S. Saw et al., Urine laminin and kallikrein, markers of tubulointerstitial damage in experimental protein overload on pre-existing renal damage, PATHOLOGY, 33(1), 2001, pp. 37-43
We studied the response of urinary protein overload on preexisting tubuloin
terstitial nephritis (TIN), which was induced in male Sprague Dawley rats b
y hexachloro-1,3-butadiene (HCBD). Five days after the development of TIN,
puromycin aminonucleoside (PAN) was administered to induce urinary protein
overload. Urinary laminin and kallikrein were measured. Urine specimens wer
e collected daily for 14 days and on day 21; and tissue specimens were coll
ected on days 1, 4, 7, 10, 14 and 21. Urinalysis was correlated with the re
nal pathology at the light microscopic level. Laminin excretion was increas
ed on day 4; one day before total protein, indicating damage to the basemen
t membrane. Kallikrein levels also fell early indicating distal tubular dam
age. There is clear evidence that urine protein overload in a previously da
maged kidney with tubulointerstitial injury leads to accelerated and more s
evere renal damage. Laminin and kallikrein are early and sensitive markers
of renal injury.