Hypouricemia, Abnormal Renal Tubular Urate Transport, and Plasma Natriuretic Factor(s) in Patients with Alzheimer's Disease

Maesaka, John K.; Wolf‐Klein, Gisele; Piccione, Joanne M.; Chan, Miranda

doi:10.1111/j.1532-5415.1993.tb01885.x

Cited by 59 publications

(84 citation statements)

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“…By contrast, ammonium sulfate precipitates of urine from neurosurgical patients with normal FEurate and normonatremia and those with SIADH did not inhibit transcellular transport of 22 Na, suggesting that the natriuretic factor was present only in the urine of patients with increased FEurate and normonatremia. These data are consistent with previous rat clearance studies, which demonstrated natriuretic activity in the plasma of neurosurgical and Alzheimer's disease patients who had increased FEurate and normonatremia as compared to two control groups, composed of (1) age-and gender-matched controls and (2) patients with multi-infarct dementia, both groups with normal FEurate and normonatremia 19,20 . These studies collectively support our proposal that an increased FEurate with normonatremia is consistent with RSW and represent an initial step to utilize the natriuretic factor as a biomarker for RSW 1,2 .…”

Section: Discussionsupporting

confidence: 81%

Demonstration of natriuretic activity in urine of neurosurgical patients with renal salt wasting

et al. 2013

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Section: Discussionsupporting

confidence: 81%

Demonstration of natriuretic activity in urine of neurosurgical patients with renal salt wasting

et al. 2013

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“…Some of the characteristic findings of prerenal azotemia are therefore not applicable in RSW. Renin production in RSW can be variable, depending on salt intake despite ECV depletion, because the major defect in salt transport resides in the proximal tubule (15,26). Thus, the salt supply to the juxtaglomerular apparatus will reflect salt intake as compared with a decreased supply in a volume-depleted patient with normal kidneys (27).…”

Section: Discussionmentioning

confidence: 99%

“…Determination of FEurate can, therefore, be a useful tool to assess proximal tubule function in various disease states, being low in prerenal azotemia with normal kidneys (38) and high in those with proximal tubule dysfunction such as RSW, or transiently high in SIADH. The administration of plasma from our patients with neurosurgical and Alzheimer's diseases who had hypourice-mia, increased FEurate, and normal serum sodium as seen in RSW resulted in a 30% increase in FElithium and a significant increase in FENa (14,15,26). Because lithium is transported mainly in the proximal tubule on a one-to-one basis with sodium in the absence of osmotic diuretics (39,40), these studies suggest that a plasma natriuretic factor reduces proximal and possibly distal tubular sodium transport in RSW.…”

Section: Discussionmentioning

confidence: 99%

“…We demonstrated the value of determining serum urate levels in hyponatremia and fortified our contention that the persistence of hypouricemia and elevated fractional excretion (FE) of urate after correction of hyponatremia differentiate RSW from SIADH, since the hypouricemia and elevated FEurate in SIADH normalize after correction of the hyponatremia (1,5,(11)(12)(13)(14)(15)(16)(17)(18). Differences in urate metabolism, however, are evident only after correction of the hyponatremia and would not contribute to differentiating SIADH from RSW on first encounter.…”

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confidence: 99%

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More on Renal Salt Wasting Without Cerebral Disease

Bitew

Imbriano

Miyawaki

et al. 2009

Clinical Journal of the American Society of Nephrology

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116

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Background and objectives: The existence and prevalence of cerebral salt wasting (CSW) or the preferred term, renal salt wasting (RSW), and its differentiation from syndrome of inappropriate antidiuretic hormone (SIADH) have been controversial. This controversy stems from overlapping clinical and laboratory findings and an inability to assess the volume status of these patients. The authors report another case of RSW without clinical cerebral disease and contrast it to SIADH. Design, setting, participants, & measurements: Three patients with hyponatremia, hypouricemia, increased fractional excretion (FE) of urate, urine sodium >20 mmol/L, and concentrated urines were infused with isotonic saline after collection of baseline data.Results: One patient with RSW had pneumonia without cerebral disease and showed increased plasma aldosterone and FEphosphate, and two patients with SIADH had increased blood volume, low plasma renin and aldosterone, and normal FEphosphate. The patient with RSW responded to isotonic saline by excretion of dilute urines, prompt correction of hyponatremia, and normal water loading test after volume repletion. Hypouricemia and increased FEurate persisted after correction of hyponatremia. Two patients with SIADH failed to dilute their urines and remained hyponatremic during 48 and 110 h of saline infusion.Conclusions: The authors demonstrate appropriate stimulation of ADH in RSW. Differences in plasma renin and aldosterone levels and FEphosphate can differentiate RSW from SIADH, as will persistent hypouricemia and increased FEurate after correction of hyponatremia in RSW. FEphosphate was the only contrasting variable at baseline. The authors suggest an approach to treat the hyponatremic patient meeting criteria for SIADH and RSW and changing CSW to the more appropriate term, RSW.

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“…11,38 The natriuretic factor has been identified as a protein and has been partially characterized. 44,45 Work is underway to isolate and identify this natriuretic factor. A natriuretic factor with characteristics similar to those observed in patients with intracranial disease has been reported in patients with Alzheimer's disease.…”

Section: Reset Osmostat Syndromementioning

confidence: 99%

The hyponatremic patient: A systematic approach to laboratory diagnosis

2003

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HYPONATREMIA (SERUM SODIUM LEVEL LESS THAN 134 MMOL/L) is a common electrolyte disturbance. Its high prevalence and potential neurologic sequelae make a logical and rigorous differential diagnosis mandatory before any therapeutic intervention. A history of concurrent illness and medication use as well as the assessment of extracellular volume status on physical examination may provide useful clues as to the pathogenesis of hyponatremia. Measurement of the effective serum tonicity (serum osmolality less serum urea level) is the first step in the laboratory evaluation. In patients with normal or elevated effective serum osmolality (280 mOsm/kg or greater), pseudohyponatremia should be excluded. In the hypo-osmolar state (serum osmolality less than 280 mOsm/kg), urine osmolality is used to determine whether water excretion is normal or impaired. A urine osmolality value of less than 100 mOsm/kg indicates complete and appropriate suppression of antidiuretic hormone secretion. A urine sodium level less than 20 mmol/L is indicative of hypovolemia, whereas a level greater than 40 mmol/L is suggestive of the syndrome of inappropriate antidiuretic hormone secretion. Levels of hormones (thyroid-stimulating hormone and cortisol) and arterial blood gases should be determined in difficult cases of hyponatremia.

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Hypouricemia, Abnormal Renal Tubular Urate Transport, and Plasma Natriuretic Factor(s) in Patients with Alzheimer's Disease

Abstract: In AD there is defective tubular urate transport and a plasma natriuretic factor(s). FE sodium and/or FE lithium in rats exposed to plasma of demented patients may differentiate AD from MID and estimate the severity of AD.

Cited by 59 publications

References 24 publications

Demonstration of natriuretic activity in urine of neurosurgical patients with renal salt wasting

Demonstration of natriuretic activity in urine of neurosurgical patients with renal salt wasting

More on Renal Salt Wasting Without Cerebral Disease

The hyponatremic patient: A systematic approach to laboratory diagnosis

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