Renal Cancer: Clinical Features

Clinical finding

Cause

A. Endocrine

Hypercalcaemia

Tumor release of parathyroid hormone (PT) and parathyroid hormone related protein (PTHrP) causing increased bone reabsorption

Hypertension

Increased renin secretion activating the renin-angiotensin-aldosterone pathway

Polycythemia

Increased erythropoietin secretion stimulates colony forming unit-erythrocyte (CFU-E)

Nonmetastatic hepatic dysfunction

Release of hepatotoxins and lysosomal enzymes by the tumor

Galactorrhea

Caused by raised prolactin levels

Cushing’s syndrome

Tumor conversion of pro-opiomelanocortin to ACTH which increases cortisol secretion

Alterations in glucose metabolism

Tumor secretion of insulin and/or (entero) glucagon

B. Non Endocrine

Amyloidosis

Occurs in 3–8 % with RCC due to prolonged stimulation of immune system by tumor growth or necrosis

Anaemia

Poor nutritional status and chronic condition; also presence of lactoferrin, an iron-binding protein produced by RCC

Neuromyopathies

Rare effects ranging from nonspecific myalgia to bilateral phrenic nerve paralysis

Vasculopathy

Rare described effects. Pathogenesis not well understood

Nephropathy

Coagulopathy

Prostaglandin elevation

Based on data from Ref. [1]

Nonmetstatic Manifestations

Hypercalcemia

This is the most common phenomenon affecting up to 20 % of patients with RCC [1]. Half of patients with hypercalcemia will have bony metastases [3]. Metastatic RCC related hypercalcemia is the result of activation of osteoclasts causing release of calcium from bone. In contrast, non-metastatic RCC related hypercalcemia is mediated by release of parathyroid hormone and parathyroid hormone-related peptides from tumour cells. These cytokines increases bone resorption, reduce renal excretion of calcium and increase phosphate wasting.

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