Test Paper 1
Teck Yew Chin, Susan Cheng Shelmerdine, Akash Ganguly, Chinedum Anosike in Get Through, 2017
Acute tubular necrosis is common in the early post-operative period and results in reduced function, which gradually recovers over the next few weeks to months. There is no graft tenderness or fever, unlike acute rejection. The scintigraphic findings are abnormal immediately after surgery. The perfusion phase is relatively maintained well; later phases show slow washout and persistent isotope accumulation. In contrast, if the isotope study is normal in the early post-operative phase and becomes abnormal subsequently, acute rejection can be diagnosed confidently.
Life Care Planning for Organ Transplantation
Roger O. Weed, Debra E. Berens in Life Care Planning and Case Management Handbook, 2018
Following kidney transplant, post-operative care focuses on monitoring urine output, replacing fluids, and maintaining normal electrolyte values. Foley catheters will be maintained for 3 to 5 days post-operatively. Transplanted kidneys may begin to function immediately, producing copious amounts of urine. Acute tubular necrosis may be seen, resulting from ischemia of the kidney tubules. Acute tubular necrosis necessitates an increased length of stay, along with dialysis for resolution and preservation of the patient's health.
Imatinib-induced podocytopathies in a patient with gastrointestinal stromal tumor
Published in Renal Failure, 2021
Gang Wang, Ning Zhuo, Ying Luo, Jie Li
As a tyrosine kinase inhibitor, imatinib is widely used in the treatment of chronic myeloid leukemia and GIST [1]. Studies by Yilmaz et al. [2] and Chen et al. [3] both showed that acute kidney injury (AKI) occurs in patients with chronic myeloid leukemia treated with tyrosine kinase inhibitors, with imatinib being more common. The exact mechanism by which imatinib causes AKI is unclear, and acute tubular necrosis (ATN) may be the major cause [4]. The proliferation and regeneration of renal proximal tubular cells depend on the activation of PDGFR, and imatinib inhibits PDGFR and blocks PDGF activation, resulting the inability of renal proximal tubular cells to proliferate and regenerate [4]. Apoptosis of renal proximal tubular cells blocks the renal tubules and eventually leads to acute tubular necrosis. However, glomerular podocyte changes caused by imatinib is very rare. How imatinib causes podocytopathies and its pathogenesis draws our attention.
Electron microscopic findings can support multiple etiologies of nephrotoxicity in renal tubules
Published in Ultrastructural Pathology, 2020
Ping L. Zhang, Timothy Pancioli, Wei Li, Hassan D. Kanaan
The light microscopy revealed unremarkable glomeruli. The proximal tubules were slightly dilated with moderate vacuolization changes in the cytoplasm on hematoxylin/eosin stained section and some diminished brush borders on PAS stained section (Figure 2a,b). Proximal tubules stained moderately positive for kidney injury molecule-1 (KIM-1), a specific marker of proximal tubular injury.24,25 The findings are consistent with moderate acute tubular injury (so-called acute tubular necrosis). Vessels were not remarkable and there was no significant interstitial fibrosis and tubular atrophy. Immunofluorescent studies showed negative staining for all panel of antibodies in the glomerular and tubulointerstitial compartments. EM revealed numerous round and dilated lysosomes containing randomly distributed whirling electron dense materials, so-called zebra bodies or myeloid bodies in proximal tubules (Figure 2c). These were found in some distal tubules as well. The myeloid bodies were measured ranging from 500 to 1000 nm in sizes. One year follow-up data indicated that patient’s sCr was returned to a normal level (Table 1).
Safety of current antiviral drugs for chronic hepatitis B
Published in Expert Opinion on Drug Safety, 2022
Chiara Masetti, Nicola Pugliese, Alessio Aghemo, Mauro Viganò
All oral antiviral agents are excreted in active form by the kidney through active uptake by proximal tubular cells and the subsequent elimination in the urinary space. Proximal renal tubule seems most commonly involved in nephrotoxicity induced by oral antiviral agents, as these cells are particularly rich in mitochondria and therefore more susceptible to damage. Renal tubular dysfunction may be difficult to detect, as early indicators, such as fractional excretion of phosphate and retinol-binding protein (RBP), are not commonly used in clinical practice, while commonly used indicators for renal function (glomerular filtration rate, eGFR, and creatinine clearance) may underestimate renal tubular injury [29]. Reductions in renal tubular function may lead to a Fanconi-like syndrome, characterized mainly by metabolic acidosis, hypophosphatemia, hyperphosphaturia, and glycosuria, which can become life-threatening. Conversely, acute tubular necrosis is more frequently observed in patients with preexistent kidney disease [12].