scholarly journals Renal salt wasting syndrome in a patient with COVID-19; a case report and review of the literature

2020 ◽  
Vol 7 (1) ◽  
pp. e02-e02
Author(s):  
Bassam Al-Helal ◽  
Emad Abdallah ◽  
Altayyeb Yousef ◽  
Reem Asad ◽  
Mahmoud Reda
Keyword(s):  
Uric Acid ◽  
Serum Sodium ◽  
Hormone Secretion ◽  
Lower Limbs ◽  
Cerebral Salt Wasting ◽  
Cerebral Disease ◽  
Salt Wasting ◽  
Renal Salt Wasting ◽  
First Case ◽  
Disease Case

Introduction: Cerebral salt wasting or renal salt wasting (RSW) syndrome, may be more common than syndrome of inappropriate antidiuretic hormone secretion (SIADH) and may even occur in the absence of cerebral disease. We report a case of RSW in a Bangladeshi patient positive for COVID-19 without clinical cerebral disease. Case Presentation: A 53 years-old Bangladeshi patient presented with history of chest pain and acute MI. On examination, the patient was conscious, alert, vitally stable, chest with fine bilateral basal crepitation and heart with additional S3 sound and abdomen was lax with no organomegaly. There was no lower limbs oedema. His serum creatinine; 68 umol/L, urea; 3.4 mmol/L, K; 4.7 mmol/L, sodium; 135 mmol/L, uric acid; 141 mmol/L and phosphate was 1.3 mmol./L. Echocardiography (ECG) revealed anterior lateral wall STEMI. PCI was done for LAD. ECG revealed ejection fraction (EF) 10-15 %. Nasopharyngeal swab for COVID-19 was positive. Serum sodium decreased from 135 to 108 with signs of hypovolemia. Work up for hyponatremia revealed serum osmolality of 237 mOsm/kg, urine NA; 109 mmol/L, urine osmolality; 295 mOsm/kg, urine uric acid; 685 umol/L, and urine phosphate; 6.5 mmol/L. Additionally serum T3, T4, TSH and serum basal cortisol were normal. The patient received normal saline infusion and fludrocortisone and serum sodium increased to 134 mmol/L. Our patient had all the important clinical and laboratory characteristics of RSW in the absence of cerebral disease which include hyponatremia associated with hypovolemia, high urinary sodium excretion, increased fraction excretion of phosphate and persistent hypouricemia with increased fractional excretion of urate after correction of hyponatremia and with normal renal, adrenal and thyroid functions. Furthermore, there was a prompt response to saline replacement and fludrocortisone and steady improvement in serum sodium with negativity and improvement of COVID-19. Our diagnosis was RSW in the absence of cerebral disease and to our knowledge; this is the first case of RSW in a patient with COVID-19 in the literature. Conclusion: RSW should be considered in patients with COVID-19 with hyponatremia and absence of cerebral disease. We suggest changing cerebral salt wasting to the more appropriate term RSW.

scholarly journals Cerebral salt wasting in a case of tubercular meningitis in a child

2017 ◽  
Vol 4 (6) ◽  
pp. 2217
Author(s):  
Kapil Bainade ◽  
V. Kotrashetti ◽  
Vijay Sonwane ◽  
Rizwan Ahmed ◽  
Prashant Abusaria
Keyword(s):  
Serum Sodium ◽  
Hormone Secretion ◽  
Final Diagnosis ◽  
Total Leukocyte Count ◽  
Fluid Restriction ◽  
Communicating Hydrocephalus ◽  
Cerebral Salt Wasting ◽  
Meningeal Enhancement ◽  
Inappropriate Antidiuretic Hormone Secretion ◽  
Salt Wasting

A 12-year-old female child presented with fever, headache, vomiting since 20 days and convulsions for 1 day. She was unimmunised and BCG scar was absent. Clinical examination showed signs of meningeal irritation, Kernigs sign and Brudzinkins sign with signs of raised intracranial tension. Fundus examination was suggestive of stage 2 papilledema. Her laboratory reports were normal on admission. LP was with hold in view of raised ICT. CT brain was done. S/O meningeal enhancement, mild communicating hydrocephalus with periventricular ooze, extra axial hyper densities in bilateral sylvian fissures along the tentorium (Basal Exudates) On day 3 of admission she had low serum sodium, serum osmolality High urinary sodium. While on lumbar puncture (LP) and cerebrospinal fluid (CSF) examination, CSF protein, and total leukocyte count (predominant lymphocytes) were all increased. On his 5th day of admission, her serum sodium was low and he had a normal urine output. Fluid restriction was tried in order to rule out syndrome of inappropriate antidiuretic hormone secretion (SIADH) but the patient did not respond to it. Keeping in view the above findings, a final diagnosis of tuberculous meningitis leading to cerebral salt wasting syndrome was made. The patient was started on anti-tuberculous therapy (ATT), IV Steroids, anticonvulsants, 3% NaCl and supportive treatment, to which she responded favourably and was later discharged. 

Cerebral Salt Wasting

2017 ◽  
Author(s):  
Mark A. Henry ◽  
Avinash B. Kumar
Keyword(s):  
Serum Sodium ◽  
Extracellular Fluid ◽  
Cerebral Salt Wasting ◽  
Delivery Of Care ◽  
Salt Wasting ◽  
Neurological Illness ◽  
Assessment And Treatment ◽  
Life Threatening ◽  
Biochemical Level ◽  
Timely Delivery

Human survival (on a biochemical level) depends on the body’s critical ability to regulate the osmolality and salinity of extracellular fluid. When functioning in a normal state, the osmoregulatory system stringently maintains the serum sodium in a narrow range. Alterations in the serum sodium and water balance have significant and sometimes life-threatening impact on patients—especially when they occur in conjunction with serious intracranial pathology. This chapter, including the case discussion, illustrates the conundrum of hyponatremia and high urine output states complicating neurological illness. A thorough understanding of the pathophysiology, assessment, and treatment of these conditions is essential for the timely delivery of care and optimal patient outcomes.

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.

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 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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