High prevalence of renal salt wasting induced by haptoglobin-related protein without signal peptide is linked to new syndrome of salt wasting in Alzheimer disease.

The subject of hyponatremia is undergoing significant changes after developing a more pathophysiologic approach that is superior to the ineffective volume approach and can more effectively identify the different causes of hyponatremia. This new approach identified cerebral salt wasting (CSW) in 24 (38%) of 62 hyponatremic patients from the medical wards of the hospital with 21 showing no evidence of cerebral disease to support our proposal to change CSW to renal salt wasting (RSW). RSW had to be differentiated from the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) because of diametrically opposite therapeutic goals of water-restricting water-logged patients with SIADH or administering salt water to volume-depleted patients with RSW. Both syndromes present with identical clinical parameters that require a difficult protocol to make such a differentiation possible. We describe rat clearance studies demonstrating natriuretic activity in the plasma of patients with neurosurgical and Alzheimer diseases (AD) and eventually identify the protein as haptoglobin-related protein without signal peptide, which can serve as a biomarker to simplify diagnosis of RSW and delivery of the proper management to improve clinical outcomes. We also discuss the introduction of a new syndrome of RSW in AD and its implications. The high prevalence of RSW and identification of the natriuretic factor have created debates over the existence of RSW with none questioning or addressing the pathophysiologic data that identified patients with RSW. We also discuss the potentially large group of patients with RSW who are normonatremic.

Haptoglobin-Related Protein without Signal Peptide as Biomarker of Renal Salt Wasting in Hyponatremia, Hyponatremia-Related Diseases and as New Syndrome in Alzheimer's Disease.

The application of pathophysiologic tenets has created significant changes in our approach to hyponatremia and hyponatremia-related conditions. This new approach incorporated the determination of fractional excretion (FE) of urate before and after the correction of hyponatremia and the response to isotonic saline infusion to differentiate the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) from renal salt wasting (RSW). FEurate simplified the identification of the different causes of hyponatremia, especially the diagnosis of a reset osmostat and Addison's disease. Differentiating SIADH from RSW has been extremely difficult because both syndromes present with identical clinical parameters, which could be overcome by successfully carrying out the difficult protocol of this new approach. A study of 62 hyponatremic patients from the general medical wards of the hospital identified 17 (27%) to have SIADH, 19 (31%) with reset osmostat, and 24 (38%) with RSW with 21 of these RSW patients presenting without clinical evidence of cerebral disease to warrant changing the nomenclature from cerebral to renal salt wasting. The natriuretic activity found in the plasma of 21 and 18 patients with neurosurgical and Alzheimer's disease, respectively, was later identified as haptoglobin-related protein without signal peptide (HPRWSP). The high prevalence of RSW creates a therapeutic dilemma of deciding whether to water-restrict water-logged patients with SIADH as compared to administering saline to volume-depleted patients with RSW. Future studies will hopefully achieve the following: 1. Abandon the ineffective volume approach; 2. Develop HPRWSP as a biomarker to identify hyponatremic and a projected large number of normonatremic patients at risk of developing RSW, including Alzheimer's disease; 3. Facilitate differentiating SIADH from RSW on the first encounter and improve clinical outcomes.

Profound hyponatremia and dehydration: A case of cisplatin induced renal salt wasting syndrome.

Cisplatin is a well-known chemotherapeutic agent that can be associated with hyponatremia. It is known to be associated with a multitude of renal disorders including acute kidney injury with reduced glomerular filtration, Fanconi syndrome, and renal tubular acidosis, nephrogenic diabetes insipidus and renal salt wasting syndrome. We report a case of an elderly male presenting with significant recurrent hyponatremia, and prerenal azotemia. With recent exposure to cisplatin along with significant hypovolemia and urinary loss of sodium, he was diagnosed to have cisplatin induced renal salt wasting syndrome.

New Approach to Hyponatremia: High Prevalence of Cerebral/Renal Salt Wasting, Identification of Natriuretic Protein That Causes Salt Wasting.

