Reset osmostat
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In water-electrolyte imbalance, Reset osmostat is a cause of hyponatremia.
"The normal osmostat for vasopressin release is fixed between 275 and 295 mOsm/kg. When the serum osmolality is below 280 mOsm/kg in normal individuals, vasopressin levels are very low"[1].
Rest osmostat have been reported in a healthy patient[2].
Pathology
Reset osmostat may be a form of the syndrome of inappropriate antidiuretic hormone (SIADH)[3] and has been proposed to possibly be either[4]:
- A type B SIADH. Type B SIADH may include reset osmostat, "characterized by a decline in plasma copeptin levels with increasing saline-stimulated serum osmolality...baseline hypovolemia could not be identified [in these patient]"[4]
- A type C SIADH. Reset osmostat may be a Type C rather than Type b, "reset osmostat may in part be considered as a less severe variant of the type C defect..., where responsivity to osmotic challenges is completely lost. Copeptin release in this subtype was stable at levels within the normal physiologic range but was not suppressed by hypotonicity or stimulated in response to osmotic stimulation; thus, it deviates from the previously described type C"[4]
Alternatively, reset osmostat may not be a type of SIADH[5]. Maesaka has proposed this due to the reliable normal fractional urate excretion (FEurate) values in reset osmostat[6].
Psychogenic polydipsia may be related to reset osmostat[7] and has similar (normal) findings with the FEurate[8].
Diagnosis
The fractional urate excretion (FEurate) in reset osmostat should be: 4%-11% (normal) and is superior to serum urate[6][8].
If the FEurate is high (higher than 11%), this suggests SIADH, thiazide-induced hyponatremia, or renal salt wasting[8].
Importance
Recognizing reset osmostat maybe important as baseline sodium < 140 mEq/L is a predictor of thiazide-induced hyponatremia during thiazide therapy[9].
See also
External links
References
- ↑ Kuthiah N, Er C (2018). "Reset Osmostat: A Challenging Case of Hyponatremia". Case Rep Med. 2018: 5670671. doi:10.1155/2018/5670671. PMC 6247647. PMID 30532786.
- ↑ Lipschutz JH, Arieff AI (1994). "Reset osmostat in a healthy patient". Ann Intern Med. 120 (7): 574–6. doi:10.7326/0003-4819-120-7-199404010-00007. PMID 8116995.
- ↑ DeFronzo RA, Goldberg M, Agus ZS (1976). "Normal diluting capacity in hyponatremic patients. Reset osmostat or a variant of the syndrome of inappropriate antidiuretic hormone secretion". Ann Intern Med. 84 (5): 538–42. doi:10.7326/0003-4819-84-5-538. PMID 1275354.
- ↑ 4.0 4.1 4.2 Fenske WK, Christ-Crain M, Hörning A, Simet J, Szinnai G, Fassnacht M; et al. (2014). "A copeptin-based classification of the osmoregulatory defects in the syndrome of inappropriate antidiuresis". J Am Soc Nephrol. 25 (10): 2376–83. doi:10.1681/ASN.2013080895. PMC 4178436. PMID 24722436.
- ↑ Maesaka JK, Imbriano L, Mattana J, Gallagher D, Bade N, Sharif S (2014). "Differentiating SIADH from Cerebral/Renal Salt Wasting: Failure of the Volume Approach and Need for a New Approach to Hyponatremia". J Clin Med. 3 (4): 1373–85. doi:10.3390/jcm3041373. PMC 4470189. PMID 26237607.
- ↑ 6.0 6.1 Imbriano LJ, Ilamathi E, Ali NM, Miyawaki N, Maesaka JK (2012). "Normal fractional urate excretion identifies hyponatremic patients with reset osmostat". J Nephrol. 25 (5): 833–8. doi:10.5301/jn.5000074. PMID 22307440.
- ↑ Hariprasad MK, Eisinger RP, Nadler IM, Padmanabhan CS, Nidus BD (1980). "Hyponatremia in psychogenic polydipsia". Arch Intern Med. 140 (12): 1639–42. PMID 7458496.
- ↑ 8.0 8.1 8.2 Maesaka JK, Imbriano LJ, Miyawaki N (2018). "Determining Fractional Urate Excretion Rates in Hyponatremic Conditions and Improved Methods to Distinguish Cerebral/Renal Salt Wasting From the Syndrome of Inappropriate Secretion of Antidiuretic Hormone". Front Med (Lausanne). 5: 319. doi:10.3389/fmed.2018.00319. PMC 6284366. PMID 30560127.
- ↑ Makam AN, Boscardin WJ, Miao Y, Steinman MA (2014). "Risk of thiazide-induced metabolic adverse events in older adults". J Am Geriatr Soc. 62 (6): 1039–45. doi:10.1111/jgs.12839. PMC 4128471. PMID 24823661. Review in: Ann Intern Med. 2014 Oct 21;161(8):JC11