Acute kidney injury (AKI), chronic renal failure, and tubular abnormalities represent the kidney disease spectrum of malignancy. Prompt diagnosis and treatment may prevent or reverse these complications. The pathogenesis of AKI in cancer is multifactorial. AKI affects outcomes in cancer, oncological therapy withdrawal, increased hospitalization rate, and hospital stay. Renal function derangement can be recovered with early detection and targeted therapy of cancers. Identifying patients at higher risk of renal damage and implementing preventive measures without sacrificing the benefits of oncological therapy improve survival. Multidisciplinary approaches, such as relieving obstruction, hydration, etc., are required to minimize the kidney injury rate. Different keywords, texts, and phrases were used to search Google, EMBASE, PubMed, Scopus, and Google Scholar for related original and review articles that serve the article’s aim well. In this nonsystematic article, we aimed to review the published data on cancer-associated kidney complications, their pathogenesis, management, prevention, and the latest updates. Kidney involvement in cancer occurs due to tumor therapy, direct kidney invasion by tumor, or tumor complications. Early diagnosis and therapy improve the survival rate. Pathogenesis of cancer-related kidney involvement is different and complicated. Clinicians’ awareness of all the potential causes of cancer-related complications is essential, and a kidney biopsy should be conducted to confirm the kidney pathologies. Chronic kidney disease is a known complication in malignancy and therapies. Hence, avoiding nephrotoxic drugs, dose standardization, and early cancer detection are mandatory measures to prevent renal involvement.

Hemolytic uremic syndrome (HUS) is a microangiopathic thrombotic disease. HUS is classified into typical, secondary, and atypical types. All types are characterized by thrombocytopenia, acute kidney impairment, and hemolysis. Infection with Shiga toxin from Escherichia coli causes typical HUS. Atypical HUS is frequently caused by abnormal complement activation via the alternative pathway because of gene mutations or autoantibodies synthesis. Secondary HUS accompanies post-transplantation, autoimmunity, cancer, etc. Endothelial cell injury initiates cells destruction stimulates procoagulant state, which activates platelet and thrombus generation, producing ischemic tissue injury. HUS pathogenesis is the result of an ineffective complement activation cycle that causes endothelial cells damage, activating platelet and thrombus formation. In some atypical HUS cases, interrupting the pathogenesis cycle of HUS by inhibiting complement activation might be beneficial, but not in those with gene mutations and patients with typical or secondary HUS. Hence, the pathogenesis of HUS types understanding is required; therefore, a comprehensive review of the differences and resemblances between the HUS types will be discussed and updated.