case_images: PMC8667226_01
case_images: Time course of the case. Time course of serum creatinine levels, trastuzumab and T-DM1 infusions, and kidney biopsy. Abbreviations: ADM, admission; ALND, axillary lymph node dissection; T-DM1, ado-trastuzumab emtansine.
case_images: fonc-11-796223-g001.jpg
case_images: PMC8667226_01_fonc-11-796223-g001.jpg
case_images: f1
case_images: Four weeks prior to admission, the patient received the first infusion with T-DM1 followed by a second infusion 1 week prior to admission ( Figure 1 ). At admission, the patient presented to our emergency department with hypertensive crisis (initial blood pressure of 211/126 mmHg), acute kidney injury (AKI) stage 1, proteinuria (4.4 g/g creatinine), and albuminuria (3.1 g/g creatinine, normal range <30 mg/g,  Figure 1  and  Table 1 ). During the further course, the patient presented with deterioration of kidney function (serum creatinine up to 2.25 mg/dl, normal range 0.5-1 mg/dl,  Figure 1 ), in addition to progressive nephrotic range proteinuria (up to >10 g/g creatinine), albuminuria (up to 6.7 g/g creatinine, normal range <30 mg/g), and hematuria. After discontinuation of T-DM1 therapy, proteinuria (down to 1.1 g/g creatinine) and albuminuria (down to 0.7 g/g creatinine) improved 3 weeks after the last T-DM1 infusion without further specific treatment, associated with improvement of kidney function (serum creatinine 1.13 mg/dl, normal range 0.5-1 mg/dl,  Figure 1 ).
case_images: Histopathological findings. (A, B) Representative kidney sections stained with periodic acid-Schiff and Masson's Trichrome showing acute tubular injury and mild interstitial fibrosis. (C) Glomeruli showed mild mesangial expansion according to Tervaert class IIa. (D) Notably, collapsing FSGS was present. (E) As shown by silver stain, no double contours of the basement membrane were detectable. (F-J) No subendothelial immune deposits (IgA, IgG, IgM, C1q, and C3c) were detectable, while IgM was entrapped in damaged glomerular capillaries. Scale bars: 100 mum. Abbreviations: C1q, complement component 1q; C3c, complement factor 3 conversion product; FSGS, focal segmental glomerulosclerosis; IgA, immunoglobulin A; IgG, immunoglobulin G.
case_images: fonc-11-796223-g002.jpg
case_images: PMC8667226_01_fonc-11-796223-g002.jpg
case_images: f2
case_images: A kidney biopsy was performed showing acute tubular injury and mild interstitial fibrosis ( Figures 2A, B ). Glomeruli showed moderate mesangial expansion according to Tervaert class IIb ( Figure 2C ). Notably, collapsing FSGS was present ( Figure 2D ). FSGS due to chemotherapy-associated thrombotic microangiopathy (TMA;  Figure 2E ). Furthermore, no subendothelial immune deposits (IgA, IgG, IgM, C1q, and C3c) were detectable, while IgM was entrapped in damaged glomerular capillaries ( Figures 2F-J ).