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Nephrotic syndrome is associated with up-regulation of the heparin-binding epidermal growth factor (HB-EGF). Erlotinib blocks the activation of the epidermal growth factor receptor (EGFR) in response to HB-EGF. This study investigates the effect of Erlotinib on the progression of proteinuria, renal dysfunction, and salt retention in doxorubicin treated nephrotic rats. Male rats were divided into 3 pair-fed groups (n = 13/group) as follows: Control rats ( Ctrl ); rats receiving intravenous doxorubicin ( Dox ); and rats receiving intravenous doxorubicin followed by daily oral Erlotinib ( Dox + Erl ). Upon establishment of high grade proteinuria, urine sodium and creatinine clearance were measured. Kidney tissue was dissected and analyzed for γ-epithelial sodium channel (γENaC), sodium-potassium -chloride co-transporter 2 (NKCC2), sodium chloride co-transporter (NCC), aquaporin 2 (AQP2), and EGFR abundances using western blot. Creatinine clearance was preserved in the  Dox + Erl  rats as compared to the  Dox  group (in ml/min:  Ctrl : 5.2±.5,  Dox : 1.9±0.3,  Dox + Erl : 3.6±0.5). Despite a minimal effect on the degree of proteinuria, Erlotinib prevented salt retention (Urinary Na in mEq/d:  Ctrl : 2.2±0.2,  Dox : 1.8±0.3,  Dox + Erl : 2.2±0.2). The cleaved/uncleaved γENaC ratio was increased by 41±16% in the  Dox  group but unchanged in the  Dox + Erl  group when compared to  Ctrl . The phosphorylated EGFR/total EGFR ratio was reduced by 74±7% in the  Dox  group and by 77±4% in the  Dox + Erl  group. In conclusion, Erlotinib preserved renal function and prevented salt retention in nephrotic rats. The observed effects do not appear to be mediated by direct blockade of EGFR.

Erlotinib Preserves Renal Function and Prevents Salt Retention in Doxorubicin Treated Nephrotic Rats