Our understanding of hyponatremic conditions has undergone major alterations. There is a tendency to treat all patients with hyponatremia because of common subtle symptoms that include unsteady gait that lead to increased falls and bone fractures and can progress to mental confusion, irritability, seizures, coma and even death. We describe a new approach that is superior to the ineffectual volume approach. Determination of fractional excretion (FE) of urate has simplified the diagnosis of a reset osmostat, Addison's disease, edematous causes such as congestive heart failure, cirrhosis and nephrosis, volume depletion from extrarenal salt losses with normal renal tubular function and the difficult task of differentiating the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) from cerebral/renal salt wasting (C/RSW). SIADH and C/RSW have identical clinical and laboratory parameters but have diametrically opposite therapeutic goals of water-restricting water-loaded patients with SIADH or administering salt water to dehydrated patients with C/RSW. In a study of nonedematous patients with hyponatremia, we utilized FEurate and response to isotonic saline infusions to differentiate SIADH from C/RSW. Twenty-four (38%) of 62 hyponatremic patients had C/RSW with 21 having no clinical evidence of cerebral disease to support our important proposal to change cerebral to renal salt wasting (RSW). Seventeen (27%) had SIADH and 19 (31%) had a reset osmostat. One each from hydrochlorothiazide and Addison's disease. We demonstrated natriuretic activity in the plasma of patients with neurosurgical and Alzheimer diseases (AD) in rat clearance studies and have now identified the natriuretic protein to be haptoglobin related protein without signal peptide (HPRWSP). We introduce a new syndrome of RSW in AD that needs further confirmation. Future studies intend to develop HPRWSP as a biomarker to simplify the diagnosis of RSW in hyponatremic and normonatremic patients and explore other clinical applications that can improve clinical outcomes.

Carboplatin-induced renal salt-wasting syndrome in pediatric patients with intracranial germ cell tumors and concomitant diabetes insipidus.

We report a case series of 14 children with intracranial germ cell tumor and concomitant central diabetes insipidus, who developed hyponatremia secondary to renal salt-wasting syndrome (RSWS) following the administration of carboplatin. Clinicians prescribing platinum-based chemotherapy for this group of patients should be alert to the risk of RSWS. Regular monitoring should be performed as hyponatremia can be asymptomatic until it is severe.

A Challenging Case of Persisting Hypokalemia Secondary to Gitelman Syndrome.

There are several causes of hypokalemia, including transcellular shift, renal loss, gastrointestinal loss, and decreased oral intake. Sometimes it is challenging to know the source of the problem; however, with detailed history, physical examination, and appropriate laboratory investigations, the physician should be able to narrow down the differentials diagnosis to reach the right one. One of the rare causes of hypokalemia is Gitelman syndrome, which is a salt-losing tubulopathy that manifests as renal potassium wasting, metabolic alkalosis, hypokalemia, hypomagnesemia, hypocalciuria, and hyperreninemic hyperaldosteronism. This disorder is inherited in an autosomal recessive pattern with an incidence of 25 instances per million population. We report a challenging case of persistent hypokalemia in a 30-year-old woman who presented with a history of palpitation, bilateral upper and lower limbs numbness, nausea, diarrhea, and generalized fatigue for three days. After history and physical examination, the patient was diagnosed with an episode of enteritis, and laboratory workups revealed low potassium and magnesium levels, and it was thought that these electrolyte abnormalities were secondary to gastrointestinal loss. Therefore, the patient was mainly treated supportively along with potassium and magnesium replacement. However, after one week of replacement, the patient still had low potassium and magnesium levels in spite of being diarrhea-free, so renal loss was suspected. Urine electrolytes revealed high renal potassium loss with low-normal blood pressure, arterial blood gases revealed metabolic alkalosis with a pH of 7.49 and bicarbonate level of 29 mEq/L. Repeated urine chemistry was done to check for chloride level and turned out to be high, and 24-hour urinary excretion of calcium was very low. Therefore, the patient was diagnosed with Gitelman syndrome and was managed with potassium and magnesium replacements intravenously, and was encouraged to consume a diet rich in these electrolytes. After complete resolutions of the symptoms and correction of potassium and magnesium levels, the patient was discharged home in stable condition.

Identification of a Novel Natriuretic Protein in Patients With Cerebral-Renal Salt Wasting-Implications for Enhanced Diagnosis.

