures including antihypertensive treatment intensity, blood pressure, serum electrolytes, and body size. Classification trees incorporating 96 patients without missing data points for any considered predictor variable were used to identify hypertensive screen-positive patients who have low to absent risk for PA as determined by confirmatory testing. Results: Patients with PA had higher serum aldosterone levels at screening (mean = 22.5 ng/dl ± SD = 11.6 vs. 15.2 ± 4.5, p < 0.001), higher BMI (35.8 kg/m 2 ± 9.9 vs. 29.9 ± 5.8, p < 0.001), lower potassium (3.9 mmol/L ± 0.5 vs. 4.1 ± 0.6, p = 0.03), and more intense antihypertensive drug therapy (defined by the World Health Organization defined daily dose [6.1 ± 3.2 vs. 4.4 ± 3.0, p = 0.01]) than hypertensive patients without PA. The optimal classification tree model performed relatively poorly at differentiating those with PA from those without PA (sensitivity = 0.76, specificity = 0.86, positive predictive value = 0.87, and negative predictive value = 0.73). However, the model did reveal a subset of individuals who consistently tested negative for PA. Out of 14 patients with serum aldosterone concentration < 25.5, serum potassium > 3.55, and BMI < 27, none had PA. Conclusion: We identified a set of readily available clinical variables for identifying hypertensive patients who screened positive for PA but in whom PA was subsequently proven to be absent. Applying these criteria to our screen-positive hypertensive cohort reduces confirmatory testing by approximately 15%. Study in a larger sample size and external validation of this model is needed prior to recommending it for use in clinical decision-making.