scholarly journals Cisplatin-Induced Renal Salt Wasting Requiring over 12 Liters of 3% Saline Replacement

2017 ◽  
Vol 2017 ◽  
pp. 1-4
Author(s):  
Phuong-Chi Pham ◽  
Pavani Reddy ◽  
Shaker Qaqish ◽  
Ashvin Kamath ◽  
Johana Rodriguez ◽  
...  
Keyword(s):  
Fanconi Syndrome ◽  
Cell Cancer ◽  
Hormone Secretion ◽  
Free Water ◽  
Severe Case ◽  
Acute Onset ◽  
Water Restriction ◽  
Inappropriate Antidiuretic Hormone Secretion ◽  
Salt Wasting ◽  
Renal Salt Wasting

Cisplatin is known to induce Fanconi syndrome and renal salt wasting (RSW). RSW typically only requires transient normal saline (NS) support. We report a severe RSW case that required 12 liters of 3% saline. A 57-year-old woman with limited stage small cell cancer was admitted for cisplatin (80 mg/m2) and etoposide (100 mg/m2) therapy. Patient’s serum sodium (SNa) decreased from 138 to 133 and 125 mEq/L within 24 and 48 hours of cisplatin therapy, respectively. A diagnosis of syndrome of inappropriate antidiuretic hormone secretion (SIADH) was initially made. Despite free water restriction, patient’s SNa continued to decrease in association with acute onset of headaches, nausea, and dizziness. Three percent saline (3%S) infusion with rates up to 1400 mL/day was required to correct and maintain SNa at 135 mEq/L. Studies to evaluate Fanconi syndrome revealed hypophosphatemia and glucosuria in the absence of serum hyperglycemia. The natriuresis slowed down by 2.5 weeks, but 3%S support was continued for a total volume of 12 liters over 3.5 weeks. Attempts of questionable benefits to slow down glomerular filtration included the administration of ibuprofen and benazepril. To our knowledge, this is the most severe case of RSW ever reported with cisplatin.

Factors predicting postoperative hyponatremia and efficacy of hyponatremia management strategies after more than 1000 pituitary operations

2013 ◽  
Vol 119 (6) ◽  
pp. 1478-1483 ◽  
Author(s):  
Arman Jahangiri ◽  
Jeffrey Wagner ◽  
Mai T. Tran ◽  
Liane M. Miller ◽  
Maxwell W. Tom ◽  
...  
Keyword(s):  
Receptor Antagonist ◽  
Hormone Secretion ◽  
Management Strategies ◽  
Free Water ◽  
Pituitary Surgery ◽  
Vasopressin Receptor ◽  
Water Restriction ◽  
Inappropriate Antidiuretic Hormone Secretion ◽  
Vasopressin Receptor Antagonist ◽  
Postoperative Hyponatremia

Object Syndrome of inappropriate antidiuretic hormone secretion–induced hyponatremia is a common morbidity after pituitary surgery that can be profoundly symptomatic and cause costly readmissions. The authors calculated the frequency of postoperative hyponatremia after 1045 consecutive operations and determined the efficacy of interventions correcting hyponatremia. Methods The authors performed a retrospective review of 1045 consecutive pituitary surgeries in the first 946 patients treated since forming a dedicated pituitary center 5 years ago. Patients underwent preoperative and daily inpatient sodium checks, with outpatient checks as needed. Results Thirty-two patients presented with hyponatremia; 41% of these patients were symptomatic. Postoperative hyponatremia occurred after 165 operations (16%) a mean of 4 days after surgery (range 0–28 days); 19% of operations leading to postoperative hyponatremia were associated with postoperative symptoms (38% involved dizziness and 29% involved nausea/vomiting) and 15% involved readmission for a mean of 5 days (range 1–20 days). In a multivariate analysis including lesion size, age, sex, number of prior pituitary surgeries, surgical approach, pathology, lesion location, and preoperative hypopituitarism, only preoperative hypopituitarism predicted postoperative hyponatremia (p = 0.006). Of patients with preoperative hyponatremia, 59% underwent medical correction preoperatively and 56% had persistent postoperative hyponatremia. The mean correction rates were 0.4 mEq/L/hr (no treatment; n = 112), 0.5 mEq/L/hr (free water restriction; n = 24), 0.7 mEq/L/hr (salt tablets; n = 14), 0.3 mEq/L/hr (3% saline; n = 20), 0.7 mEq/L/hr (intravenous vasopressin receptor antagonist Vaprisol; n = 22), and 1.2 mEq/L/hr (oral vasopressin receptor antagonist tolvaptan; n = 9) (p = 0.002, ANOVA). While some patients received more than 1 treatment, correction rates were only recorded when a treatment was given alone. Conclusions After 1045 pituitary operations, postoperative hyponatremia was associated exclusively with preoperative hypopituitarism and was most efficiently managed with oral tolvaptan, with several interventions insignificantly different from no treatment. Promptly identifying hyponatremia in high-risk patients and management with agents like tolvaptan can improve safety and decrease readmission. For readmitted patients with severely symptomatic hyponatremia, the intravenous vasopressin receptor antagonist Vaprisol is another treatment option.

