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.
|Original language||English (US)|
|Number of pages||2|
|State||Published - Oct 27 1996|
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