Pathological findings of initial-phase postrenal acute kidney injury
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IMAGES IN NEPHROLOGY
Pathological findings of initial‑phase postrenal acute kidney injury Takaya Iida1 · Kenichiro Miura1 · Motoshi Hattori1 Received: 27 May 2020 / Accepted: 13 June 2020 © Japanese Society of Nephrology 2020
Keywords Acute kidney injury · Renal pathology · Obstructive nephropathy A 19-year-old woman with bilateral renal hypoplasia underwent living donor kidney transplantation. On post-transplant day 2, her serum creatinine level was 1.5 mg/dL. On posttransplant day 6, her graft function deteriorated, and serum creatinine level increased to 3.7 mg/dL. A biopsy of the transplanted kidney did not reveal any evidence of rejection. Computed tomography showed mild dilatation of the renal pelvis and calix, with a renal pelvic anteroposterior diameter of 15 mm. Her graft function dramatically improved after drainage with a double-J stent, and the serum creatinine level decreased to 0.72 mg/dL on post-transplant day 11. After 2 weeks, laparoscopy revealed necrosis of the transplanted ureter. We concluded that the cause of graft dysfunction was postrenal acute kidney injury (AKI). Few studies have described the pathological findings of initial-phase postrenal AKI in humans. Glomerular tuft shrinking, tubular dilatation, and flattened epithelium have been observed in the initial-phase of postrenal AKI induced by ureter ligation in rabbits [1]. Similar findings were observed in our case (Fig. 1a). Moreover, although the focal expression of Tam–Horsfall protein (THP) in some glomeruli has been observed in a series of human kidney biopsies [2], marked expression of THP in some glomeruli observed by immunohistochemistry in this case may suggest urine backflow (Fig. 1b). These observations may contribute to a better understanding of the pathophysiology of postrenal AKI.
Compliance with ethical standards Conflict of interest All the authors have declared no competing interest. Ethical standards This article does not contain any studies with animals performed by any authors. Informed consent Informed consent was obtained from the patient.
Reference 1. Nagle RB, Bulger RE, Cutler RE, Jervis HR, Benditt EP. Unilateral obstructive nephropathy in the rabbit. I. Early morphologic, physiologic, and histochemical changes. Lab Invest. 1973;28(4):456–67. 2. Micanovic R, LaFavers K, Garimella PS, Wu XR, El-Achkar TM. Uromodulin (Tamm–Horsfall protein): guardian of urinary and systemic homeostasis. Nephrol Dial Transplant. 2020;35(1):33–43. Publisher’s Note Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.
* Motoshi Hattori [email protected] 1
Department of Pediatric Nephrology, Tokyo Women’s Medical University, 8‑1 Kawada‑cho, Shinjuku‑ku, Tokyo 162‑8666, Japan
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Clinical and Experimental Nephrology
Fig. 1 a Light microscopy shows glomerular tuft shrinking, tubular dilatation, and flattened epithelium (Periodic acid-Schiff stain; original magnification × 200). b Anti-Tamm–Horsfall protein stain was positive in the
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