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1 l tolerated, with only one grade 4 toxicity (hyponatremia).
2 s LGI1 antibodies were associated with serum hyponatremia.
3 were alcoholics and 33 (92%) presented with hyponatremia.
4 hildren due to the risk of hospital-acquired hyponatremia.
5 udies primarily focused on the importance of hyponatremia.
6 al at risk for the unexpected development of hyponatremia.
7 in patients with euvolemic and hypervolemic hyponatremia.
8 hat cerebral salt wasting is a rare cause of hyponatremia.
9 e two grade 4 toxicities: duodenal ulcer and hyponatremia.
10 d in patients with euvolemic or hypervolemic hyponatremia.
11 AVP receptor antagonism in the treatment of hyponatremia.
12 ectrolyte-free water--might be of benefit in hyponatremia.
13 med to identify risk factors associated with hyponatremia.
14 rmone secretion (SIADH) is a common cause of hyponatremia.
15 the mortality risk previously attributed to hyponatremia.
16 Risk varied continuously with worsening hyponatremia.
17 ia with renal involvement, coagulopathy, and hyponatremia.
18 e central nervous system typical of clinical hyponatremia.
19 ners tend to develop conditions that lead to hyponatremia.
20 ese rats had significant water retention and hyponatremia.
21 outcome was a primary position diagnosis of hyponatremia.
22 atients are normonatremic and never manifest hyponatremia.
23 lydipsic schizophrenic patients with chronic hyponatremia.
24 der that can occur after rapid correction of hyponatremia.
25 d encephalopathy that is caused by untreated hyponatremia.
26 e risk for myelinolysis due to correction of hyponatremia.
27 ally evolve several days after correction of hyponatremia.
28 wer elimination, prolonged antidiuresis, and hyponatremia.
29 ere is a research gap regarding heat-related hyponatremia.
30 associated with an immediate exacerbation of hyponatremia.
31 mphocyte count, anemia, hypoalbuminemia, and hyponatremia.
32 s constitute a leading cause of drug-induced hyponatremia.
33 ebo in outpatients with chronic SIAD-induced hyponatremia.
34 UTs are a promising drug target for treating hyponatremia.
35 clearance, and four patients developed mild hyponatremia.
36 to differentiate hypotonic from nonhypotonic hyponatremia.
37 e complication of overly rapid correction of hyponatremia.
38 ting with concurrent grade 3 hypokalemia and hyponatremia.
39 e 3 nonhematologic toxicity was asymptomatic hyponatremia.
40 ic patients and may result in fewer cases of hyponatremia.
41 ntiate between depletional versus dilutional hyponatremia.
42 included hospitalization with hypokalemia or hyponatremia.
43 rload edemas and high-vasopressin-associated hyponatremias.
44 wo patients in the hypotonic group developed hyponatremia, 1 in each group developed hypernatremia, 2
48 rum sodium (>135 mEq/L) at OLT, whereas mild hyponatremia (125-134 mEq/L) was present in 615 (28.3%)
50 ences were observed in the primary outcomes (hyponatremia 44% vs 67% (p=0.29); liver toxicity 6% vs 0
51 encephalopathy (50% versus 27.5%; P = 0.04), hyponatremia (67.5% versus 22.5%; P < 0.001), acute kidn
52 ic encephalopathy (50% vs. 27.5%; P = 0.04), hyponatremia (67.5% vs. 22.5%; P < 0.001), acute kidney
53 cases in patients receiving dabrafenib) and hyponatremia (8 and 6 cases, respectively) were also rep
58 G5 treatment-related AE (TRAE), one G4 TRAE (hyponatremia, A), and 53% (A) versus 41% (B) G3 TRAEs.
59 ed hazard ratio, 3.06 [CI, 2.04 to 4.58]) or hyponatremia (adjusted hazard ratio, 1.68 [CI, 1.24 to 2
61 he risk for illness and death from untreated hyponatremia against the risk for myelinolysis due to co
65 ndrome that can cause hypotension and shock, hyponatremia, altered mental status, and death if untrea
67 nts included in the study, 1,215 (11.2%) had hyponatremia and 277 (2.5%) had hypernatremia at admissi
69 an increased urine Na+ concentration despite hyponatremia and a decreased urine K+ concentration desp
70 f 1.5 L/d or more was identified to estimate hyponatremia and AKI in the included patients with devic
71 inage of 1.5 L/d or more was associated with hyponatremia and AKI, even after adjusting for various c
73 aintain cell volume, and that in response to hyponatremia and EtOH withdrawal their volume increases
74 ing toxicities (n = 1 for each) were grade 3 hyponatremia and herpes zoster reactivation and grade 4
77 outcomes were mean sodium level at 24 hours, hyponatremia and hypernatremia, weight gain, hypertensio
78 as the association of increasing severity of hyponatremia and in-hospital mortality assessed using mu
80 r the treatment of chronic rather than acute hyponatremia and is more likely to occur with a rapid ra
82 ice were fed a low-salt diet, they developed hyponatremia and mild metabolic alkalosis, symptoms char
83 t this stage, investigations commonly showed hyponatremia and MRI hippocampal high T2 signal; functio
85 nown reasons, in schizophrenic patients with hyponatremia and polydipsia, thereby placing them at inc
88 arathon runners to estimate the incidence of hyponatremia and to identify the principal risk factors.
