{"id":9036,"date":"2026-11-08T13:26:32","date_gmt":"2026-11-08T13:26:32","guid":{"rendered":"https:\/\/zamzam.edu.sd\/2026\/?page_id=9036"},"modified":"2026-11-08T15:42:23","modified_gmt":"2026-11-08T15:42:23","slug":"cancer-chemotherapy-and-acute-kidney-injury-nephrotoxic-mechanisms-the-limits-of-prevention-and-mechanism-informed-renoprotection-zamzam-medical-journal","status":"publish","type":"page","link":"https:\/\/zamzam.edu.sd\/2026\/?page_id=9036","title":{"rendered":"Cancer Chemotherapy and Acute Kidney Injury: Nephrotoxic Mechanisms, the Limits of Prevention, and Mechanism-Informed Renoprotection \u2013 Zamzam Medical Journal"},"content":{"rendered":"<p style=\"margin:1.5em 0;\"><a href=\"https:\/\/zamzam.edu.sd\/2026\/wp-content\/uploads\/2026\/11\/ZMJ-V1I1-9036-chemotherapy-aki.pdf\" target=\"_blank\" rel=\"noopener\" style=\"display:inline-block;padding:10px 22px;border-radius:4px;text-decoration:none;font-family:Georgia,serif;font-size:0.95em;font-weight:bold;margin:0 8px 8px 0;background:#8B1A1A;color:#fff;\">\u2b07 Download Article PDF (pp. 22\u201328)<\/a><\/p>\n<div style=\"background:#f8f8f8;border-left:4px solid #8B1A1A;padding:1.2em 1.5em;margin:1.5em 0;font-family:Georgia,serif;\">\n<p style=\"font-weight:bold;font-size:1em;margin:0 0 0.7em;color:#8B1A1A;text-transform:uppercase;letter-spacing:0.05em;\">Abstract<\/p>\n<p style=\"margin:0 0 0.8em;line-height:1.7;\">Acute kidney injury (AKI) is among the most frequent and consequential organ toxicities of cancer chemotherapy, contributing to dose reduction, treatment discontinuation, chronic kidney disease, and mortality. Chemotherapy-induced AKI is, in most cases, not idiosyncratic: it reflects a mechanistically defined pharmacological injury determined by the interaction between a nephrotoxic agent and specific renal transport, metabolic, and vascular pathways. Cisplatin enters proximal tubular cells through organic cation transporter 2 (OCT2) and copper transporter 1 (CTR1), triggering mitochondrial dysfunction and apoptosis; ifosfamide generates the tubular toxin chloroacetaldehyde, producing Fanconi syndrome; high-dose methotrexate precipitates within the acidic tubular lumen; antiangiogenic agents disrupt podocyte-endothelial vascular endothelial growth factor (VEGF) signaling, producing proteinuria, hypertension, and thrombotic microangiopathy; and immune checkpoint inhibitors provoke acute interstitial nephritis. However, mechanistic intelligibility should not be conflated with clinical preventability. For several agents \u2014 most notably ifosfamide tubulopathy and checkpoint inhibitor nephritis \u2014 no effective prophylaxis exists, and even for cisplatin, AKI occurs in approximately a quarter to a third of patients despite optimal hydration. This review therefore advances a deliberately calibrated thesis: mechanistic understanding reliably guides monitoring and mitigation, and identifies rational renoprotective targets, but does not yet render chemotherapy-induced AKI reliably preventable across agents. We critically evaluate the evidence for established renoprotective strategies, the real-world limitations of emerging biomarkers and rescue therapies including glucarpidase, the diagnostic pitfalls of creatinine-based AKI definition in sarcopenic cancer patients, and the underappreciated transition from AKI to chronic kidney disease in cancer survivors. A four-domain framework for nephrotoxicity risk stratification is proposed, with explicit attention to where current evidence is strong and where it remains aspirational.<\/p>\n<p style=\"margin:0.5em 0 0;font-size:0.9em;\"><strong>Keywords:<\/strong> acute kidney injury; chemotherapy nephrotoxicity; cisplatin; organic cation transporter 2; thrombotic microangiopathy; tumor lysis syndrome; chronic kidney disease; renoprotection<\/p>\n<p style=\"margin:0.5em 0 0;font-size:0.9em;\"><strong>Authors:<\/strong> Khalid Omer Alfarouk, Amel A. Mohamed<\/p>\n<p style=\"margin:0.5em 0 0;font-size:0.9em;\"><strong>Affiliation:<\/strong> Zamzam University College, Khartoum, Sudan; King Salman Armed Forces Hospital, Tabuk, Saudi Arabia<\/p>\n<p style=\"margin:0.5em 0 0;font-size:0.9em;color:#555;\">Vol. 1, Issue 1 \u00b7 June 2026 \u00b7 pp. 22\u201328<\/p>\n<\/div>\n","protected":false},"excerpt":{"rendered":"<p>\u2b07 Download Article PDF (pp. 22\u201328) Abstract Acute kidney injury (AKI) is among the most frequent and consequential organ toxicities of cancer chemotherapy, contributing to dose\u2026<\/p>\n","protected":false},"author":27,"featured_media":0,"parent":0,"menu_order":0,"comment_status":"closed","ping_status":"closed","template":"","meta":{"footnotes":""},"class_list":["post-9036","page","type-page","status-publish","hentry"],"_links":{"self":[{"href":"https:\/\/zamzam.edu.sd\/2026\/index.php?rest_route=\/wp\/v2\/pages\/9036","targetHints":{"allow":["GET"]}}],"collection":[{"href":"https:\/\/zamzam.edu.sd\/2026\/index.php?rest_route=\/wp\/v2\/pages"}],"about":[{"href":"https:\/\/zamzam.edu.sd\/2026\/index.php?rest_route=\/wp\/v2\/types\/page"}],"author":[{"embeddable":true,"href":"https:\/\/zamzam.edu.sd\/2026\/index.php?rest_route=\/wp\/v2\/users\/27"}],"replies":[{"embeddable":true,"href":"https:\/\/zamzam.edu.sd\/2026\/index.php?rest_route=%2Fwp%2Fv2%2Fcomments&post=9036"}],"version-history":[{"count":5,"href":"https:\/\/zamzam.edu.sd\/2026\/index.php?rest_route=\/wp\/v2\/pages\/9036\/revisions"}],"predecessor-version":[{"id":9195,"href":"https:\/\/zamzam.edu.sd\/2026\/index.php?rest_route=\/wp\/v2\/pages\/9036\/revisions\/9195"}],"wp:attachment":[{"href":"https:\/\/zamzam.edu.sd\/2026\/index.php?rest_route=%2Fwp%2Fv2%2Fmedia&parent=9036"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}