Publication of the Symplicity HTN-11 and HTN-22 trials showed the feasibility of catheter-based renal sympathetic denervation (RDN) in patients with drug-resistant hypertension and unleashed an unprecedented wave of enthusiasm. Advocates of the technique, driven by legions of marketers, proposed numerous potential applications of RDN, including atrial fibrillation, heart failure, metabolic syndrome and diabetes mellitus, obstructive sleep apnea, and even polycystic ovary syndrome. In this issue of the Journal, Portasiewicz and colleagues3 report the first case of RDN of the native kidneys in a 58-year-old kidney graft recipient. Before the procedure, blood pressure remained uncontrolled despite substitution of cyclosporine with tacrolimus and prescription of 5 antihypertensive drug classes. Renal function was altered, partly because of allograft rejection, with an estimated glomerular filtration rate (eGFR) of 38 ml/min/1.73m2. Using the Symplicity system, radiofrequency energy was applied at 6 different locations in the right renal artery and at 5 sites in the left renal artery. Twenty-four-hour ambulatory blood pressure decreased by 20/15 mm Hg at 3 months and by 16/12 mm Hg at 6 months, left ventricular mass declined, and antihypertensive drug treatment was tapered to 2 drugs, whereas eGFR remained unchanged (39 ml/min/1.73m2) at 6 months. This “first-in-man” case report3 leaves several questions unanswered. The authors did not report on urinary sodium excretion and therefore did not exclude excessive salt intake, which is a major cause of treatment resistance, especially in patients with chronic kidney disease.4 Furthermore, one wonders why the Polish investigators did not try using angiotensin-converting enzyme inhibitors, an established blood pressure–lowering treatment in kidney transplant recipients,5 or use thiazide instead of loop diuretics. Besides stenosis of the artery of the renal graft, other less frequent causes of secondary hypertension in kidney transplant recipients should have been excluded, in particular pheochromocytoma, which can cause resistant hypertension and recurrent hypertensive crises.6 Finally, the authors did not assess adherence, for instance by measuring drug levels in urine or witnessing drug intake,7 nor did they use single-pill drug combinations that improve adherence to treatment. Although the authors must be complimented on bringing their case report to publication, the clinical implications are minimal. The short follow-up of 6 months, the unstandardized method of blood pressure measurement, the absence of a strategy to taper antihypertensive drug treatment after the procedure, and the lack of imaging of the native kidneys at 6 months hamper the extrapolation of the case report to clinical practice. It has been suggested that the RDN might be particularly efficient in patients with chronic kidney disease because this condition is characterized by inappropriate sympathetic activation and because afferent denervation in animal models of chronic kidney disease produced promising results.8 Several authors also highlighted the potential interest of RDN in renal transplant recipients.9 Indeed, in this population, hypertension is frequent, often treatment resistant, and associated with deterioration of the graft function.5 Although the renal transplant itself is denervated, the native kidneys may still cause activation of the sympathetic nervous system through afferent signaling, thereby contributing to the maintenance of high blood pressure.5 Previous studies in kidney transplant recipients10 showed a decrease in peripheral arterial