89 7%) due to hyperkalemia, in 1 (0.37%) due to hyponatremia, and in 0 due to reduction in kidney functi
90 7%) due to hyperkalemia, in 2 (0.37%) due to hyponatremia, and in 3 (0.56%) due to reduction in kidne
93 ism, colitis, diarrhoea, decreased appetite, hyponatremia, and pneumonitis (each in two [1%]) in thos
94 ia, hyperbilirubinemia, renal insufficiency, hyponatremia, and prothrombin time prolongation (all P <
97 ic reactions included hypotension, vomiting, hyponatremia, anemia, thrombocytopenia, and infection at
98 ients sustaining rapid correction of chronic hyponatremia are at risk of osmotic demyelination syndro
99 al agents currently used in the treatment of hyponatremia are limited by inconsistent response and ad
100 lele were 2.4-6.4 times as likely to exhibit hyponatremia as subjects without the minor allele (after
107 dose-limiting toxicity was reported (grade 3 hyponatremia at the 20 mg dose), therefore the maximum t
112 for patients with head injury, alkalosis, or hyponatremia, but in large volumes may lead to metabolic
114 represent a new approach to the treatment of hyponatremia by blocking tubular reabsorption of water b
115 d hyponatremia (HAH) with community-acquired hyponatremia (CAH) in HF patients with respect to outcom
116 me expansion, excessive water retention with hyponatremia can occur in the absence of increases in aq
117 ent hyponatremia in previous studies, and 2) hyponatremia can significantly alter brain morphology on
119 d with a marked increased rate of subsequent hyponatremia compared to use of other medications indica
120 come of mild, moderate, and severe admission hyponatremia compared with normonatremia among coronavir
121 iew discusses the diagnosis and treatment of hyponatremia, comparing the two guidelines and highlight
122 e a difference; regardless of volume status, hyponatremia complicating intracranial disease should be
128 recommend limiting the correction of severe hyponatremia during the first 24 hours to prevent osmoti
129 xibility protects against the development of hyponatremia even in the face of water intake that can a
130 controlling for confounders including pre-LT hyponatremia, every 5 mmol/L increase in delta sodium as
133 eport a newborn with severe hyperkalemia and hyponatremia from autosomal recessive pseudohypoaldoster
134 en requiring IVFs are at risk for developing hyponatremia from numerous stimuli for arginine vasopres
135 The improvement was more pronounced in the hyponatremia group with respect to ADL (DeltaADL: 14.3 +
136 n-small cell lung cancer) who presented with hyponatremia had inappropriately elevated levels of AVP.
137 The present study compares hospital-acquired hyponatremia (HAH) with community-acquired hyponatremia
140 experience with AVP receptor antagonists for hyponatremia has shown that these agents augment free wa
141 Patients with polydipsia and intermittent hyponatremia have greater ventricle-brain ratios (VBRs)
142 xis), ascites and some of its complications (hyponatremia, hepatic hydrothorax), hepatorenal syndrome
143 factor even in patients without preexisting hyponatremia; however, isolated hypernatremia may be sol
146 dosterone deficiency, signs of which include hyponatremia, hyperkalemia, hypovolemia, elevated plasma
147 or a composite of hypokalemia, hyperkalemia, hyponatremia, hypernatremia, hypomagnesemia, hypophospha
151 findings included diarrhea, hypoalbuminemia, hyponatremia, hypokalemia, hypocalcemia, and hypomagnese
152 f inducing severe hypokalemia in addition to hyponatremia, hypotension, and worsening renal function.
153 he condition of patients with mild or marked hyponatremia improved (P<0.001 for all comparisons).