BACKGROUND: The most vexing problem in hyponatremic conditions is to differentiate the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) from cerebral/renal salt wasting (C-RSW). Both have identical clinical parameters but diametrically opposite therapeutic goals of water- restricting water-logged patients with SIADH or administering salt and water to dehydrated patients with C-RSW. While C-RSW is considered a rare condition, the report of a high prevalence of C-RSW in the general hospital wards creates an urgency to differentiate one syndrome from the other on first encounter. We decided to identify the natriuretic factor (NF) we previously demonstrated in plasma of neurosurgical and Alzheimer diseases (AD) who had findings consistent with C-RSW. METHODS: We performed the same rat renal clearance studies to determine natriuretic activity (NA) in serum from a patient with a subarachnoid hemorrhage (SAH) and another with AD and demonstrated NA in their sera. The sera were subjected to proteomic and SWATH (Sequential Windowed Acquisition of All) analyses which identified increased levels of haptoglobin related protein (Hpr) without signal peptide (Hpr-WSP). RESULTS: Recombinant Hpr with His tag at the N terminus had no NA. Hpr-WSP had a robust NA in a dose-dependent manner when injected into rats. Serum after recovery from C-RSW in the SAH patient had no NA. CONCLUSIONS: Hpr-WSP may be the NF in C-RSW which should be developed as a biomarker to differentiate C-RSW from SIADH on first encounter, introduces a new syndrome of C-RSW in AD and can serve as a proximal diuretic to treat congestive heart failure.

Lessons from Wolfram Syndrome: Initiation of DDAVP Therapy Causes Renal Salt Wasting Due to Elevated ANP/BNP Levels, Rescued by Fludrocortisone Treatment.

Initiation of desmopressin acetate (DDAVP) for untreated diabetes insipidus (DI) in Wolfram syndrome (WS) causes abrupt volume expansion resulting in particularly high secretion of Atrial Natriuretic Peptide (ANP) and/or Brain Natriuretic Peptide (BNP), which in turn blocks all stimulators of zona glomerulosa steroidogenesis, resulting in secondary mineralocorticoid deficiency and acute hyponatremia, causing renal salt wasting (RSW). Two sisters, a 19-y-old girl (A) and a 7-y-old girl (B) with WS, presented with severe polyuria-polydipsia due to never treated DI. Both had neurogenic bladder and "B" had severe hydronephrosis secondary to untreated grade III bilateral vesicoureteral reflux. They initiated therapy with oral melt DDAVP which resulted in RSW. ANP was found ×50 and BNP ×2-4 fold elevated. Fludrocortisone 100-200 × 2 µg/d controlled natriuresis and restored electrolytes to normal within 48 h. Fludrocortisone treatment rescues otherwise potentially life-threatening hyponatremia due to RSW and the secondary mineralocorticoid deficiency driven by elevated ANP and/or BNP, caused by sudden volume expansion following DDAVP initiation.

Differentiating syndrome of inappropriate ADH, reset osmostat, cerebral/renal salt wasting using fractional urate excretion.

OBJECTIVES: Clinical and laboratory data of reset osmostat (RO) and cerebral/renal salt wasting (C/RSW) mimic syndrome of inappropriate antidiuretic hormone (SIADH) and can pose diagnostic challenges because of significant overlapping between clinical and laboratory findings. Failure to correctly diagnose hyponatremia may result in increased mortality risk, longer hospital stay, and is cost-effective. We aim to illustrate clinical and laboratory similarities and difference among patients with hyponatremic disorders and discuss the diagnostic value of factional uprate excretion (FEurate) to differentiate SIADH from RO and C/RSW. CASE PRESENTATIONS: We report the use of FEurate in the evaluation of three patients with hyponatremia and elevated urine osmolality in the absence of edema or clinical evidence of dehydration to differentiate SIADH from RO and C/RSW. CONCLUSIONS: Measurement of FEurate may offset in part the diagnostic confusion imparted by the diagnoses of SIADH, RO, and C/RSW.

The challenges of diagnosis and management of Gitelman syndrome.

