Acute hyponatremia post craniotomy resulting in a unilateral fixed and dilated pupil: A case study on diagnosis and management.

Background: Postoperative hyponatremia is a known complication of intracranial surgery, which can present with depressed mental status. Hyponatremia resulting in focal neurologic deficits is less frequently described. Case Description: We describe a patient who, after a bifrontal craniotomy for olfactory groove meningioma, developed acute hyponatremia overnight with a decline in mental status from Glasgow coma scale (GCS) score 15 to GCS 7 and a unilateral fixed dilated pupil. Head computed tomography showed expected postoperative changes without new acute or localizing findings, such as unilateral uncal herniation. The patient's mental status and pupil immediately improved with the administration of mannitol; however, there was a subsequent decline in mental status with a preserved pupil later that morning. Hypertonic saline reversed the neurologic change, and the patient was eventually discharged without a neurologic deficit. Focal neurologic deficits need not always arise following a craniotomy from a postoperative hematoma, stroke, or other finding with radiographic correlate. Conclusion: Post-craniotomy hyponatremia should now be seen as a postoperative complication that can result in both a general neurologic decline in mental status, as well as with focal neurologic signs such as a fixed, dilated pupil, which can be reversed with hyperosmolar therapy and correction of the hyponatremia.

Associations between Baseline Hyponatremia and Activities of Daily Living and Muscle Health in Convalescent Stroke Patients.

Objectives: Evidence is scarce regarding the association between hyponatremia and functional outcomes among older hospitalized patients. We aimed to evaluate the associations between baseline hyponatremia and improvement in activities of daily living (ADL) and muscle health in hospitalized post-stroke patients. Methods: This retrospective cohort study included hospitalized post-stroke patients. Serum sodium concentrations were extracted from medical records based on blood tests performed within 24 h of admission, with hyponatremia defined as a serum sodium concentration below135 mEq/L. Primary outcome was the discharge ADL as assessed by the motor domain of the Functional Independence Measure (FIM-motor) and its corresponding gain during hospitalization. Other outcomes encompassed the discharge scores for skeletal muscle mass (SMI) and handgrip strength (HGS). Multivariate linear regression analyses were used to determine the association between hyponatremia and outcomes of interest, adjusted for potential confounders. Results: Data from 955 patients (mean age 73.2 years; 53.6% men) were analyzed. The median baseline blood sodium level was 139 [interquartile range: 137, 141] mEq/L, and 84 patients (8.8%) exhibited hyponatremia. After full adjustment for confounders, baseline hyponatremia was significantly and negatively associated with FIM-motor at discharge (ß=-0.036, P=0.033) and its gain during hospital stay (ß=-0.051, P=0.033). Baseline hyponatremia exhibited an independent and negative association with discharge HGS (ß=-0.031, P=0.027), whereas no significant association was found between baseline hyponatremia and discharge SMI (ß=-0.015, P=0.244). Conclusions: Baseline hyponatremia demonstrated a correlation with compromised ADL and muscle health in individuals undergoing rehabilitation after stroke.

A case of early repolarization syndrome in which hyponatremia and coronary vasospasms induced ventricular fibrillation.

A 60-year-old man was referred to our hospital presenting with unconsciousness due to severe hyponatremia. The twelve­lead ECG on admission exhibited prominent J waves in the inferolateral leads. During the treatment for hyponatremia, ventricular fibrillation (VF) occurred and the electrogram (ECG) after the VF incident exhibited marked ST elevation in the inferolateral leads. An Ach provocation test induced vasospasms in the right and left coronary arteries and J wave augmentation, suggesting a high risk for vasospastic angina. Finally, a subcutaneous implantable cardioverter defibrillator was implanted in the patient. We hereby discuss the possible contribution of hyponatremia to VF episodes in early repolarization syndrome based on the present case.

Incidence and Risk Factors for Hyponatremia in Postoperative Spinal Surgery Patients.

Introduction: The incidence of hyponatremia after orthopedic surgery is high. Hyponatremia may prolong hospitalization and increase mortality, but few reports have identified risk factors for hyponatremia after spinal surgery. This study aims to determine the incidence and risk factors for hyponatremia after spinal surgery. Methods: A total of 200 patients aged 20 years or older who underwent spinal surgery at our hospital from 2020-2021 were recruited. Data on age, sex, height, weight, body mass index, operation duration, blood loss, albumin level, the geriatric nutritional risk index (GNRI), potassium level, the estimated glomerular filtration rate (eGFR), sodium level, length of hospital stay, history of hypertension, dialysis status, the occurrence of delirium during hospital stay, and oral medication use were collected. Comparisons between the postoperative hyponatremia group and the postoperative normonatremia group were conducted to evaluate the impact of hyponatremia on clinical outcomes. Results: Postoperative hyponatremia was observed in 56 (28%) of the 200 patients after spinal surgery. Comparison between the postoperative hyponatremia group with the postoperative normonatremia group revealed that the patients in the postoperative hyponatremia group were significantly older (72 versus 68.5 years, p<0.01). Postoperative hyponatremia was significantly associated with low GNRI values (100.8 versus 109.3, p<0.01), low eGFR values (59.2 versus 70.8 mL/min/1.73 m2, p<0.01), preoperative hyponatremia (138.5 vs. 141 mEq/L, p<0.01), and a high incidence of delirium (12.5% versus 2.7%, p=0.01). Older age (odds ratio=1.04, p=0.01) and preoperative hyponatremia (odds ratio=0.66, p value<0.01) were risk factors for postoperative hyponatremia. Conclusions: In addition to older age and preoperative hyponatremia, the study identified new risk factors for postoperative hyponatremia, which are preoperative undernutrition and impaired renal function. The incidence of delirium was significantly higher in the postoperative hyponatremia group, suggesting that correcting preoperative hyponatremia and ensuring good nutrition may prevent delirium and thereby shorten hospital stays.

