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The endocrine system
Published in Laurie K. McCorry, Martin M. Zdanowicz, Cynthia Y. Gonnella, Essentials of Human Physiology and Pathophysiology for Pharmacy and Allied Health, 2019
Laurie K. McCorry, Martin M. Zdanowicz, Cynthia Y. Gonnella
A nephrogenic form of diabetes insipidus also occurs in which ADH production is normal but the kidneys do not respond to the effects of ADH. Nephrogenic diabetes insipidus may occur with renal inflammation or injury
Endocrinology
Published in Fazal-I-Akbar Danish, Essential Lists of Differential Diagnoses for MRCP with diagnostic hints, 2017
Nephrogenic diabetes insipidus:1 Primary: X-linked/autosomal dominant (→ childhood onset).2 Secondary: a Electrolyte disturbance (↓ K+; ↑ Ca2+).b Renal pathology (ADPKD; obstructive uropathy; chronic pyelonephritis; sarcoidosis).c Drug-induced (lithium; demeclocycline; glibenclamide; aminoglycosides; amphotericin).
ENTRIES A–Z
Published in Philip Winn, Dictionary of Biological Psychology, 2003
Diabetes insipidus may result from intrinsic kidney disease (nephrogenic diabetes insipidus) but is more commonly due to a deficiency of VASOPRESSIN (known also as antidiuretic hormone). This is a peptide synthesized in the supraoptic and paraventricular nuclei of the posterior HYPOTHALAMUS, especially in response to increased plasma osmotic pressure or decreased blood volume. The peptide is carried by axonal transport to the posterior PITUITARY GLAND (neurohypophysis) where it enters the bloodstream. On reaching the kidney it serves to increase the concentration of the urine by promoting the resorption of water from the renal filtrate (see OSMOREGULATION). Vasopressin also promotes VASOCONSTRICTION and haemostasis and has been assigned a number of more dubious cognitive functions. In the absence of vasopressin, urine output may exceed 10 litres daily but revert to normal with replacement therapy, administered by injection or intranasal spray.
An unusual case of severe hypercalcemia: as dehydrated as a bone
Published in Journal of Community Hospital Internal Medicine Perspectives, 2021
Roshan Acharya, Dylan M Winters, Cameron Rowe, Nathan Buckley, Smita Kafle, Bhaskar Chhetri
It is well known that hypercalcemia causes a nephrogenic diabetes insipidus which may lead to dehydration. There is also evidence hypercalcemia can cause natriuresis and subsequent dehydration [11]. We propose that an initial insult such as dehydration leading to hypercalcemia can precipitate further dehydration as a result of hypercalcemia interfering with the kidney's ability to concentrate urine. This sets up a vicious loop whereby dehydration leading to hypercalcemia becomes worsened by decreasing renal function and worsening hypercalcemia. This patient being dehydrated allowed for such a dramatic rise in serum calcium. The degree hypercalcemia was out of proportion of kidney injury, and furthermore normalization of serum calcium did not correlate with normalization of kidney function. Therefore, we assumed that the hypercalcemia was due to dehydration and the feedforward mechanism which worsened both dehydration and hypercalcemia.
Electrolyte handling in the isolated perfused rat kidney: demonstration of vasopressin V2-receptor-dependent calcium reabsorption
Published in Upsala Journal of Medical Sciences, 2020
Krister Bamberg, Lena William-Olsson, Ulrika Johansson, Anders Arner, Judith Hartleib-Geschwindner, Johan Sällström
The most well-described hormonal regulator of renal calcium handling is parathyroid hormone (PTH), which promotes active calcium reabsorption (8). The parathyroid gland, discovered in Uppsala in 1877 by Ivar Sandström (9), secretes PTH in response to low serum calcium concentrations. Several lines of evidence demonstrate that also AVP stimulates calcium reabsorption. Earlier studies in Brattleboro rats with diabetes insipidus demonstrated that when long-term administration of the selective V2R agonist desmopressin (DDAVP) was ceased, the excretion of calcium increased (1). In a more recent clinical trial, patients with central diabetes insipidus (CDI) and nephrogenic diabetes insipidus (NDI) were challenged with DDAVP administration (2); CDI patients demonstrated a reduced excretion of calcium, whereas no change was observed in the NDI patients. Several channels have been identified for calcium transport along the nephron (10), and mechanistic studies have indicated a stimulatory role of AVP both in the cortical thick ascending limb (cTAL) (11) and the collecting duct (12). The specific effects of AVP on calcium handling in the kidney are, however, not fully understood. The isolated kidney model provides unique possibilities to explore the effects of AVP given that it is possible to precisely control the concentration in the perfusate, which is not possible in vivo where systemic variations in hormone levels occur.
Treatment of Refractory Acute Retinal Necrosis with Intravenous Foscarnet or Cidofovir
Published in Ocular Immunology and Inflammation, 2018
Tomasz P. Stryjewski, Nathan L. Scott, Miriam B. Barshak, Ellis H. Tobin, Joshua O. Mali, Lucy H. Young, C. Stephen Foster, Ivana K. Kim, Marlene L. Durand
A 72-year-old immunocompetent man was admitted in 2012 with PCR-positive VZV ARN OD (OD count fingers, OS 20/20; Figure 1a-b). Intravenous acyclovir 10 mg/kg q8 h plus oral prednisone 60 mg daily were started; IV acyclovir was continued for 14 days and then switched to valacyclovir 1g po tid. The retinitis OD stabilized, but at a clinic visit on day 15, early ARN OS (Figure 1c-d) was seen. Valacyclovir 1 g po tid was continued for 5 more days but retinitis OS progressed, therefore IV foscarnet 60 mg/kg q8 h and intravitreal foscarnet 2.4 mcg/0.1 ml were given. Foscarnet-induced nephrogenic diabetes insipidus developed but renal function remained normal. After 3 weeks of IV foscarnet (reduced to 90 mg/kg once daily during week 3) and three intravitreal foscarnet injections, he was discharged on oral valacyclovir 1 g po tid. He required readmission 10 days later for relapse of retinitis OS and a branch retinal artery occlusion; IV foscarnet 60 mg/kg q8 h was resumed, intravitreal foscarnet 2.4 mcg/0.1 ml was given, and retinitis regressed. Intravenous foscarnet 60 mg/kg once daily was continued for 2 months (Figure 1e-f) followed by life-long famciclovir 500 mg po bid therapy. At the last follow-up 3 years later, vision was 20/125 OD, 20/40 OS.