J. Herman et al., Dysplasia of tubular cells in a kidney-transplanted patient treated with recombinant human growth hormone, PEDIAT TRAN, 5(6), 2001, pp. 463-466
After renal transplantation (Tx), children with growth retardation can be s
uccessfully treated with recombinant human growth hormone (rhGH). However,
the impact of this treatment on kidney allograft function remains a source
of concern. We report on one boy who received a cadaveric kidney transplant
at 12 yr of age, after developing end-stage focal and segmental glomerulos
clerosis and hyalinosis. The early post-transplant period was complicated b
y thrombosis or an arterial branch of the graft and two acute rejection epi
sodes. Because of poor growth, the boy was treated with rhGH starting 22 mo
nths after the Tx. The renal function remained relatively stable for 22 mon
ths after initiation of rhGH therapy and then progressively deteriorated ov
er a period of 10 months, with the patient ending up on dialysis. Several b
iopsies. performed for rejection episodes or before the start of rhGH, or t
o elucidate the deterioration of the renal function, were analyzed, Histolo
gically, a progressive increase in the amount of hypertrophy of the tubules
and of the glomeruli was seen after initiation of rhGH. Hyperplasia of the
tubular epithelium with crowding of cells of the proximal tubules, hyperch
romasia and irregularities in the shape of the nuclei, and abrupt changes o
f chromatism along the tubuli were also observed. These lesions of tubular
dysplasia are extremely unusual in transplanted kidneys and are unlikely to
be caused by compensatory hypertrophy secondary to destruction of renal ti
ssue. They may be an effect of rhGH treatment. The prognostic significance
of these lesions is unknown but merits attention.