Apelin and Copeptin Levels in Patients With Chronic SIAD Treated With Empagliflozin.

Background: Empagliflozin increases sodium levels in patients with a chronic syndrome of inappropriate antidiuresis (SIAD), and dapagliflozin increases apelin levels in patients with diabetes mellitus. Exogenous apelin increases sodium levels in rats with SIAD. We aimed to investigate whether an increase in plasma apelin concentration may contribute to the efficacy of empagliflozin in SIAD. Methods: Post hoc secondary analysis of a double-blind, crossover, placebo-controlled trial performed from December 2017 to August 2021 at the University Hospital Basel, Switzerland, investigating the effect of 4-week treatment with empagliflozin 25 mg/day as compared to placebo in 14 outpatients with chronic SIAD (NCT03202667). The objective was to investigate the effect of empagliflozin on plasma apelin and copeptin concentrations and their ratio. Results: Fourteen patients, 50% female, with a median [interquartile range] age of 72 years [65-77] were analyzed. Median apelin concentration was 956 pmol/L [853, 1038] at baseline. Median [interquartile range] apelin relative changes were +11% [0.7, 21] and +8% [-5, 25] (P = .672) at the end of the placebo and empagliflozin phases, respectively. Median copeptin concentration was 2.6 [2.2, 4.5] pmol/L at baseline and had a relative change of +5 [-2. 11]% and +25% [10, 28] (P = .047) over the placebo and empagliflozin phases, respectively. Conclusion: Empagliflozin did not lead to significant changes in apelin or the apelin/copeptin ratio in patients with chronic SIAD but led to an increase in copeptin. This suggests that the efficacy of empagliflozin in SIAD is independent of apelin and is not blunted by the adaptative increase in copeptin.

Hyponatremia in the emergency department: an overview of diagnostic and therapeutic approach.

INTRODUCTION: Hyponatremia, defined as a serum sodium concentration <135 mmol/l, is a frequent electrolyte disorder in patients presenting to an emergency department (ED). In this context, appropriate diagnostic and therapeutic management is rarely performed and challenging due to complex pathophysiologic mechanisms and a variety of underlying diseases. OBJECTIVE: To implement a feasible pathway of central diagnostic and therapeutic steps in the setting of an ED. METHODS: We conducted a narrative review of the literature, considering current practice guidelines on diagnosis and treatment of hyponatremia. Underlying pathophysiologic mechanisms and management of adverse treatment effects are outlined. We also report four cases observed in our ED. RESULTS: Symptoms associated with hyponatremia may appear unspecific and range from mild cognitive deficits to seizures and coma. The severity of hyponatremia-induced neurological manifestation and the risk of poor outcome is mainly driven by the rapidity of serum sodium decrease. Therefore, emergency treatment of hyponatremia should be guided by symptom severity and the assumed onset of hyponatremia development, distinguishing acute (<48 hours) versus chronic hyponatremia (>48 hours). CONCLUSIONS: Especially in moderately or severely symptomatic patients presenting to an ED, the application of a standard management approach appears to be critical to improve overall outcome. Furthermore, an adequate work-up in the ED enables further diagnostic and therapeutic evaluation during hospitalization.

Suspected cerebral salt wasting syndrome secondary to traumatic brain injury in a dog.

OBJECTIVE: To describe a dog with suspected cerebral salt wasting syndrome (CSWS) secondary to traumatic brain injury (TBI). CASE SUMMARY: A 2-month-old intact male Chihuahua-American Pitbull Terrier mix weighing 1.94 kg presented to a veterinary teaching emergency room after suffering bite wound-penetrating trauma to the head. Treatment was initiated with hyperosmotic agents, fluid resuscitation, and analgesia. The dog's neurologic dysfunction warranted hospitalization and continuous monitoring. Within 24 hours, the dog developed hyponatremia (133 mmol/L compared to 143 mmol/L on presentation [reference interval 142-149 mmol/L]). As the dog had concurrent tachycardia, increase in urine sodium concentration, polyuria, and weight loss, a diagnosis of cerebral salt wasting was suspected. A 2% hypertonic saline constant rate infusion was administered for volume replacement, and the patient showed improvement in clinical signs and blood sodium concentration. The dog was discharged on Day 5. Recheck examination showed significant neurologic improvement with sodium just below the low end of the reference range (141 mmol/L [reference interval 142-149 mmol/L]). NEW OR UNIQUE INFORMATION PROVIDED: This is the first description of suspected CSWS in veterinary medicine. Hyponatremia is a common finding in critically ill neurologic people, including those with TBI, and is typically associated with either syndrome of inappropriate antidiuretic hormone or CSWS. As treatment recommendations for syndrome of inappropriate antidiuretic hormone and CSWS are diametrically opposed, identifying the presence of hyponatremia and distinguishing between these 2 clinical entities is critical for improving patient care for those with TBI. This case highlights the characteristics and clinical progression regarding the diagnosis and management of suspected CSWS.

