The cause of reduced Tamm-Horsfall protein excretion in patients suffering
from uric acid diathesis is still unknown. Our investigation was conducted
based on the hypothesis that the solubility of uric acid is increased by Ta
mm-Horsfall protein and that an increased uric acid content in the urine mi
ght cause a decrease in Tamm-Horsfall protein. In 20 patients with uric cal
culi the excretion of Tamm-Horsfall protein, uric acid, calcium, and citrat
e was measured. 65% of the patients had pure uric acid stones (group I) and
35% showed mixed stones with at least 30% of uric acid (group II). Reduced
Tamm-Horsfall protein excretion was found in 63% of the patients of group
I and in 43% of the patients of group II. The excretion of Tamm-Horsfall pr
otein was significantly reduced in pure uric acid stone formers compared to
normal subjects (p < 0.0001). The excretion of uric acid was elevated in 6
1% of the patients of group I and in 86% of the patients of group II. There
was no significant correlation between Tamm-Horsfall protein excretion and
uric acid excretion (r = 0.2139). Calcium excretion was elevated in 57% of
the patients with mixed stones. The excretion of citrate was reduced in al
most all of the patients of groups I and II. Ou results do not support the
hypothesis that an increased content of uric acid in the urine causes a dec
rease in Tamm-Horsfall protein. In our opinion the lower excretion of Tamm-
Horsfall protein in some of the stone patients might be caused by damage in
the distal tubular epithelium. Moreover, it has to be supposed that there
are defects both in the distal and the proximal tubule in patients prone to
develop uric acid calculi.