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

F1000Research ◽  
2013 ◽  
Vol 2 ◽  
pp. 126 ◽  
Author(s):  
Steven J Youmans ◽  
Miriam R Fein ◽  
Elizabeth Wirkowski ◽  
John K Maesaka
Keyword(s):  
Ammonium Sulfate ◽  
Hormone Secretion ◽  
Transcellular Transport ◽  
Inappropriate Antidiuretic Hormone Secretion ◽  
Salt Wasting ◽  
Renal Salt Wasting ◽  
Natriuretic Factor ◽  
Potential Biomarker ◽  
Neurosurgical Patients

We have utilized the persistent elevation of fractional excretion (FE) of urate, > 10%, to differentiate cerebral/renal salt wasting (RSW) from the syndrome of inappropriate antidiuretic hormone secretion (SIADH), in which a normalization of FEurate occurs after correction of hyponatremia.  Previous studies suggest as well  that an elevated FEurate with normonatremia, without pre-existing hyponatremia, is also consistent with RSW, including studies demonstrating induction of RSW in rats infused with plasma from normonatremic neurosurgical and Alzheimer’s disease patients.  The present studies were designed to test whether precipitates from the urine of normonatremic neurosurgical patients, with either normal or elevated FEurate, and patients with SIADH, display natriuretic activity.  Methods: Ammonium sulfate precipitates from the urine of 6 RSW and 5 non-RSW Control patients were dialyzed (10 kDa cutoff) to remove the ammonium sulfate, lyophilized, and the reconstituted precipitate was tested for its effect on transcellular transport of 22Na across LLC-PK1 cells grown to confluency in transwells.Results: Precipitates from 5 of the 6 patients with elevated FEurate and normonatremia significantly inhibited the in vitro transcellular transport of 22Na above a concentration of 3 μg protein/ml, by 10-25%, versus to vehicle alone, and by 15-40% at concentrations of 5-20 μg/ml as compared to precipitates from 4 of the 5 non-RSW patients with either normal FEurate and normonatremia (2 patients) or with SIADH (2 patients).Conclusion: These studies provide further evidence that an elevated FEurate with normonatremia is highly consistent with RSW.  Evidence in the urine of natriuretic activity suggests significant renal excretion of the natriuretic factor. The potentially large source of the natriuretic factor that this could afford, coupled with small analytical sample sizes required by the in-vitro bioassay used here, should facilitate future experimental analysis and allow the natriuretic factor to be investigated as a potential biomarker for RSW.

scholarly journals Differential diagnosis between syndrome of inappropriate antidiuretic hormone secretion and cerebral/renal salt wasting syndrome in children over 1 year: proposal for a simple algorithm

2021 ◽  
Author(s):  
Flaminia Bardanzellu ◽  
Maria Antonietta Marcialis ◽  
Roberta Frassetto ◽  
Alice Melis ◽  
Vassilios Fanos
Keyword(s):  
Differential Diagnosis ◽  
Antidiuretic Hormone ◽  
Hormone Secretion ◽  
Extracellular Volume ◽  
Simple Algorithm ◽  
Diagnostic Algorithm ◽  
Clinical Approach ◽  
Inappropriate Antidiuretic Hormone Secretion ◽  
Salt Wasting ◽  
Renal Salt Wasting

AbstractHyponatremia, especially if acute and severe, can be a life-threatening condition. Several conditions can trigger hyponatremia. In this review, we will discuss two conditions that can determine euvolemic hyponatremia: the cerebral/renal salt wasting (CRSW) syndrome and the syndrome of inappropriate secretion of antidiuretic hormone (SIADH), including the two subtypes: reset osmostat (RO) and nephrogenic syndrome of inappropriate antidiuresis (NSIAD) and their differential diagnoses. Despite the passage of over 70 years since its first description, to date, the true etiopathogenesis of CRSW syndrome, a rare cause of hypovolemic/euvolemic hyponatremia, is almost unknown. SIADH, including RO and NSIAD, is sometimes difficult to differentiate from CRSW syndrome; in its differential diagnosis, the clinical approach based on the evaluation of the extracellular volume (ECV) was proven insufficient. We therefore suggest a simple diagnostic algorithm based on the assessment of the degree of hyponatremia, urinary osmolality, and the assessment of the fraction of urate excretion (FEUa) in conditions of hyponatremia and after serum sodium correction, to be applied in children over 1 year of life.