Gitelman syndrome is an inherited tubulopathy characterized by renal salt wasting from the distal convoluted tubule. Defects in the sodium chloride cotransporter (encoded by SLC12A3) underlie this autosomal recessive condition. This article focuses on the specific challenges of diagnosing and treating Gitelman syndrome, with use of an illustrative case report. Symptoms relate to decreased serum potassium and magnesium levels, which include muscle weakness, tetany, fatigue and palpitations. Sudden cardiac deaths have been reported. Making a diagnosis may be difficult given its rarity but is important. A knowledge of the serum and urine biochemical picture is vital to distinguish it from a broad differential diagnosis, and application of genetic testing can resolve difficult cases. There is a group of Gitelman syndrome heterozygous carriers that experience symptoms and electrolyte disturbance and these patients should be managed in a similar way, though here genetic investigations become key in securing a difficult diagnosis. Potassium and magnesium replacement is the cornerstone of treatment, though practically this can be hard for patients to manage and often does not fully relieve symptoms even when serum levels are normalized. Challenges arise due to the lack of randomized controlled trials focussing on treatment of this rare disease; hence, clinicians endorse strategies in line with correction of the underlying pathophysiology such as sodium loading or pharmacological treatments, which seem to help some patients. Focussed dietary advice and knowing the best tolerated preparations of potassium and magnesium medications are useful tools for the physician, as well as an awareness of the specific burdens that this patient group face in order to signpost appropriate support.

Syndrome of inappropriate antidiuretic hormone secretion as a side effect of chemotherapy for testicular cancer: A case report.

INTRODUCTION: Inappropriate antidiuretic hormone secretion syndrome can be a serious adverse event of cisplatin-based chemotherapy. Cisplatin had to be changed to other drugs or chemotherapy completely discontinued in earlier reported cases. CASE PRESENTATION: Three cycles of bleomycin, etoposide, and cisplatin chemotherapy were planned for a 40-year-old man with a diagnosis of lymph node recurrence of testicular cancer. On day 9, he suffered from vomiting and mental disturbance. Severe hyponatremia (110 mEq/L) with low plasma osmolality led to a diagnosis of a syndrome of inappropriate antidiuretic hormone secretion, and infusions of hypertonic saline and salt intake were prescribed. Second and third courses of bleomycin, etoposide, and cisplatin chemotherapy could then be given with careful electrolyte management. CONCLUSION: Continuation of cisplatin administration with precise electrolyte adjustment can be a treatment option in regimens where cisplatin is essential for achieving optimal antitumor efficacy.

Determining Fractional Urate Excretion Rates in Hyponatremic Conditions and Improved Methods to Distinguish Cerebral/Renal Salt Wasting From the Syndrome of Inappropriate Secretion of Antidiuretic Hormone.

Our evaluation of hyponatremic patients is in a state of confusion because the assessment of the volume status of the patient and determinations of urine sodium concentrations (UNa) >30-40 mEq/L have dominated our approach despite documented evidence of many shortcomings. Central to this confusion is our inability to differentiate cerebral/renal salt wasting (C/RSW) from the syndrome of inappropriate secretion of antidiuretic hormone (SIADH), syndromes with diametrically opposing therapeutic goals. The recent proposal to treat most or all hyponatremic patients makes differentiation even more important and reports of C/RSW occurring without cerebral disease leads to a clinically important proposal to change cerebral to renal salt wasting (RSW). Differentiating SIADH from RSW is difficult because of identical clinical parameters that characterize both syndromes. Determination of fractional urate excretion (FEurate) is central to a new algorithm, which has proven to be superior to current methods. We utilized this algorithm and differences in physiologic response to isotonic saline infusions between SIADH and RSW to evaluate hyponatremic patients from the general medical wards of the hospital. In 62 hyponatremic patients, 17 (27%) had SIADH, 19 (31%) had reset osmostat (RO), 24 (38%) had RSW, 1 due to HCTZ and 1 Addison's disease. Interestingly, 21 of 24 with RSW had no evidence of cerebral disease and 10 of 24 with RSW had UNa < 20 mEqL. We conclude that 1. RSW is much more common than is perceived, 2.the term cerebral salt wasting should be changed to RSW 3. RO should be eliminated as a subclass of SIADH, 4. SIADH should be redefined 5. The volume approach is ineffective and 6. There are limitations to determining UNa, plasma renin, aldosterone or atrial/brain natriuretic peptides. We also present data on a natriuretic peptide found in sera of patients with RSW and Alzheimer's disease.

Chronic hyponatremia in a patient with renal salt wasting and without cerebral disease: relationship between RSW, risk of fractures and cognitive impairment.

