Acute pancreatitis and hyperamylasemia in renal homograft recipients

Abstract

In a series of 301 renal homograft recipients, 17 (5.6%) had acute pancreatitis at some time after transplantation. Eleven of these patients died, for a mortality of 64.7%. In each instance, pancreatitis was a major factor in a complex chain of lethal events to which immunosuppression invariably contributed. An additional 43 patients (14.3%) developed asymptomatic hyperamylasemia after transplantation and, undoubtedly, some of these recipients also had pancreatitis. The factors causing pancreatitis in the renal transplantation patient include uremia, hyperparathyroidism, pancreatic injury by drugs, infections resulting from chronic immunosuppression, gallstones, and operative trauma to the pancreas. In cases of preexisting pancreatitis, transplantation is not necessarily precluded, but efforts should be made to find a specific cause of the pancreatitis and take corrective measures, such as biliary tract surgery or parathyroidectomy if indicated, in advance of transplantation.

Fig 1

In this patient, abscess in left labium majus was drained 75 days after transplantation ➀. Sinogram demonstrated an extensive proximal extension of abscess (Fig 2), which was drained through incision in left flank ➁. Large retroperitoneal abscess arising from pancreas was drained 16 days later ➂. All three abscesses communicated. Serum amylase level remained elevated for prolonged periods. Graft function deteriorated during treatment of abscesses.

Fig 2

Sinogram demonstrating a tract (arrows) extending from left labium majus retroperitoneally into left flank. Same patient as Fig 1.

Fig 3

Course of 24-year-old woman who underwent bilateral nephrectomies, splenectomy, and renal transplantation from her father. Major asymptomatic rise in serum amylase level followed operation. One month after operation, enzyme levels returned to normal. Maximal amylase elevations occurred when renal function was poor. Hypercalcemia necessitated emergency parathyroidectomy 46 days after transplantation.

Fig 4

Course of 11-year-old girl who underwent transplantation for renal failure caused by cystinosis. Donor (maternal grandmother) developed hepatitis 30 days after operation. Forty-one days later the patient was readmitted with same diagnosis. Pancreatitis developed approximately 100 days after transplantation. Severe hypocalcemia (serum calcium level below 2.4 mEq/liter), marked metabolic acidosis, and falling hematocrit were observed. Patient died 109 days after transplantation. Autopsy confirmed presence of hepatitis and acute hemorrhagic pancreatitis with fat necrosis.