A 56-year-old man comes to the office for follow up of hypertension. The patient had undergone kidney transplantation one year ago for focal segmental glomerulosclerosis. He was originally seen in the office 8 weeks ago for hypertension and had a blood pressure of 210/110 mm Hg; initially he was given amlodipine, but the patient continued to have hypertension. Two weeks ago, he was also started on lisinopril. In addition, he takes tacrolimus and low-dose prednisone. The patient currently feels well. Today, blood pressure is 160/90 mm Hg, pulse is 78/min, and respirations are 16/min. Examination shows normal jugular venous pressure, vesicular breath sounds, and normal heart sounds. The transplant site is nontender. Laboratory studies reveal a serum creatinine level of 2.4 mg/dL (2 weeks ago: 1.5 mg/dL). Serum tacrolimus level is within the normal therapeutic range. Which of the following is the most appropriate next step in management of this patient?
This patient with a history of renal transplant has severe, persistent hypertension. In association with the acute kidney injury (AKI) that developed after initiation of lisinopril, this presentation suggests renovascular hypertension due to transplant renal artery stenosis (RAS). Although most cases of RAS occur in elderly men with diffuse atherosclerotic disease, it can also occur in patients with a transplanted kidney and is commonly associated with operative abnormalities (eg, trauma during organ procurement, abnormal suture placement), viral infection (cytomegalovirus, BK virus), and atherosclerosis of the donor artery. Transplant RAS typically occurs in the first 2 years after transplantation.
Similar to RAS due to other causes, transplant RAS typically manifests with resistant hypertension. A decline in renal function after the addition of ACE inhibitors or angiotensin II receptor blockers is highly suggestive of the diagnosis. Other findings that suggest RAS include a lateralizing abdominal bruit and recurrent flash pulmonary edema. The diagnosis is made with renal vascular imaging (eg, renal Doppler ultrasonography). Management of transplant RAS usually includes angioplasty, possibly with stent placement.
(Choice A) Kidney biopsy is indicated to evaluate for AKI due to acute allograft rejection, which is somewhat less likely in the absence of graft tenderness or fever. In addition, biopsy is invasive, and noninvasive methods of assessment (eg, imaging) should be performed prior to biopsy.
(Choice B) Because transplant RAS is the equivalent of bilateral RAS in a non-transplant patient, the initiation of an ACE inhibitor is likely to trigger AKI. Increased lisinopril dosing would likely further worsen this patient's renal function.
(Choices C and E) High-dose prednisone is a common cause of hypertension; however, low doses are not typically associated with marked hypertension. Toxicity to calcineurin inhibitors (eg, tacrolimus) can cause hypertension and AKI; however, such adverse effects are more common with elevated plasma drug levels. In addition, the timing of this patient's AKI following initiation of lisinopril makes RAS more likely than an adverse effect of immunosuppression.
Educational objective:
Renal artery stenosis (RAS) can occur in the renal allograft, typically within 2 years of transplant. Like other forms of RAS, suggestive findings include persistently elevated blood pressure, decline in renal function with the addition of ACE inhibitors, a lateralizing abdominal bruit, and recurrent flash pulmonary edema. The diagnosis is made with renal vascular imaging (eg, renal Doppler ultrasonography).