Transplant renal artery stenosis presenting with hypokalemic alkalosis

Question

A 71-year-old man with a history of ESRD secondary to diabetes and hypertension presents for follow-up 6 months after a deceased donor kidney transplant. He received immunosuppression induction with thymoglobulin and had immediate graft function, with a nadir serum creatinine level of 1.1 mg/dL and nadir urine protein-to-creatinine ratio of 0.1 mg/mg (reference range, <0.2). Medications include tacrolimus 3 mg twice daily, mycophenolate mofetil 1 g twice daily, prednisone 5 mg daily, amlodipine 10 mg daily, and carvedilol 12.5 mg twice daily. The patient is adherent to medications and a 2 g/day sodium diet but reports his home BP has averaged 160/94 mm Hg for the last several weeks. On physical examination, BP is 164/96 mm Hg, which is confirmed with a repeat measurement after several minutes of resting in a quiet place. Cardiac and respiratory examinations are unremarkable. He has a well-healed surgical incision and a nontender allograft in the right lower quadrant. He has 1–2+ edema of his lower extremities bilaterally. Laboratory data: sodium 139 mEq/L (reference 136–145); potassium 3.0 mEq/L (3.5–5.0); chloride 103 mEq/L (98–106); total CO₂ 32 mEq/L (23–28); BUN 18 mg/dL (8–20); creatinine 1.4 mg/dL (0.7–1.3); tacrolimus 7 ng/mL (5–15, >3 months after transplantation). Urinalysis is negative for protein, WBCs, and RBCs. In addition to optimization of his BP regimen, which ONE of the following is the MOST appropriate next step in diagnosis or management?

Accepted Answer

C. Duplex Doppler kidney ultrasound — The most appropriate next step in this patient with post-transplant hypertension, hypokalemia, and elevated total CO₂ would be transplant kidney ultrasound with duplex Doppler study.

Hypertension after kidney transplantation is common, with overall prevalence, defined as use of antihypertensive agents, as high as 85%. Risk factors for post-transplant hypertension include pretransplant hypertension, elevated body mass index, male sex, African-American race, and older donor age. Transplant-specific risk factors include delayed graft function, calcineurin inhibitor and steroid use, acute rejection, recurrent kidney disease, and post-transplant proteinuria. Transplant renal artery stenosis (TRAS) is the most common and potentially curable cause of secondary hypertension after kidney transplantation, accounting for 1%–5% of post-transplant hypertension and affecting up to 23% of kidney transplant recipients in total.

TRAS usually occurs between 3 months and 2 years after transplant but can present at any time. It typically presents as worsening hypertension with increased renin, angiotensin II, and aldosterone production and manifesting with hypokalemia, metabolic alkalosis, and decreased kidney function with reduced perfusion pressure, especially in the setting of ACEI or ARB use. Although arterial bruit may suggest TRAS, it is neither a sensitive nor a specific finding. TRAS can be diagnosed by Doppler ultrasound of the kidney or with CT or MR angiography. Definitive diagnosis and treatment can be attempted with renal angiography.

In this patient with a therapeutic tacrolimus level and benign urinalysis, suspicion for acute rejection is not high enough to warrant empiric IV steroids. Similarly, although allograft biopsy is generally warranted for the evaluation of allograft dysfunction, the presence of worsening hypertension, hypokalemia, metabolic alkalosis, and a mild increase in the serum creatinine suggest TRAS as the most likely diagnosis.

Although ambulatory BP monitoring can be a useful tool if white coat or masked hypertension are suspected, this patient's home and clinic BP readings are concordant, so this technique would not be expected to advance his diagnosis or management.

Transplant renal artery stenosis presenting with hypokalemic alkalosis

Explanation

Why each option

More Transplant questions

Browse other topics