Nowadays, chronic kidney disease (CKD) and osteoporosis have become crucial health-related issues globally. CKD-induced osteoporosis is a systemic disease characterized by the disruption of mineral, hormone, and vitamin homeostasis that elevates the likelihood of fracture. Here, we review recent studies on the association of CKD and osteoporosis. In particular, we focus on the pathogenesis of CKD-associated osteoporosis, including the homeostasis and pathways of several components such as parathyroid hormone, calcium, phosphate, vitamin D, fibroblast growth factor, and klotho, as well as abnormal bone mineralization, remodeling, and turnover. In addition, we explore the diagnostic tools and possible therapeutic approaches for the management and prevention of CKD-associated osteoporosis. Patients with CKD show higher osteoporosis prevalence, greater fracture rate, increased morbidity and mortality, and an elevated occurrence of hip fracture. We also rule out that increased severity of CKD is related to a more severe condition of osteoporosis. Furthermore, supplements such as calcium and vitamin D as well as lifestyle modifications such as exercise and cessation of smoking and alcohol help in fracture prevention. However, new approaches and advancements in treatment are needed to reduce the fracture risk in patients with CKD. Therefore, further collaborative multidisciplinary research is needed in this regard.

The communication between the gastrointestinal tract and the central nervous system (CNS) allows for certain peptide hormones to influence neurocognitive function. Ghrelin, also known as the ‘hunger hormone,' has the unique ability to enter the CNS and interact with the growth hormone secretagogue receptor (GHS-R) within the hippocampus. Upon interaction with ghrelin, a conformational change in the receptor causes an increase in transcription factors to foster a wide array of physiologic changes in response to caloric deprivation. With the GHS-R in a relatively high concentration within the hippocampus, ghrelin can promote memory, spatial, learning, and behavioral effects. In fact, ghrelin appears to also have a neuroprotective and neuromodulatory response once active within the hippocampal dentate gyrus. Through the GHS-R, higher levels of ghrelin may alter cognitive circuitry and offer a possible link to the treatment of some pathologies implicated in neurological dysfunction. Alzheimer’s disease (AD) is already becoming a significant target for ghrelin neuroreceptor therapy. In such experimental models, ghrelin has been shown to combat this degenerative process by eliciting an ameliorative and regenerative response. Although trials and research are still ongoing, further studies are indicated as early research into this adjuvant therapy is promising.The research team explored the effects of ghrelin by reviewing the downstream signaling modifications of ghrelin's interaction with a specific CNS receptor, the GHS-R. Although the GHS-R is found in multiple locations within the CNS, the team investigated the role of the GHS-R within the hippocampus to focus solely on the neurocognitive implications of ghrelin. The team noted which signaling pathways in particular that ghrelin initiated and used this approach to determine whether ghrelin may have any therapeutic benefits. The team explored the possible therapeutic indications of ghrelin by looking at studies conducted with a specific neurodegenerative disease known to target the hippocampus.

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Granulomatosis with polyangiitis (GPA, Wegener’s granulomatosis) presenting as rapidly progressive glomerulonephritis is not uncommon. The recognition of multisystem disease involving joints, kidney, and lung is critical for diagnosing Wegener's vasculitis. Here, we report a case study of a 52-year-old Bangladeshi man presented with a history of progressively worsening fever, recurrent cough, and hemoptysis. He developed renal failure within a month which was successfully treated with high-dose steroids, cyclophosphamide, and trimethoprim-sulfamethoxazole (TMP-SMX). Rapidly progressive glomerulonephritis can be a fulminant manifestation of GPA, in which case an immediate and aggressive treatment with pulse steroids, high-dose cyclophosphamide and TMP-SMX can be lifesaving.

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Among several inflammatory bowel diseases, Crohn’s disease is associated with inflammation that may take place in any region of the gastrointestinal tract. The inflammatory process is most commonly associated with the ileum, often spreading deep into the bowel tissues, extending into multiple forms, such as strictures and penetrations. Currently, Crohn’s disease has no known cure. Various medical and surgical procedures are used to manage the condition. The underlying mechanisms of the disease are yet to be identified, with recent studies suggesting the influence of genetics, environmental factors, and the possible activity of pathogens. Newer studies also offer strong evidence that suggests a relationship between Crohn’s disease and the nucleotide-binding oligomerization domain-containing protein 2 (NOD2) gene, also known as inflammatory bowel disease protein 1 (IBD1) or caspase recruitment domain-containing protein 15 (CARD15). NOD2 is responsible for the mechanism in which the immune system identifies foreign microorganisms through the sensing of pathogen-associated molecular patterns in microorganisms. NOD2 can detect intracellular muramyl dipeptide (MDP) in the bacterial wall, thereby causing an inflammatory response. Three major mutations associated with the NOD2 gene are known to have an influence on Crohn’s disease (SNP8, SNP12, and SNP13). This article will discuss a number of studies to identify whether there is a relationship between Crohn’s disease and the NOD2 gene.

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