Renal salt wasting syndrome (RSW) is defined as a renal loss of sodium leading to hyponatremia and a decrease in extracellular fluid volume (ECV). Differentiation of this disorder from the syndrome of inappropriate antidiuretic hormone secretion (SIADH), a common cause of hyponatremia, can be difficult because both can present with hyponatremia and concentrated urine with natriuresis. Our clinical case about a 78-year-old woman with a recent fracture of the right femur not only confirms that this syndrome can occur in patients without intracranial pathologies (CT documented), but depicts how the hyponatremia caused by RSW can show a chronic, oscillating course. This is an interesting point of view because it suggests to us to consider RSW in the differential diagnosis of patients with chronic hyponatremia.

High Prevalence of Renal Salt Wasting Without Cerebral Disease as Cause of Hyponatremia in General Medical Wards.

BACKGROUND: The approach to hyponatremia is in a state of flux, especially in differentiating syndrome of inappropriate antidiuretic hormone secretion (SIADH) from cerebral-renal salt wasting (RSW) because of diametrically opposite therapeutic goals. Considering RSW can occur without cerebral disease, we determined the prevalence of RSW in the general hospital wards. METHODS: To differentiate SIADH from RSW, we used an algorithm based on fractional excretion (FE) of urate and nonresponse to saline infusions in SIADH as compared to excretion of dilute urines and prompt increase in serum sodium in RSW. RESULTS: Of 62 hyponatremic patients, (A) 17 patients (27%) had SIADH, 11 were nonresponsive to isotonic saline, and 5 normalized a previously high FEurate after correction of hyponatremia; (B) 19 patients (31%) had a reset osmostat based on normal FEurates and spontaneously excreted dilute urines; (C) 24 patients (38%) had RSW, 21 had no clinical evidence of cerebral disease, 19 had saline-induced dilute urines; 2 had undetectable plasma ADH levels when urine was dilute, 10 required 5% dextrose in water to prevent rapid increase in serum sodium, 11 had persistently increased FEurate after correction of hyponatremia and 10 had baseline urinary sodium < 20 mEq/L; (D) 1 patient had Addison disease with a low FEurate and (E) 1 patient (1.6%) had hyponatremia due to hydrochlorothiazide. CONCLUSIONS: Of the 24 patients with RSW, 21 had no cerebral disease, supporting our proposal to change cerebral-renal salt wasting to renal salt wasting. Application of established pathophysiological standards and a new algorithm based on determination of FEurate were superior to the volume approach for determination of urinary sodium when identifying the cause of hyponatremia.

Post-cytokine-release Salt Wasting as Inverse Tumor Lysis Syndrome in a Non-cerebral Natural Killer-cell Neoplasm.

The pathogenesis of cerebral/renal salt-wasting syndrome remains unknown. We herein present a case of salt-wasting syndrome with a natural killer-cell neoplasm without cerebral invasion. A 78-year-old man with hemophagocytic syndrome received two cycles of chemotherapy that did not induce tumor lysis syndrome, but repeatedly caused polyuria and natriuresis. The expression of tumor necrosis factor-α in the neoplasm led us to hypothesize that an oncolysis-induced cytokine storm may have caused renal tubular damage and salt wasting. Our theory may explain the pathogenic mechanism of cerebral/renal salt-wasting syndrome associated with other entities, including cerebral disorders, owing to the elevation of cytokine levels after subarachnoid hemorrhage.

Application of established pathophysiologic processes brings greater clarity to diagnosis and treatment of hyponatremia.

Hyponatremia, serum sodium < 135 mEq/L, is the most common electrolyte abnormality and is in a state of flux. Hyponatremic patients are symptomatic and should be treated but our inability to consistently determine the causes of hyponatremia has hampered the delivery of appropriate therapy. This is especially applicable to differentiating syndrome of inappropriate antidiuresis (SIAD) from cerebral salt wasting (CSW) or more appropriately, renal salt wasting (RSW), because of divergent therapeutic goals, to water-restrict in SIAD and administer salt and water in RSW. Differentiating SIAD from RSW is extremely difficult because of identical clinical parameters that define both syndromes and the mindset that CSW occurs rarely. It is thus insufficient to make the diagnosis of SIAD simply because it meets the defined characteristics. We review the pathophysiology of SIAD and RSW, the evolution of an algorithm that is based on determinations of fractional excretion of urate and distinctive responses to saline infusions to differentiate SIAD from RSW. This algorithm also simplifies the diagnosis of hyponatremic patients due to Addison's disease, reset osmostat and prerenal states. It is a common perception that we cannot accurately assess the volume status of a patient by clinical criteria. Our algorithm eliminates the need to determine the volume status with the realization that too many factors affect plasma renin, aldosterone, atrial/brain natriuretic peptide or urine sodium concentration to be useful. Reports and increasing recognition of RSW occurring in patients without evidence of cerebral disease should thus elicit the need to consider RSW in a broader group of patients and to question any diagnosis of SIAD. Based on the accumulation of supporting data, we make the clinically important proposal to change CSW to RSW, to eliminate reset osmostat as type C SIAD and stress the need for a new definition of SIAD.

