Hyperkalemia is the most frequent
electrolyte abnormality found in whole organ transplant recipients receiving either
cyclosporine (CsA) or
tacrolimus (
FK506). Recipients of a simultaneous pancreas kidney (SPK) transplant with bladder drainage may be particularly susceptible to
hyperkalemia secondary to
sodium loss from the bladder-drained pancreas, leading to decreased
sodium delivery to
potassium secretory sites of the kidney. We looked at the incidence of
hyperkalemia in 34 type I diabetic SPK recipients transplanted at our center over the period from 1993 to 1995 and compared this with a cohort of 25 type I diabetic recipients of a kidney alone (K(Tx)) transplant. The incidence of
hyperkalemia was 73.5% in recipients of an SPK, while it was 44% in K(Tx) recipients (P<0.05). CsA levels were higher, on average, in the SPK group (339 ng/ml+/-62 versus 272 ng/ml+/-58 in the K(Tx) group, P<0.05). However, CsA levels were not different between groups at the time of
hyperkalemia, 320+/-74 versus 298+/-49 for SPK and K(Tx), respectively. CsA levels at the time of
hyperkalemia were not different from those at the time of normokalemia. Other medications, serum
bicarbonate, and renal function were not different in the groups. SPK recipients appear to have a greater incidence of
hyperkalemia than kidney alone transplant recipients. This difference cannot be explained by higher acute CsA levels, other medications, or worse renal function. The increased incidence of
hyperkalemia may, in part, be secondary to decreased
sodium delivery to the transplanted kidney.