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Published in Samar Razaq, Difficult Cases in Primary Care, 2021
The acronym HOP helps remember the presenting features of nephrotic syndrome. The triad of hypoalbuminaemia (and hyperlipidaemia), oedema and proteinuria indicate the presence of nephrotic syndrome. In children it is caused mainly by two idiopathic diseases: (1) minimal change nephrotic syndrome and (2) focal segmental glomerulosclerosis. An increased risk of infectious complications among children with nephrotic syndrome has long been recognised. Cellulitis and spontaneous bacterial peritonitis are not too infrequent complications of nephrotic syndrome and one should be on guard against their development. Children should receive pneumococcal vaccination. Overwhelming bacterial infection in nephrotic syndrome still carries a significant mortality rate and hence should not be taken lightly when seen in primary care. Thromboembolic complications are also more common in nephrotic syndrome because of the hypercoagulable state it encourages. They are, however, less common in children than in adults. Hyperlipidaemia, hypertension, hypercoagulability and use of steroids as treatment all increase the cardiovascular risk in sufferers of nephrotic syndrome. Vitamin D deficiency due to loss of vitamin D–binding protein through the kidney may lead to secondary hyperparathyroidism. Progression to end-stage renal disease may be inevitable for some children who end up requiring dialysis. Children who respond to steroids will tend to have the best long-term prognosis.
Role of Vitamin D and Antioxidants in the Prevention and Treatment of Alzheimer’s Disease
Published in Abhai Kumar, Debasis Bagchi, Antioxidants and Functional Foods for Neurodegenerative Disorders, 2021
Shilia Jacob Kurian, Ruby Benson, Sonal Sekhar Miraj, Mahadev Rao
The cholecalciferol further gets hydroxylated to 25-hydroxycholecalciferol [25(OH) vitamin D] in the liver and later to 1,25-dihydroxycholecalciferol (calcitriol) by 1α-hydroxylase in the kidney (Cherniack and Troen 2016). The metabolites of vitamin D are transported in the blood bound to the vitamin D binding protein (85%–88%) and albumin (12%–15%) (Bikle 2018). 1,25-dihydroxycholecalciferol, the fat-soluble active form of vitamin D, crosses the phospholipid layers and enters the nucleus where it binds to the vitamin D receptor (VDR) to exert its genomic effects (Cherniack and Troen 2016). Once bound, VDR forms a heterodimer complex with retinoid X receptor (RXR) resulting in the formation of the VDR-RXR complex. This attaches to the vitamin D responsive elements that are specific sequences on the DNA. The non-genomic rapid effects are seen when it binds to the membrane-associated, rapid-response steroid-binding (MARRS) receptor on the cell surface (de Abreu et al. 2009).
Pathogenesis: Molecular mechanisms of osteoporosis
Published in Peter V. Giannoudis, Thomas A. Einhorn, Surgical and Medical Treatment of Osteoporosis, 2020
Anastasia E. Markatseli, Theodora E. Markatseli, Alexandros A. Drosos
Vitamin D in the circulation is bound to the vitamin D binding protein. The inactive form 25(OH)D3 is the circulating form of vitamin D whose levels are used to determine vitamin D status. Although the lower normal limit of 25(OH)D3 is 20 ng/mL according to most laboratories, this limit is preferred to be set at 30 ng/mL, since it has been shown that levels of inactive vitamin D less than 30 ng/mL induce secondary hyperparathyroidism (79–81).
Vitamin D attenuates biofilm-associated infections via immunomodulation and cathelicidin expression: a narrative review
Published in Expert Review of Anti-infective Therapy, 2023
Ruby Benson, Mazhuvancherry Kesavan Unnikrishnan, Shilia Jacob Kurian, Saleena Ummer Velladath, Gabriel Sunil Rodrigues, Raghu Chandrashekar Hariharapura, Anju Muraleedharan, Dinesh Bangalore Venkateshiah, Barnini Banerjee, Chiranjay Mukhopadhyay, Aieshel Serafin Johnson, Murali Munisamy, Mahadev Rao, Benson Mathai Kochikuzhyil, Sonal Sekhar Miraj
Vitamin D in food/skin is activated by two successive stages of hydroxylation. Ingested vitamin D gets bound to vitamin D binding protein (VDBP), a serum glycoprotein with a single binding site for all vitamin D metabolites [23–25]. First, vitamin D is hydroxylated at the C-25th position in the liver by cytochrome P450 (CYP) 2R1 to form 25-hydroxy vitamin D, or calcidiol. Secondly, in the kidney, CYP27B1 adds a hydroxyl group at C-1 to generate 1,25-dihydroxy vitamin D, the functional form that mediate genomic actions [26–28]. Hypocalcemia, fibroblast growth factor 23, and parathyroid hormone, regulate renal hydroxylases [29]. VDBP’s high affinity for 25-hydroxy vitamin D increases the levels of circulating 25-hydroxy vitamin D, thereby assuaging vitamin D deficiency [24,25].
Health implication of vitamin D on the cardiovascular and the renal system
Published in Archives of Physiology and Biochemistry, 2021
Raghad Khalid Al-Ishaq, Peter Kubatka, Martina Brozmanova, Katarina Gazdikova, Martin Caprnda, Dietrich Büsselberg
Vitamin D is synthesised and activated by three steps. Skin exposed to ultraviolet B radiation produces cholecalciferol (Takeyama et al.1997, Holick 2007). Vitamin D-binding protein attaches to cholecalciferol while it is transported to the liver to be absorbed. In the liver, 25-hydroxylase activates the inactive circulating vitamin D producing 25-hydroxyvitamin (25(OH)D) (Bikle 2016). In the kidney 1α-hydroxylase converts this molecule to the active form of vitamin D (1α,25-dihydroxyvitamin D (1,25(OH)2D) (Figure 1). Parathyroid hormone regulates the production of 1,25(OH)2D in the kidney (Prosser and Jones 2004). 1,25(OH)2D enters the cells either by diffusion or by an active transport system (endocytic receptor), where it binds to a vitamin-D-receptor (VDR) for vitamin D gene transcription (Christakos et al.2010).
Controversies related to vitamin D deficiency effect on the maternal and feto-placental unit – an update
Published in Journal of Obstetrics and Gynaecology, 2020
Shabnum Sibtain, Prabha Sinha, Madhavi Manoharan, Aaleen Azeez
Vitamin D binding protein (DBP) takes Vitamin D3 in the blood to the liver. There are two enzymatic hydroxylations in the body for its activation. The first takes place in the liver, mediated by the 25-hydroxylase which forms 25-hydroxyvitamin D (25OHD). The second reaction takes place in the kidney, mediated by 1α-hydroxylase, which converts 25OHD to the biologically active hormone, calcitriol (1,25-dihydroxyvitamin D (1,25(OH) 2 D) and inactive 24,2S-dihydroxycholecalciferol. After synthesis of calcitriol in the kidneys, it binds to DBP and transports to the target organs. This dissociates from DBP at target organs and binds to a Vitamin D Receptor (VDR). Vitamin D Receptors are present at numerous tissues including in the placenta, prostate, breast, colon, lung, bone, parathyroid, pancreas, immune system, and vascular wall (Bergwitz and Jüppner 2010).