Uric Acid Homeostasis in the Evaluation of Diuretic-Induced Hyponatremia

Liamis, Georgé; Christidis, Dimitrios; Alexandridis, George; Bairaktari, Eleni; Madias, Nicolaos E.; Elisaf, Moses

doi:10.2310/6650.2007.06027

Cited by 27 publications

(19 citation statements)

References 26 publications

(42 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Usually, low-normal serum creatinine and hypouricemia are observed in patients with HCTZ-induced hyponatremia. 12, 26 In the present study, however, the significant elevations of the serum creatinine and uric acid levels following the addition of 12.5 mg of HCTZ to ARB treatment were larger in patients with low salt intake than in those without low salt intake. Therefore, patients with a low salt intake might remain in a dehydrated state to compensate for the hypo-osmolar state associated with the reduction in the srNa levels by the addition of a diuretic.…”

Section: Resultscontrasting

confidence: 45%

Low Salt Intake and Changes in Serum Sodium Levels in the Combination Therapy of Low-Dose Hydrochlorothiazide and Angiotensin II Receptor Blocker

Nakayama

Tomiyama

Kuwajima

et al. 2013

Circ J

View full text Add to dashboard Cite

Section: Resultscontrasting

confidence: 45%

Low Salt Intake and Changes in Serum Sodium Levels in the Combination Therapy of Low-Dose Hydrochlorothiazide and Angiotensin II Receptor Blocker

Nakayama

Tomiyama

Kuwajima

et al. 2013

Circ J

View full text Add to dashboard Cite

“…Six patients presented very low uric acid levels (≤2 wmg/dL) after correction of SNa (Nr 1,8,[12][13][14][15]. When patients are separated not for their uric acid levels but for their urea levels, we observed a significant increase in BW with the treatment (0.84 kg) in the patients with an urea level higher than 30 mg/dL, when compared with the patients with a low urea value (-0.2 kg; p < 0.05; Table 4).…”

Section: Resultsmentioning

confidence: 99%

“…Patients taking drugs other than the diuretics known to influence serum uric acid levels were excluded [8] as were patients with diabetes, cardiac failure, cirrhosis, or nephrotic syndrome. All patients took the diuretic for treatment of HTA and normalized SNa completely before leaving the hospital.…”

Section: Methodsmentioning

confidence: 99%

“…It is unclear, whether solute depletion is a major contributing factor to the pathogenesis of diuretic-induced hyponatre-DOI: 10.1159/000490203 mia in patients whom serum urea and uric acid levels are rather low and fractional excretions (FE) of urea [4,5] and uric acid [6] rather high, like in SIADH. It is believed, that the first class (with a uric acid level higher than 4 mg/dL) should be treated mainly by solute repletion and the second [7,8] mainly by water restriction both combined with a withdrawal of the diuretic. We observe, that even with an SIADH-like biochemistry, diuretic-induced hyponatremia mainly reflects solute loss and not water excess.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Severe Solute Depletion in Patients with Hyponatremia Due to Diuretics Despite Biochemical Pictures Similar Than Those Observed in the Syndrome of Inappropriate Secretion of Antidiuretic Hormone

Musch¹,

Decaux²

2018

Nephron

View full text Add to dashboard Cite

Background/AIMS: Hyponatremia secondary to distal diuretics intake could have a biochemical picture similar to the one observed in the syndrome of inappropriate secretion of antidiuretic hormone (SIADH). In these patients, water retention is considered to be the main causal factor and solute depletion a secondary one. Methods. We compared the level of cation (Na + K) depletion and water balance in patients with high or low uric acid levels (< 4 mg/dL or 238 µmol/L) or with high or low (< 30 mg/dL or 5 mmol/L) urea levels. Data were collected from 15 consecutive patients treated in a similar way by a daily infusion of 2 L isotonic saline with potassium chloride until SNa reached at least 132 mmol/L. The same procedure was performed in 6 patients with hyponatremia due to salt depletion not related to diuretic intake. Results: Hyponatremia, associated with low or high uric acid level is mainly due to severe cation depletion (around 600 mmol) and not due to water retention, since body weight did not change significantly (SNa 122 ± 2.0 mEq/L). If patients were classified according to serum urea levels those with higher urea levels (≥30 mg/dL) presented with a mild increase in BW (0.84 ± 0.37 kg). In patients with salt depletion and hyponatremia not related to diuretic intake, we observe as expected an increase in BW (1.5 ± 0.3 kg) and similar cation retention with the treatment. Conclusion: We therefore suggest that diuretic induced hyponatremia with an SIADH-like biochemical profile, should be treated mainly by solute repletion.

show abstract

“…Total body water expansion and potassium depletion (vomiting, diarrhea, urinary potassium loss) may act as potent blocks to aldosterone secretion by adrenal glands in kala-azar patients. Hypochloremia and low urea serum levels may be evidence of decreased protein ingestion and/or body water expansion 18 . Hypouricemia and increased fractional urinary uric acid excretion are other features of kala-azar patients.…”

Section: Discussionmentioning

confidence: 99%

Hyponatremia in visceral leishmaniasis

Verde

Veronese

et al. 2010

Rev. Inst. Med. trop. S. Paulo

View full text Add to dashboard Cite

SUMMARYThere are few reports linking hyponatremia and visceral leishmaniasis (kala-azar). This is a study of 55 consecutive kala-azar patients and 20 normal individuals as a control group. Hyponatremia and serum hypo-osmolality were detected in 100% of kalaazar patients. High first morning urine osmolality (750.0 ± 52.0 vs. 894.5 ± 30.0mOsm/kg H 2 O, p < 0.05), and high 24-hour urine osmolality (426.0 ± 167.0 vs. 514.6 ± 132.0 mOsm/kg H 2 O, p < 0.05) demonstrated persistent antidiuretic hormone secretion. Urinary sodium was high (82.3 ± 44.2 vs.110.3 ± 34.7 mEq/L, p < 0.05). Low seric uric acid occurred in 61.8% of patients and increased fractional urinary uric acid excretion was detected in 74.5% of them. Increased glomerular filtration rate was present in 25.4% of patients. There was no evidence of extracellular volume depletion. Normal plasma ADH levels were observed in kala-azar patients. No endocrine or renal dysfunction was detected. It is possible that most hyponatremic kala-azar patients present the syndrome of inappropriate antidiuretic hormone secretion.

show abstract

Uric Acid Homeostasis in the Evaluation of Diuretic-Induced Hyponatremia

Abstract: Diuretics are the most common cause of community-developed hyponatremia. The serum uric acid level effectively discriminates between two biochemical profiles of diuretic-induced hyponatremia, one consistent with extracellular volume depletion and another that simulates SIADH.

Cited by 27 publications

References 26 publications

Low Salt Intake and Changes in Serum Sodium Levels in the Combination Therapy of Low-Dose Hydrochlorothiazide and Angiotensin II Receptor Blocker

Low Salt Intake and Changes in Serum Sodium Levels in the Combination Therapy of Low-Dose Hydrochlorothiazide and Angiotensin II Receptor Blocker

Severe Solute Depletion in Patients with Hyponatremia Due to Diuretics Despite Biochemical Pictures Similar Than Those Observed in the Syndrome of Inappropriate Secretion of Antidiuretic Hormone

Hyponatremia in visceral leishmaniasis

Contact Info

Product

Resources

About