These co-factors are shown to play an important role in the pathogenetic process attached to senile osteoporosis as they enhance the action of the parathyroid hormone.The intake of calcium in elder people is quite low, and this problem is worsened by a reduced capability to ingest it. This, attached to a decrease in the absorption of vitamin D concerning metabolism, are also factors that contributes to a diagnosis of osteoporosis type II. Risk factors
While senile osteoporosis (type II) is mainly attributed to age, other risks include medical, pharmacological, genetic, and environmental factors. Peak bone mass is a major determinant of bone density, which starts in utero and is typically complete by the age 40. Medical
Though secondary osteoporosis is a separate category when it comes to osteoporosis diagnosis, it can still be a contributing factor to primary osteoporosis. Secondary osteoporosis can be present in pre- and post-menopausal women and in men and have found to be factors contributing to osteoporosis in both sexes (50-80% of men and 30% of post-menopausal women). Therefore, when treating people over 70, it is important to exclude secondary causes of osteoporosis which include endocrine disorders (e.g. hyperthyroidism and diabetes mellitus), gastrointestinal, hepatic and nutritional disorders (e.g. celiac disease and inflammatory bowel disease), hematological disorders (e.g. systemic mastocytosis), renal disorders (e.g. chronic kidney disease), and autoimmune disorders (e.g. rheumatoid arthritis and systemic lupus erythematosus). Medications
Medications that can contribute to bone loss include aluminum (found in antacids), aromatase inhibitors, cyclosporine, depo-medroxyprogesterone (premenopausal), glucocorticoids, lithium, proton pump inhibitors, serotonin reuptake inhibitors, tacrolimus, and tamoxifen (premenopausal).
Pathogenesis
Different molecular mechanisms are involved in PRCC development, which further result in distinct histologic features and clinical outcomes.Type 1 PRCC is caused by a genetic mutation or a gain in chromosome 7 where the MET gene is positioned, resulting in the promotion of oncogenic pathways in renal epithelial cells. Typically, the MET gene is upregulated for renal tissue repair and regeneration by encoding the receptor tyrosine kinase c-MET of hepatocyte growth factor. However, activation of the oncogenic pathway in the MET gene will manifest invasion, anti-apoptosis, angiogenesis, and metastasis.Type 2 PRCC is associated with irregularity of several signaling pathways, which includes CDKN2A silencing, mutation in chromatin-modifying genes, and a GpG island methylator phenotype (CIMP). CDKN2A is a tumor suppressor gene, while loss of its expression results in enhanced tumorigenesis and metastasis. Moreover, mutation of gene involved in chromatin remodeling (SETD2, BAP1, or PBRM) may lead to higher rate of TFE3/TFEB fusion. Additionally, CIMP papillary renal cell carcinoma tumors exhibited somatic FH gene mutation, which is closely associated with HLRCC syndrome. Diagnosis
Currently, cross-sectional imaging with computed tomography (CT) and magnetic resonance imaging (MRI) is known as the best option for diagnosing papillary renal tumors. Computed tomography (CT)
Contrast-enhanced computed tomography (CT) is most commonly used to identify the subtypes of RCC. PRCC can be differentiated from other types of RCC due to its distinguishing features, displaying a small hypovascular renal tumor on T2 weighted images.