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Malignant Renal Mass

Malignant Renal Mass: Pathogenesis & clinical findings ↑ Central Chronic renal adiposity Smoking Hypertension failure ↑ Glomerular blood flow in nephron of ↑ Insulin Accumulation Induction of Formation of kidney ↑ Adipokines ↑ Cytokines ↑ Oxidative state resistance of heavy metals metabolic changes renal cysts ↑ Availability of insulin-like growth factor promotes cellular proliferation Aberrant proliferation causes mass effect Mass compresses various structures Obstructs the collecting system of the kidney (including ureter, ureteropelvic junction, renal pelvis, renal calyces) & prevents flow of urine ↑ Leptin & vasfatin promote cellular metabolism to attempt to meet energy demands of proliferating cells ↑ IL-15 & VEGF promote inflammation ↑ VEGF in response to energy demands causes ↑ angiogenesis (blood vessel growth) causing cellular damage & ↑ angiogenesis Cadmium & arsenic in renal tissue disrupt metal & ion homeostasis causing cell damage which initiates injury- repair cycle Generation of reactive oxygen species causes oxidative damage to genes regulating cell cycle ↓ Oxidative phosphorylation promotes glycolysis/ survival in hypoxic conditions typical of tumor microenvironment Altered amino acid metabolism in cells enhances biosynthetic capabilities & promotes cell proliferation ↑ Pressure causes hypoxic conditions as tubular electrolyte load is ↑ & ↑ Atypical energy demand on renal epithelial cell tubular cells is ↑ proliferation promotes tumor suppressor gene mutations Hypoxia stimulates VEGF to ↑ angiogenesis ↑ Blood flow damages endothelial cells & initiates the injury-repair cycle which ↑ the risk of cell mutations ↑ Angiogenesis ↑ Cellular metabolism ↓ Fidelity of DNA repair mechanisms ↑ Cellular damage results in DNA mutations Altered metabolism promotes survival in tumor microenvironment ↑ Proliferation of cancer cells (typically from proximal tubular epithelial cells, as in clear cell renal cell carcinoma) Malignant Renal Mass Metastasis to distal sites (most commonly bone, lungs, liver, brain) Cancer cells release proteolytic (protein degrading) enzymes including MMPs, cathepsins, & uPA Degradation of healthy renal tissue & vasculature surrounding collecting system of kidneys impairing flow of urine and causing blood loss into collecting system Inactivation of VHL gene ↑ VEGF expression & causes ↑ angiogenesis ↑ Vascular permeability due to uninhibited growth ↑ Muscle & fat wasting from ↑ inflammatory cytokines activates JAK/STAT & NF-κB pathways Gain of function mutations to PI3K/AKT/mTOR cause ↑ glucose uptake & drive insulin resistance without hyperinsulinemia (↑ blood insulin Cancer cells release of adipose triglyceride lipase & hormone- sensitive lipase Tumor-generated ↑Secretion of Tumor- cell death releases parathyroid generated cell proinflammatory hormone- death ↑ IL-6 cytokines & ↓ renal related protein levels & cell production of (PTHrP) initiates ↑ erythropoietin (EPO) production of ↑ lipolysis & browning (protein regulating PTHrP is thrombopoietin of white adipose tissue red blood cell Weaker vessels form (conversion to homologous to (protein production) Hydronephrosis within the kidney metabolically active parathyroid regulating ↑ Creatinine (hydrostatic collecting system & state by ↑ UCP1 hormone (PTH) platelet dilation of the subsequently rupture expression) & competes production) renal pelvis & ↓ Erythropoiesis (red with PTH to calyces) blood cell production) bind to PTH from ↓ EPO receptors Thrombocytosis (↑ platelets) Compresses posterior abdominal wall nerves Imbalance of anabolic & catabolic metabolism, reducing body mass due to ↑ catabolism Brown adipose tissue thermogenic properties ↑ body temperature Flank pain Hematuria (presence of blood in urine) Anemia Bleeding at site of metastasis Weight loss Drenching night sweats PTH receptor activation promotes ↑ bone resorption & renal Ca2+ reabsorption ↑ Ca2+ Published Aug 31, 2025 on www.thecalgaryguide.com Familial Renal Carcinoma Syndrome Genetic mutations conferred from birth Authors: Kaiden Jobin Sergio F. Sharif Reviewers: Jessica Revington Nimira Alimohamed* *MD at time of publication Gain of function for proto- oncogenes Loss of function for tumor suppressor genes Compresses stomach/ esophagus Compresses bladder Compresses diaphragm ↑ Urinary Early satiety Cough frequency Legend: Malignant renal cells produce ↑ EPO & subsequently ↑ erythropoiesis Polycythemia (↑ red blood cells) Neoplastic proximal tubule cells secrete ↑ renin Intrarenal ischemia (reduced blood flow) due to tumor growth compressing renal blood supply Hypertension ↑ Tumor cell secretion of hepatotoxins, lysosomal enzymes, & IL-6 Secreted products hepatocellular injury, releasing cell contents IL-6 triggers immune response against hepatocellular cell contents in response to injury ↑ ALT ↑ AST ↑ ALP ↑ Prothrombin time ↑ Bilirubin Pathophysiology Mechanism Sign/Symptom/Lab Finding Complications