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(diabetes insipidus)
9,818 results
  • Transient diabetes insipidus after discontinuation of vasopressin in neurological ICU patients: Case series and literature review. [Journal Article]
  • WNWorld Neurosurg 2016 Oct 11
  • Bohl MA, Forseth J, Nakaji P
  • CONCLUSIONS: Recognition of this phenomenon has caused us to change our clinical management of neurosurgical patients on AVP. We hypothesize that tDI is caused by downregulation of the V2 receptor mass in the renal distal convoluted tubule and collecting duct cells. When AVP is discontinued, patients develop nephrogenic tDI secondary to decreased V2 receptor binding, which explains why desmopressin is effective in correcting tDI. Future research includes a large prospective study to determine risk factors for tDI, its incidence, and its pathophysiology.
  • Extreme hypernatremia as a probable cause of fatal arrhythmia: a case report. [Journal Article]
  • JMJ Med Case Rep 2016 Oct 1; 10(1):272
  • Arambewela MH, Somasundaram NP, Garusinghe C
  • CONCLUSIONS: Extreme hypernatremia is rare, and the literature on electrocardiographic changes occurring at such high levels of sodium is scarce. At present there are no established guidelines on rate and mode of correction of such high sodium levels. This case highlights the electrocardiographic changes observed during extreme hypernatremia, controversies in managing increased intracranial pressure with hypertonic saline, and dilemmas encountered in managing extreme hypernatremia.
  • Amiloride modifies the progression of lithium-induced renal interstitial fibrosis. [Journal Article]
  • NNephrology (Carlton) 2016 Sep 28
  • Kalita-DE Croft P, Bedford JJ, … Walker RJ
  • CONCLUSIONS: In this study, the 5 months of amiloride therapy partially mitigated the lithium-induced NDI and limited the further progression of lithium-induced kidney fibrosis. This improvement was associated with decreased expression of the pro-fibrotic connective tissue growth factor (CTGF), along with reduced myofibroblast infiltration and decreased collagen deposition around the distended cortical collecting ducts. This may, in part, be mediated by modifying lithium-induced alterations in β-catenin activity through its effects on GSK-3β.
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