Uraemic patients may have markedly elevated serum GH concentrations ye
t, for hitherto unknown reasons, they do not develop acromegaly. We di
scuss the diagnostic dilemma presented by a 33-year-old Caucasian male
with chronic renal failure (creatinine clearance 10 ml/min) secondary
to polycystic kidney disease, elevated GH concentrations (fasting con
centration of 22.6 rising to 77.9 mU/l 30 minutes after a 75-g oral gl
ucose load) as well as acromegalic features. Review of the patient's r
elatives and the findings of a normal serum IGF-I concentration and a
normal pituitary fossa on magnetic resonance imaging, suggest that the
patient's acromegalic appearance is a familial trait and his abnormal
GH dynamics a result of his renal failure rather than acromegaly. The
patient's normal GH bioactivity and reduced GH binding protein concen
tration supports the current belief that chronic renal failure leads t
o an increase in peripheral tissue resistance to GH due to decreased G
H receptor numbers. These changes, together with reduced IGF-I bioacti
vity, may explain why patients with chronic renal failure do not devel
op acromegaly in the presence of abnormally elevated levels of GH.