Plasma natriuretic factor(s) in patients with intracranial disease, renal salt wasting and hyperuricosuria

Maesaka, John K.; Venkatesan, Jeyanti; Piccione, Joanne M.; Decker, Robert W.; Wetherington, Jeffrey D.

doi:10.1016/0024-3205(93)90008-q

Cited by 33 publications

(37 citation statements)

References 18 publications

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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: 92%

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

et al. 2013

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Section: Discussionsupporting

confidence: 92%

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

et al. 2013

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“…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: 85%

“…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%

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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“…We administered the plasma of these patients and of age- and gender-matched normal controls to rats and studied the effect of plasma on sodium and lithium transports by clearance technique [69]. The success of these studies depended on the adherence to pharmacological principles of dose and time to effectiveness of drugs.…”

Section: Plasma Natriuretic Factormentioning

confidence: 99%

“…Sodium and lithium excretion rates increased significantly above control levels approximately 4.5 h after first exposure of the rats to the plasma of the neurosurgical patients. This effect lasted for an additional 180 min after termination of the infusion of plasma [69]. The time course could not be altered by other maneuvers such as rapid intravenous administration of the full dose of plasma.…”

Section: Plasma Natriuretic Factormentioning

confidence: 99%

Cerebral Salt-Wasting Syndrome: Does It Exist?

Maesaka

Gupta

Fishbane³

1999

Nephron

Self Cite

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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Plasma natriuretic factor(s) in patients with intracranial disease, renal salt wasting and hyperuricosuria

Cited by 33 publications

References 18 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

Cerebral Salt-Wasting Syndrome: Does It Exist?

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