List of EGFR inhibitors: View by Brand | Generic. Although the mechanism responsible for development of hypocalcemia is unclear, several explanations are proposed [51] such as: (i) ‘hypomagnesemic hypocalcemia’ related to PTH resistance due to hypomagnesemia and which usually responds to Mg replacement, (ii) end-organ unresponsiveness to PTH with altered release of PTH or (iii) an impaired formation of 1, 25-dihydroxy vitamin D3. Tubular and electrolyte disorders are common and mainly a complication of MAbs while glomerular lesions are unusual and related to various anti-EGFR agents. However, the clinical effects of EGFR inhibitors on ESCC are controversial. It should be pointed out that the two anti-EGFR MAbs cetuximab and panitumumab are commonly employed along with cytotoxic chemotherapy, the latter potentially being able to contribute, directly or through the induction of adverse events such as vomiting and diarrhea, to kidney injury [51]. In one case of MCN with gefitinib withdrawal alone, without immunosuppressive use, complete remission of NS was observed 8 weeks later. Two patients (cetuximab and erlotinib, one case each) required transient hemodialysis (3 weeks for cetuximab, unknown for erlotinib). Dimke H, van der Wijst J, Alexander TR et al. gefitinib (Iressa™), erlotinib (Tarceva™) and Afatinib], and monoclonal antibodies (MAbs) [i.e. The incidence of grade 3/4 hypomagnesemia events compared with controls was 4.8 versus 0.7% with an increased RR of grade 3/4 hypomagnesemia events (RR 6.10, 95% CI 4.37–8, 52, P < 0.001) in all cancers types [52]. This is an orally active, reversible EGFR-TKI marketed by OSI, Genentech and Roche for stage IIIb/IV NSCLC patients, which was approved worldwide as second- or third-line treatment of advanced NSCLC based on the Phase III, randomized BR.21 study [18], and as a first-line treatment for patients with EGFR exon 19 deletion and L858R mutation based on OPTIMAL [19] and EURTAC studies [20]. Treatment of hypomagnesemia involves the temporary discontinuation of anti-EGFR therapy and replacement with either oral or intravenous magnesium [51, 54, 60, 65, 66]. Selected EGFR tyrosine kinase inhibitors in NSCLC (and other cancers). Diagnoses are primarily clinical, with typical timing and clinical presentations as described below. Thus, the authors postulated that inhibitors of the EGFR cascade may actually be useful for preventing severe renal damage and renal failure [10]. 2017 Jun;114:102-113. doi: 10.1016/j.critrevonc.2017.03.032. Sixteen months later, the patient continued to have proteinuria and microhematuria, while renal dysfunction remained unchanged [79]. The EGFR is a transmembrane glycoprotein and a member of the erbB family of receptor tyrosine kinases (TKs). Groenestege WM, Thebault S, van der Wijst J et al. The mechanisms of NS related to anti-EGFR agent are unclear. FDA approved (2007, metastatic breast cancer), Phase II (metastatic gastric, cholangiocarcinoma), Third-generation/mutant-selective EGFR TKIs,