Mechanisms of Hypouricemia in the Syndrome of Inappropriate Secretion of Antidiuretic Hormone

Decaux, Guy; Dumont, Isabelle; Waterlot, Yves; Hanson, Bernard

doi:10.1159/000183365

Cited by 28 publications

(18 citation statements)

References 19 publications

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“…49 Likewise, although vasopressin reduces uric acid excretion in healthy subjects, 60 in the syndrome of inappropriate antidiuretic hormone, serum uric acid is low, and urinary uric acid excretion is high. 61,62 Thus, whether uric acid has a role in water handling remains unclear and deserves additional studies.…”

Section: Vasopressin: the Survival Hormonementioning

confidence: 99%

Metabolic and Kidney Diseases in the Setting of Climate Change, Water Shortage, and Survival Factors

Johnson

Stenvinkel

Jensen

et al. 2016

JASN

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Climate change (global warming) is leading to an increase in heat extremes and coupled with increasing water shortage, provides a perfect storm for a new era of environmental crises and potentially, new diseases. We use a comparative physiologic approach to show that one of the primary mechanisms by which animals protect themselves against water shortage is to increase fat mass as a means for providing metabolic water. Strong evidence suggests that certain hormones (vasopressin), foods (fructose), and metabolic products (uric acid) function as survival signals to help reduce water loss and store fat (which also provides a source of metabolic water). These mechanisms are intricately linked with each other and stimulated by dehydration and hyperosmolarity. Although these mechanisms were protective in the setting of low sugar and low salt intake in our past, today, the combination of diets high in fructose and salty foods, increasing temperatures, and decreasing available water places these survival signals in overdrive and may be accelerating the obesity and diabetes epidemics. The recent discovery of multiple epidemics of CKD occurring in agricultural workers in hot and humid environments may represent harbingers of the detrimental consequences of the combination of climate change and overactivation of survival pathways.

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Section: Vasopressin: the Survival Hormonementioning

confidence: 99%

Metabolic and Kidney Diseases in the Setting of Climate Change, Water Shortage, and Survival Factors

Johnson

Stenvinkel

Jensen

et al. 2016

JASN

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“…This finding suggests that expansion of the extracellular volume was responsible for the increase in fractional uric acid excretion. The increase in uric acid fractional excretion in the SIADH is due to a decrease in tubular reabsorption (42), mainly localized at presecretory and postsecretory sites of the tubule, whereas urate secretion seems to be appropriate for the level of uricemia (43).…”

Section: Serum Creatinine Urea and Uratementioning

confidence: 99%

Clinical Laboratory Evaluation of the Syndrome of Inappropriate Secretion of Antidiuretic Hormone

Decaux

Musch²

2008

Clinical Journal of the American Society of Nephrology

145

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Hyponatremia secondary to the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) is a frequent cause of hypotonicity. Although the differential diagnosis with other causes of hypotonicity such as salt depletion is sometimes challenging, some simple and readily available biologic parameters can be helpful in the diagnosis of SIADH. In SIADH, urea is typically low; this is less specific for elderly patients, for whom lower clearance of urea accounts for higher values. Low levels of uric acid are more often seen in SIADH (70%) compared with salt-depleted patients (40%). Typically, patients with SIADH will show a lower anion gap with nearly normal total CO 2 and serum potassium, this despite dilution. In patients with hyponatremia secondary to hypocorticism, total CO 2 is usually lower than in nonendocrine SIADH despite low urea and uric acid levels. Urine biology can also be helpful in diagnosis of SIADH because patients with SIADH have high urine sodium (Na; >30 mEq/L), and most of them will have a high fractional excretion of Na (>0.5% in 70% of cases), reflecting salt intake. Conversely, low urine Na in patients with SIADH and poor alimentation is not rare. Finally, measurement of urine osmolality is useful for the diagnosis of polydipsia and reset osmostat and could further help in the choice of therapeutic strategy because patients with low urine osmolality will benefit from water restriction or urea, whereas those with high urine osmolality (>600 mOsm/kg) would be good candidates for V 2 antagonist.

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“…Serum sodium and uric acid are uniquely linked in patients with SIADH and after experimental induction of hyponatremia by exogenous deamino- D -arginine vasopressin (DDAVP) administration and water loading in normal subjects [48, 49, 50, 51, 52, 53, 54, 55, 56, 57]. The decrease in serum uric acid is largely a result of a defect in net renal urate transport or an increase in fractional excretion of uric acid (FEurate).…”

Section: Uric Acid Metabolism In Siadh and Renal Salt Wastingmentioning

confidence: 99%

“…The decrease in serum uric acid is largely a result of a defect in net renal urate transport or an increase in fractional excretion of uric acid (FEurate). Interestingly, FEurate and serum urate return to normal after correction of the hyponatremia by water restriction [48, 49]. Beck [48]made the interesting observation that in 16 out of 17 patients with SIADH the serum urate levels were in the hypouricemic range (<4 mg/dl) as compared with other causes of hyponatremia.…”

Section: Uric Acid Metabolism In Siadh and Renal Salt Wastingmentioning

confidence: 99%

Cerebral Salt-Wasting Syndrome: Does It Exist?

Maesaka

Gupta

Fishbane³

1999

Nephron

125

121

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Cerebral salt-wasting syndrome (CSWS) has been regarded as a misnomer of the syndrome of inappropriate secretion of antidiuretic hormone (SIADH). We take the position that CSWS does exist and might be more common than SIADH. Differentiation between groups has been difficult because of overlapping signs, symptoms, and associated diseases. Euvolemia in SIADH and hypovolemia in CSWS may be the only contrasting variables. However, clinical assessment of extracellular volume is accurate in about 50% of these patients. Determination of serum urate and fractional excretion rates of urate can differentiate one group from the other. In both groups, hyponatremia coexists with hypouricemia and increased fractional excretion of urate. When the hyponatremia is corrected by water restriction, hypouricemia and elevated FEurate correct in SIADH but persist in CSWS. Persistent hypouricemia and elevated FEurate were commonly noted with pulmonary and/or intracranial diseases. The absence of intracranial diseases in some patients suggests that renal salt wasting might be a more appropriate term than CSWS. A review of renal/CSWS reveals three studies involving hyponatremic neurosurgical patients who had decreased blood volume, decreased central venous pressure, and inappropriately high urinary sodium concentrations in the majority of them, suggesting that CSWS was more common than SIADH in neurosurgical patients. Evidence for the presence of a plasma natriuretic factor in CSWS is presented.

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Mechanisms of Hypouricemia in the Syndrome of Inappropriate Secretion of Antidiuretic Hormone

Cited by 28 publications

References 19 publications

Metabolic and Kidney Diseases in the Setting of Climate Change, Water Shortage, and Survival Factors

Metabolic and Kidney Diseases in the Setting of Climate Change, Water Shortage, and Survival Factors

Clinical Laboratory Evaluation of the Syndrome of Inappropriate Secretion of Antidiuretic Hormone

Cerebral Salt-Wasting Syndrome: Does It Exist?

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