Kidney Cancer
GMJ News knowledge hub · last reviewed September 2026 · Georgian Medical Journal
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Renal cell carcinoma (RCC) accounts for around 90% of kidney cancers and approximately 430,000 new cases worldwide each year, and its epidemiology has been transformed by imaging: the classical triad of flank pain, haematuria and a palpable mass is now rare, and more than half of all renal cancers are discovered incidentally on ultrasound or CT performed for unrelated reasons (WHO). This stage migration has driven two major shifts in management: nephron-sparing partial nephrectomy has replaced radical nephrectomy wherever technically feasible, because preserving renal function measurably reduces long-term cardiovascular mortality; and small renal masses under 4cm in older or comorbid patients are increasingly managed by active surveillance, since many grow slowly and a substantial minority are benign. In metastatic disease, combination immune checkpoint inhibitor regimens — alone or with tyrosine kinase inhibitors — have replaced cytokine therapy and produced durable responses previously unattainable.
Key messages
More than half of renal cancers are now found incidentally
The classical triad of flank pain, visible haematuria and a palpable mass is present in under 10% of cases and indicates advanced disease. Widespread cross-sectional imaging means over half of renal cell carcinomas are now detected incidentally on scans performed for unrelated reasons — producing stage migration towards smaller, organ-confined tumours with far better prognosis. Roughly 430,000 new cases occur worldwide annually. Risk factors: smoking, obesity, hypertension, acquired cystic disease in end-stage kidney disease, and inherited syndromes.
Partial nephrectomy wherever feasible — preserving nephrons saves lives
Nephron-sparing partial nephrectomy has replaced radical nephrectomy as the standard for T1 tumours wherever technically feasible. The rationale is not oncological — cancer outcomes are equivalent — but the recognition that removing a whole kidney induces chronic kidney disease, and CKD is a powerful independent driver of cardiovascular events and all-cause mortality. Patients undergoing radical nephrectomy for small tumours have measurably worse long-term non-cancer survival. This is a clear example of an oncological decision that must account for competing causes of death.
Small renal masses — active surveillance is legitimate, and up to 20% are benign
For small renal masses under 4cm, particularly in older or comorbid patients, active surveillance is an established option. Growth is typically slow (around 3mm per year), metastatic progression during surveillance is uncommon, and around 15-20% of small renal masses turn out to be benign lesions — angiomyolipoma or oncocytoma. Renal mass biopsy, historically avoided over unfounded fears of tract seeding, is now recommended before ablation or surveillance and increasingly before surgery in ambiguous cases, and can spare patients an unnecessary operation.
Metastatic RCC — immunotherapy combinations replaced cytokines
Metastatic renal cell carcinoma is chemotherapy-resistant but immunologically responsive. Interferon and interleukin-2 gave low response rates with severe toxicity. Targeted VEGF tyrosine kinase inhibitors (sunitinib, pazopanib, cabozantinib, axitinib) then transformed outcomes. First-line therapy is now combination immunotherapy: dual checkpoint blockade (ipilimumab plus nivolumab) or a checkpoint inhibitor combined with a TKI (pembrolizumab-axitinib, nivolumab-cabozantinib, pembrolizumab-lenvatinib), producing durable responses and improved overall survival. Risk stratification (IMDC criteria) guides regimen choice. Cytoreductive nephrectomy is now selective rather than routine following the CARMENA trial.
Hereditary syndromes — screen young patients and bilateral or multifocal disease
Around 5-8% of renal cancers are hereditary, and identification changes surveillance for the patient and the whole family. Von Hippel-Lindau: clear cell RCC (often bilateral, multifocal, young onset), CNS and retinal haemangioblastomas, phaeochromocytoma, pancreatic lesions. Hereditary leiomyomatosis and RCC (HLRCC, fumarate hydratase): cutaneous and uterine leiomyomas with an aggressive type 2 papillary RCC requiring early wide excision rather than surveillance. Birt-Hogg-Dubé (folliculin): fibrofolliculomas, lung cysts, spontaneous pneumothorax, chromophobe and hybrid oncocytic tumours. Hereditary papillary RCC (MET). Refer for genetic assessment if: age under 46, bilateral or multifocal tumours, a family history, or suggestive syndromic features.
Paraneoplastic syndromes and unusual presentations
RCC is sometimes called the internist's tumour because of its protean presentations. Paraneoplastic features: hypercalcaemia (PTHrP-mediated); polycythaemia (ectopic erythropoietin); Stauffer syndrome (non-metastatic hepatic dysfunction with raised alkaline phosphatase, reversible after nephrectomy); hypertension (renin); pyrexia of unknown origin; and AA amyloidosis. Structural presentations: a new left-sided varicocele that does not decompress on lying down, suggesting left renal vein obstruction; tumour thrombus extending into the renal vein and inferior vena cava, occasionally reaching the right atrium and requiring cardiopulmonary bypass. Any unexplained hypercalcaemia or polycythaemia warrants consideration of renal imaging.
Key statistics
Partial > radical
nephron-sparing surgery preserves renal function and reduces long-term cardiovascular mortality
EAU/AUA5-8%
of renal cancers are hereditary — refer under-46s, bilateral or multifocal disease for genetics
EAU/NCCNIO combinations
checkpoint inhibitor combinations are first-line in metastatic RCC, replacing cytokines and TKI monotherapy
NEJM/EAURenal cell carcinoma — approximate 5-year survival by stage
Glossary of key terms
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