Natural history and etiology of hyperuricemia following pediatric renal transplantation

Abstract

A retrospective review was conducted to determine the incidence, etiology, natural history and complications of hyperuricemia after pediatric renal transplantation. Of 81 active transplant recipients aged 10.1 +/- 4.8 (mean +/- SD) years being followed by St. Christopher's Hospital for Children, 57 (70%) were males and 59 (73%) Caucasian. Their immunosuppression consisted of azathioprine, cyclosporine A and prednisone. Mean serum uric acid concentrations peaked at 6 months post transplantation (6.2 +/- 2.6 mg/dl), when 39% of the patients had hyperuricemia and 60% were receiving diuretics, and decreased thereafter. At 30 months, 23% of the patients had hyperuricemia and 17% required diuretics. When we compared 42 normouricemic (group A) with 24 hyperuricemic (group B) patients at 18 months post transplantation, we found that patients in group B were older (11.6 +/- 4.2 vs. 8.6 +/- 5.2 years, P = 0.01), had worse renal function (77 +/- 25 vs. 96 +/- 36 ml/min per 1.73 m2, P = 0.03) and required diuretics more frequently (63% vs. 21%, P = 0.001), but had identical blood levels of cyclosporine A (82 +/- 28 vs. 84 +/- 35 ng/ml, P = 0.78). A family history of gout did not affect the prevalence of hyperuricemia after transplantation. Asymptomatic hyperuricemia is common following pediatric renal transplantation and is more likely attributable to reduced renal function and diuretic therapy than to the known hyperuricemic effect of cyclosporine A. Of these variables, only diuretic therapy is readily controllable and should be closely regulated following pediatric renal transplantation.

Hyperuricemia and gout following pediatric renal transplantation

“…Consistent with previous studies, impaired renal function -i.e. chronic transplant nephropathy -was the most important factor contributing to hyperuricemia [5,9,13,14]. The fact that our control patients showed no difference in plasma uric acid concentration from our transplant patients when there was a similar degree of CRF in the native kidneys supports this notion.…”

“…At 30 months, significantly fewer patients had hyperuricemia (23%) or were on diuretics (17%) [5]. Our study differed from that of Edvardsson on a number of points: (1) our Time after transplantation (year) Plasma uric acid (µmol/l) patients were studied after a median period of almost 5 years following the transplantation; (2) the calculated GFR was lower; (3) only one patient was on diuretics; (4) one-third of the patients were on TAC.…”

“…As primates lack the hepatic enzyme uricase, uric acid in humans is mainly excreted via the renal pathway. The main handling of renal elimination of uric acid, either by reabsorption or secretion, takes place in the proximal tubule [5,6]. During childhood, hyperuricemia is uncommon as children have an increased fractional excretion rate of uric acid [6].…”

“…Hoyer et al [9] described an increased net tubular absorption of uric acid in 28 CSAtreated pediatric renal transplant recipients. A retrospective study from Edvardsson et al [5] revealed hyperuricemia in 23% of children on CSA 30 months following renal transplantation. There is only one report describing gout in five adolescent kidney transplant recipients [10].…”

Hyperuricemia in Pediatric Renal Transplant Recipients

“…Hoyer and associates 6 have described fully increased tubular reabsorption of UA in pediatric renal transplant recipients receiving CsA. Edvardsson and associates 7 also have described hyperuricemia in 23% of pediatric renal transplant recipients on CsA treatment 30 months after a renal transplant. Sparta and associates 8 have described hyperuricemia in 47% of 32 pediatric renal transplant recipients.…”