Hiponatremia luego de uso de cisplatino: a propósito de un caso / Hyponatraemia after cisplatin use: a case report

Paciente de 26 años con diagnóstico de teratoma inmaduro de ovario derecho. Se le realizó resección del tumor más salpingooforectomía en junio de 2014. Recibió manejo adyuvante con carboplatino y ciclofosfamida por un ciclo en enero de 2015, pero sin respuesta. Se realizó laparotomía exploradora por obstrucción intestinal evidenciándose masa pélvica e implantes peritoneales a nivel hepático. Valoró oncología clínica del INC en febrero del 2015, se inicia manejo con esquema PEB; recibió el primer ciclo sin complicaciones. El segundo ciclo fue retrasado por infección en la pared abdominal. Empezó tratamiento con sodio sérico normal, con posterior descenso sin alteración en el resto de electrolitos, función renal, ni estado ácido base. La paciente no presentó síntomas neurológicos y estuvo euvolémica. Se inició estudio de hiponatremia haciéndose diagnóstico de SIADH. Se indicó manejo con restricción hídrica y dieta hipersódica, con posterior ascenso gradual de niveles séricos de Na, considerándose SIADH secundario a uso de cisplatino.

The case is presented of a 26 year-old patient diagnosed with an immature teratoma of the right ovary. Tumour resection plus salpingo-oophorectomy was performed in June 2014. She received one cycle of adjuvant treatment with carboplatin and cyclophosphamide, but with no response. An exploratory laparotomy was performed due to an intestinal obstruction, which showed a pelvic mass and peritoneal implants at hepatic level. She was assessed in the oncology clinic of the Colombian National Institute (INC) in February 2015, and treatment with a platinol (cisplatin), etoposide, and bleomycin (PEB) scheme was started. She received the first cycle without complications, but the second cycle was delayed due to an infection in the abdominal wall. She started the treatment with a normal serum sodium, with a subsequent decrease with no changes in the rest of the electrolytes, kidney function, or acid-base status. The patient showed no neurological signs and was euvolaemic. A hyponatraemia study was performed, ending up making the diagnosis of inappropriate antidiuretic hormone secretion (IADHS). A water restriction and high sodium diet was indicated, with the subsequent gradual increase in the serum Na levels. The IADHS was considered secondary to the use of cisplatin.

[Hyponatremia in children: from pathophysiology to therapy]. / Hyponatremie u detí: od patofyziologie k lécbe.

This present review analyzes the etiology, diagnostics and management of conditions associated with hyponatremia. Excess water and/or sodium wasting lead to the development of hyponatremia in children. There are diverse etiologies associated with hyponatremia, correct diagnosis is based on detailed history, physical examination and basic laboratory tests. Symptomatic hyponatremia can be a life threatening emergency and thus requires fast and vigorous management. Inappropriate treatment may cause fatal consequences.

Central Diabetes Insipidus and Cisplatin-Induced Renal Salt Wasting Syndrome: A Challenging Combination.

We describe a 2-year-old female with a suprasellar primitive neuroectodermal tumor and central diabetes insipidus (DI) who developed polyuria with natriuresis and subsequent hyponatremia 36 hr after cisplatin administration. The marked urinary losses of sodium in combination with a negative sodium balance led to the diagnosis of cisplatin-induced renal salt wasting syndrome (RSWS). The subsequent clinical management is very challenging. Four weeks later she was discharged from ICU without neurological sequela. The combination of cisplatin-induced RSWS with DI can be confusing and needs careful clinical assessment as inaccurate diagnosis and management can result in increased neurological injury.