Shh is released to human urine during acute kidney injury independent of cirrhotic liver damage.

A) Chronic ethanol ingestion in rodent models enhances Shh release into urine. Urine was collected from rats (top) or mice (bottom) ingesting ethanol for 28 or 25 days, respectively, and immunoblotted for Shh as in Figs 5 and 6. B) Humans with acute kidney injury release Shh into to urine. Spot urine samples from normal health controls or hospitalized patients diagnosed with cirrhosis, acute kidney injury (AKI), or with both cirrhosis and acute kidney injury were western blotted for Shh as in the preceding panel. The position of molecular size markers (10 kDa, 20 kDa) are depicted at the right side of the gels. Active Shh as a lipidated protein migrates between these size markers. C) Shh in patient urine correlates to acute kidney injury. Left. Statistical analysis of digitized immunoblots of urinary Shh in panel B among healthy controls, patients diagnosed with acute kidney injury, liver cirrhosis or a combination of the two diseases. N = 10 * p<0.05. Right. Shh density in immunoblots normalized by urine production using the Shh/creatinine ratio (S2 Table) and plotted as a bar and whisker graph showing the median and quartiles. N = 9 * p<0.05.