Syndrome of Inappropriate Antidiuretic Hormone Secretion Associated With Congenital Hydrocephalus in a Dog

2009 ◽  
Vol 45 (5) ◽  
pp. 249-252 ◽  
Author(s):  
Robert E. Shiel ◽  
Manuel Pinilla ◽  
Carmel T. Mooney
Keyword(s):  
Antidiuretic Hormone ◽  
Hormone Secretion ◽  
Diagnostic Testing ◽  
Clinical Signs ◽  
Abnormal Behavior ◽  
Water Restriction ◽  
Current Case ◽  
Inappropriate Antidiuretic Hormone Secretion ◽  
Antidiuretic Hormone Secretion ◽  
Truncal Ataxia

A 13-month-old, male bichon frise was examined for the investigation of intermittent seizures, ataxia, abnormal behavior, polyuria, and polydipsia. At presentation, clinical and neurological examinations were unremarkable with the exception of mild truncal ataxia and a domed skull. Severe hyponatremia and hypoosmolality were identified, and following diagnostic testing a diagnosis of the syndrome of inappropriate antidiuretic hormone secretion (SIADH) was made. Magnetic resonance imaging revealed changes consistent with severe hydrocephalus. Water restriction resulted in increased serum osmolality and a reduction in severity of clinical signs. The current case report documents SIADH associated with hydrocephalus in a dog. Structural brain disease should be excluded before a diagnosis of idiopathic SIADH is made.

scholarly journals Cerebral salt wasting in a patient with myeloproliferative neoplasm

2019 ◽  
Author(s):  
Lea Orlik ◽  
Reto Venzin ◽  
Thomas Fehr ◽  
Karin Hohloch
Keyword(s):  
Hormone Secretion ◽  
Myeloproliferative Neoplasm ◽  
Visual Disturbance ◽  
Mental Condition ◽  
Microcirculatory Disturbance ◽  
Volume Depletion ◽  
Severe Hyponatremia ◽  
Cerebral Salt Wasting ◽  
Inappropriate Antidiuretic Hormone Secretion ◽  
Salt Wasting

Abstract Background: Cerebral salt wasting (CSW) is a rare metabolic disorder with severe hyponatremia and volume depletion usually caused by brain injury like trauma, cerebral lesion, tumor or a cerebral hematoma. The renal function is normal with excretion of very high amounts of sodium in the urine. Diagnosis is made by excluding other reasons for hyponatremia, mainly the syndrome of inappropriate antidiuretic hormone secretion (SIADH). Case report: A 60-year-old patient was admitted to the emergency room with pain in the upper abdomen and visual disturbance two weeks after knee replacement. The patient was confused with severe hematoma at the site of the knee endoprosthesis. Laboratory values showed massive thrombocytosis, leukocytosis, anemia, severe hyponatremia and no evidence of infection. CT scan of the abdomen was inconspicuous. Head MRI showed no ischemia or bleeding, but a mild microangiopathy. A myeloproliferative neoplasm (MPN) was suspected and confirmed by bone marrow biopsy. Cerebral salt wasting syndrome was identified as the cause of severe hyponatremia most likely provoked by cerebral microcirculatory disturbance. The hematoma at the operation site was interpreted as a result of a secondary von Willebrand syndrome (vWS) due to the myeloproliferative neoplasm with massive thrombocytosis. After starting cytoreductive therapy with hydroxycarbamide, thrombocytosis and blood sodium slowly improved along with normalization of his mental condition. Conclusion: To the best of our knowledge this is the first description of a patient with CSW most likely caused by a microcirculatory disturbance due to a massive thrombocytosis in the context of a myeloproliferative neoplasm.

scholarly journals Cerebral salt wasting in a patient with myeloproliferative neoplasm

2019 ◽  
Author(s):  
Lea Orlik ◽  
Reto Venzin ◽  
Thomas Fehr ◽  
Karin Hohloch
Keyword(s):  
Hormone Secretion ◽  
Myeloproliferative Neoplasm ◽  
Volume Depletion ◽  
Severe Hyponatremia ◽  
Cerebral Salt Wasting ◽  
Inappropriate Antidiuretic Hormone Secretion ◽  
Salt Wasting ◽  
Cerebral Hematoma ◽  
Very High ◽  
Rare Metabolic Disorder

Abstract Background Cerebral salt wasting (CSW) is a rare metabolic disorder with severe hyponatremia and volume depletion usually caused by brain injury like trauma, cerebral lesion, tumor or a cerebral hematoma. The renal function is normal with excretion of very high amounts of sodium in the urine. Diagnosis is made by excluding other reasons for hyponatremia, mainly the syndrome of inappropriate antidiuretic hormone secretion (SIADH).

scholarly journals Cerebral salt wasting in a patient with myeloproliferative neoplasm

2019 ◽  
Author(s):  
Lea Orlik ◽  
Reto Venzin ◽  
Thomas Fehr ◽  
Karin Hohloch
Keyword(s):  
Hormone Secretion ◽  
Myeloproliferative Neoplasm ◽  
Volume Depletion ◽  
Severe Hyponatremia ◽  
Cerebral Salt Wasting ◽  
Inappropriate Antidiuretic Hormone Secretion ◽  
Salt Wasting ◽  
Cerebral Hematoma ◽  
Very High ◽  
Rare Metabolic Disorder

Abstract Background Cerebral salt wasting (CSW) is a rare metabolic disorder with severe hyponatremia and volume depletion usually caused by brain injury like trauma, cerebral lesion, tumor or a cerebral hematoma. The renal function is normal with excretion of very high amounts of sodium in the urine. Diagnosis is made by excluding other reasons for hyponatremia, mainly the syndrome of inappropriate antidiuretic hormone secretion (SIADH).

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