Arterial hypertension (HTN) is common after organ transplantation, affecting from 50 to 85% of kidney transplant recipients (1, 2). As one of the most important non-immunological risk factors of transplant failure, HTN contributes significantly to the development of graft loss in these patients. Moreover, HTN significantly increases the risk of serious cardiovascular events, which are the most common cause of death in kidney transplant recipients (3). A retrospective study conducted in over 1600 patients demonstrated that the risk of graft loss or death increases by 5% for every 10 mmHg increment in blood pressure (4). Generally, HTN etiology in kidney recipients is complex and includes graft-dependent factors, recipient-dependent factors and the hypertensive effect of some immunosuppressant drugs. The key factors associated with HTN pathogenesis in kidney transplant recipients are shown in table 1.

A 23-year-old male after kidney transplantation (4 years previously) demonstrated impaired kidney graft excretory function during a routine follow-up visit at the Transplantation Outpatient Clinic (increased serum creatinine levels from 280 to 445 μmol/L; eGFR_MDRD = 13 ml/min/1.73 m²) and high blood pressure values (240/120 mmHg). The patient was urgently admitted to the Department of Nephrology, Endocrinology and Metabolic Diseases, Silesian Medical University in Katowice. On admission, he denied dysuria and fever and reported no decrease in urine volume, no peripheral edema, or pain. Past medical history showed earlier incident of impaired renal excretory function and elevated hypertension after 14 months of kidney transplantation. Doppler ultrasonography and computed tomography angiography (CTA) of the kidney graft allow to make a final diagnosis of transplanted of transplant renal artery stenosis (TRAS) (by approximately 50%) in the vicinity of the anastomosis. Following percutaneous transluminal renal angioplasty (PTRA) of the transplanted kidney with metal stent placement, both the blood pressure and serum creatinine levels returned to the levels observed prior to the described TRAS. During the patient’s present stay on the ward (July 2012), due to ineffective control of hypertension with oral antihypertensive drugs (captopril, nitrendipine, doxazosin, metoprolol, furosemide), parenteral urapidil followed by a continuous nitroglycerine were administered; however, complete blood pressure control was not achieved. The Doppler ultrasound examination showed reduced vascularization of the segmental arteries of the kidney graft; the renal artery anastomosis or the segment distal to the anastomosis were not visualized. Due to a suspected restenosis of the stent placed in the graft artery in 2009, the patient was qualified for a double procedure of angiography and angioplasty. Angiography revealed a critical intrastent stenosis of the graft renal artery at the site of its anastomosis with the left external iliac artery, while the distal segment of the graft renal artery was normal (fig. 1). At the same time, a successful 5 x 20 mm balloon angioplasty of the stenosed segment was performed. No complications were observed following the procedure, and the blood pressure did not exceed 150/95 mmHg. After the procedure, dual antiplatelet therapy (acetylsalicylic acid and clopidogrel) and the antihypertensive treatments with metoprolol (at a dose 2 x 50 mg p.o.) and furosemide (at a dose 2 x 40 mg p.o.) were administered to achieve effective blood pressure control. Seven days after the balloon angioplasty, serum creatinine levels decreased from 445 μmol/L measured on admission to the Nephrology ward, to 329 μmol/L. During follow-up visits at the Transplantation Outpatient clinic 1 and 5 months after the procedure, blood pressure did not exceed 140/90 mmHg and the kidney graft excretory function returned to the level observed during the 12 months preceding the described TRAS episode (maximum creatinine level 287 μmol/L).