160 ICE 8: Diagnostic workup for the etiology of hyponatremia in cirrhosis should include dietary and med
163 ient management of asymptomatic hypervolemic hyponatremia in liver cirrhosis entails both sodium and
164 gement of severe or symptomatic hypervolemic hyponatremia in liver cirrhosis includes both sodium and
168 in patients with polydipsia and intermittent hyponatremia in previous studies, and 2) hyponatremia ca
169 Our objective was to quantify the rate of hyponatremia in routine clinical care for patients presc
171 nts who have euvolemia and hypervolemia with hyponatremia in the short term (</=30 days), but their s
178 , we showed that rapid correction of chronic hyponatremia induces severe alterations in proteostasis
179 CF due to elevated sweat chloride, recurrent hyponatremia, infantile FTT and lung disease identified
186 imal and human studies revealed that chronic hyponatremia is a previously unrecognized cause of osteo
200 findings indicate that oxcarbazepine-induced hyponatremia is not attributable to the syndrome of inap
201 At present, therapy for acute and chronic hyponatremia is often ineffective and poorly tolerated.
204 ium deficiency, is the culprit in dilutional hyponatremia, isotonic saline administration may further
205 d 88 hospitalized patients with SIAD-induced hyponatremia <130 mmol/L at the University Hospital Base
209 PRACTICE ADVICE 11: Recurrent or refractory hyponatremia management should involve a multidisciplina
212 complications, specifically volume overload, hyponatremia, metabolic alkalosis, uremia, and hyperglyc
227 ients, including four with fatigue, two with hyponatremia, one with muscle spasm, and one with atrial
228 oor outcomes than the rate of development of hyponatremia or the absolute decrease in the serum sodiu
230 d AHF patients may have renal insufficiency, hyponatremia, or an inadequate response to traditional d
233 lar filtration rate <60 ml/min/1.73 m(2); 2) hyponatremia; or 3) diuretic resistance (urine output </
235 C-reactive protein (CRP) (P = .0009); worse hyponatremia (P = .02); higher KSHV VL (P = .016), and h
240 rminal pro-B natriuretic peptide levels, and hyponatremia reflected greater neurohormonal activation.
243 servational study investigated the impact of hyponatremia resolution on the results of a comprehensiv
245 e; this may help to attenuate the developing hyponatremia resulting from water loading when vasopress
248 alyzed, there were 1274 patients (0.8%) with hyponatremia (serum sodium <135 mmol/L), 162,829 (97.3%)
249 ted with serum sodium concentration and with hyponatremia (serum sodium concentration < or =135 mEq/L
252 xperience suggest that correction of chronic hyponatremia should be kept at a rate less than 10 mmol/
253 es, hepatic hydrothorax, volume overload, or hyponatremia should be referred for to transjugular intr
254 For most patients, the approach to managing hyponatremia should consist of treating the underlying c
257 ate (sodium level, 125-129 mEq/L) and severe hyponatremia (sodium level, <125 mEq/L), where the cumul
259 we present a practical approach to managing hyponatremia that centers on two elements: a diagnostic
260 rements is associated with increased risk of hyponatremia that results in morbidity and mortality in
261 d at the pathogenesis and putative causes of hyponatremia, the case-specific clinical and laboratory
263 rst-line treatment for most forms of chronic hyponatremia, therapy to increase renal free water excre
264 ize sodium from bone stores during prolonged hyponatremia, thereby leading to a resorptive osteoporos
265 ments for hypertension, but thiazide-induced hyponatremia (TIH), a clinically significant adverse eff
266 In patients with euvolemic or hypervolemic hyponatremia, tolvaptan, an oral vasopressin V2-receptor
269 ocin is not receptor-selective and may cause hyponatremia via V2 receptor mediated antidiuresis.
271 ing for age, sex, region, and comorbidities, hyponatremia was a significant independent predictor of
272 inositol content in animals with uncorrected hyponatremia was about 50% of that found in normonatremi
283 A clear seasonal pattern of heat-related hyponatremia was evident among older patients, especiall
284 d clinical trials, a high incidence of acute hyponatremia was observed in response to MDMA, which may
286 orrection and very slow correction of severe hyponatremia were associated with an increased risk of m
288 ic patients with polydipsia and intermittent hyponatremia were first assigned to either normal fluid
289 sweat chloride, infantile FTT, and recurrent hyponatremia were homozygous for a novel missense varian
290 ic patients with (n = 6) and without (n = 8) hyponatremia were identified based on past and current i
291 rmalization of serum sodium in patients with hyponatremia were observed in the tolvaptan group but no
292 history of tick bite, thrombocytopenia, and hyponatremia were often absent at initial presentation.
294 c fluid associated with a lower incidence of hyponatremia when compared with hypotonic fluid for main
295 monstrated that hypotonic fluids cause acute hyponatremia, whereas 0.9% sodium chloride (NaCl) effect
296 ody-mass-index extremes were associated with hyponatremia, whereas female sex, composition of fluids
297 with oxcarbazepine showed the development of hyponatremia, which in most instances was asymptomatic.
298 opeptin concentrations from 50 patients with hyponatremia who underwent hypertonic saline infusion.
299 ts preceding the seizure were remarkable for hyponatremia, with a blood sodium level of 122 mEq/L (12
300 luid is associated with a lower incidence of hyponatremia, without evidence of an increase in adverse