A 53-year-old Caucasian man comes to the office for intermittent generalized headaches 8 months after deceased donor kidney transplantation. The patient's post-transplantation course was complicated by an episode of acute rejection at 2 months that was treated effectively with high-dose corticosteroids. He has diabetes mellitus and hypertension. His medications include insulin, atenolol, cyclosporine, mycophenolate mofetil, and vitamin D. No changes were made to his medications recently and his immunosuppressants are at therapeutic levels. The kidney donor had no personal or family history of hypertension. The patient's temperature is 36.1 C (97 F), blood pressure is 180/110 mm Hg, and heart rate is 90/min. Examination shows no abnormalities. His serum laboratory values are: The patient is started on sodium restriction, amlodipine, and enalapril to control the hypertension. One week later, he returns with a blood pressure of 138/86 mm Hg. His serum creatinine level is 2.4 mg/dL. Which of the following is the most likely underlying cause of this patient's hypertension?

Question

A 53-year-old Caucasian man comes to the office for intermittent generalized headaches 8 months after deceased donor kidney transplantation.  The patient's post-transplantation course was complicated by an episode of acute rejection at 2 months that was treated effectively with high-dose corticosteroids.  He has diabetes mellitus and hypertension.  His medications include insulin, atenolol, cyclosporine, mycophenolate mofetil, and vitamin D.  No changes were made to his medications recently and his immunosuppressants are at therapeutic levels.  The kidney donor had no personal or family history of hypertension.  The patient's temperature is 36.1 C (97 F), blood pressure is 180/110 mm Hg, and heart rate is 90/min.  Examination shows no abnormalities.  His serum laboratory values are:  The patient is started on sodium restriction, amlodipine, and enalapril to control the hypertension.  One week later, he returns with a blood pressure of 138/86 mm Hg.  His serum creatinine level is 2.4 mg/dL.  Which of the following is the most likely underlying cause of this patient's hypertension?

Quizplus · Accepted Answer

Explanation: 11ec2b69_c1c1_d9e7_8f63_bd61f1287e0d_MD0005_00 About 90%-95% of patients with a kidney transplant have hypertension secondary to specific transplant-related factors or recipient characteristics. This patient presents with severe hypertension and normal baseline renal function (creatinine of 1.1 mg/dL), which is unlikely to be seen in allograft rejection. This patient developed acute kidney injury (creatinine increased to 2.4 mg/dL) after the initiation of an ACE inhibitor. This is highly suggestive of underlying transplant renal artery stenosis as the cause of his hypertension. renal artery stenosis Renal hypoperfusion due to renal artery stenosis stimulates the renin-angiotensin-aldosterone system that in turn causes hypertension and maintains the glomerular capillary pressure and glomerular filtration rate (GFR). In patients with bilateral renal artery stenosis or renal artery stenosis in a solitary kidney (eg, patients with transplant), administration of ACE inhibitors lowers the angiotensin II level acutely, leading to a significant decrease in GFR (by >30%) and acute kidney injury. Renal artery stenosis should also be suspected in transplant recipients with resistant hypertension, flash pulmonary edema, or progressive loss of renal function. Transplant renal artery stenosis causes hypertension in 10%-12% of patients usually within the first 2 years after kidney transplantation. Improper surgical anastomosis is an important cause. It can also occur in acute rejection and cytomegalovirus infection. (Choices A and E) Corticosteroids cause hypertension by stimulating sodium and water retention. Transplant renal dysfunction causes hypertension due to a decreased ability to excrete sodium and water. In either case, the increased extracellular fluid volume can increase preload and cardiac output. Currently, many transplant protocols avoid long-term use of corticosteroids, as in this patient. (Choices B and C) Acute and chronic calcineurin inihibitor toxicity can also cause hypertension by increasing vasoconstrictor endothelin, inhibiting nitric oxide activity, and increasing sympathetic outflow. Acute toxicity is unlikely in a patient with stable serum cyclosporin levels. Chronic toxicity causing hypertension is accompanied by a rise in serum creatinine over time. This patient's baseline normal serum creatinine goes against chronic toxicity. Educational objective: Renal artery stenosis leads to stimulation of the renin-angiotensin-aldosterone system, which results in hypertension. Marked increase in serum creatinine after initiation of ACE inhibitor therapy is highly suggestive of renal artery stenosis (typically bilateral or unilateral stenosis of a solitary kidney or a transplant). References: Hypertension after kidney transplant. (http://www.ncbi.nlm.nih.gov/pubmed/21251543)

A 53-Year-Old Caucasian Man Comes to the Office for Intermittent