A case of SIADH following uncomplicated mild traumatic brain injury: Did cognitive bias delay treatment?

To optimize clinical care, it is imperative for providers to recognize their own inherent cognitive biases and the impact that has on their clinical decision making, thereby minimizing complications such as prolonged hospitalization, unnecessary healthcare spending, and impaired patient satisfaction and functional outcomes.

Severe Syndrome of Inappropriate Antidiuretic Hormone Secretion (SIADH) Following the Initiation of Valbenazine for Tardive Dyskinesia: A Case Report.

Hyponatremia, a common electrolyte disorder, usually has a benign clinical course. However, patients with the syndrome of inappropriate antidiuretic hormone secretion (SIADH) can suffer unfavorable outcomes, including mortality. Atypical antipsychotics, which are among the drugs associated with SIADH, also cause tardive dyskinesia, a condition that physicians can now effectively manage with the recently approved agent - valbenazine. We herein report a case of severe hyponatremia due to SIADH in a 58-year-old man who developed hyponatremia-induced generalized seizures six weeks after valbenazine was added to his regimen to mitigate olanzapine-associated tardive dyskinesia. His electrolyte derangement and clinical course improved following prompt recognition and treatment of SIADH. The temporal association between the commencement of valbenazine and the onset of SIADH suggests a possible but previously unreported link between valbenazine and the development of SIADH. Awareness of this uncommon association is relevant to patient safety.

Severe Hyponatremia Triggered by Immune Checkpoint Inhibitor Therapy in a Patient With Mulvihill-Smith Syndrome.

Background/Objective: Immune checkpoint inhibitors (ICI), including Programmed Cell Death 1, Programmed Cell Death Ligand 1, and Cytotoxic T-lymphocyte Associated Antigen 4 inhibitors, upregulate T-cell responses against tumor cells and are becoming a cornerstone in the treatment of various advanced solid and hematological cancers. Mulvihill-Smith Syndrome (MSS) is a rare genetic syndrome that has been associated with metabolic abnormalities and early-onset tumors, including malignancies. We report the first known case of ICI-induced hyponatremia attributable to syndrome of inappropriate antidiuretic hormone ADH release (SIADH) in a patient with MSS. Case Report: A 23-year-old female patient with MSS and hepatocellular carcinoma presented with recurrent hyponatremia. Assessment of fluid status and electrolytes revealed a euvolemic, hypotonic process consistent with SIADH shortly after initiating adjuvant therapy with atezolizumab, a Programmed Cell Death Ligand 1 inhibitor. Discussion: Endocrine etiologies for euvolemic hypotonic hyponatremia, including adrenal insufficiency and hypothyroidism, were excluded. The diagnosis of SIADH was confirmed based on electrolyte and osmolality studies. Sodium levels normalized with fluid restriction. Given the onset of hyponatremia 30 days after atezolizumab initiation, we posit that atezolizumab triggered severe hyponatremia due to SIADH. Conclusion: With the expanding utilization of ICIs, including in patients predisposed to malignancies such as MSS, vigilant monitoring for ICI-mediated electrolyte imbalances is crucial. Monitoring for hyponatremia and SIADH in the setting of ICI therapy is recommended.

Hyponatremia With Anticonvulsant Medications: A Narrative Review.

Hyponatremia is an adverse effect of many antiseizure medications (ASMs). It occurs with interference with the normal balance of electrolytes within the body. Various risk factors associated with the development of hyponatremia in patients taking these medications include age, gender, dosage, and combinations with other drugs. ASMs such as carbamazepine (CBZ), oxcarbazepine (OXC), and valproic acid have a higher risk of hyponatremia. Hyponatremia induced by an antiseizure medication can occur through various mechanisms depending on the drug's specific mechanism of action. Hyponatremia can be a potentially fatal side effect. Patients taking these medications need to be monitored closely for the signs and symptoms of hyponatremia. Acute hyponatremia, defined as developing in <48 hours, is more likely to show symptoms than chronic hyponatremia. Signs of acute hyponatremia include delirium, seizures, decerebrate posturing, and cerebral edema with uncal herniation. Chronic hyponatremia, defined as developing in >48 hours, can cause lethargy, dizziness, weakness, headache, nausea, and confusion. Hyponatremia is associated with longer hospital stays and increased mortality. Treatment varies based on the degree of severity of hyponatremia. Choosing a treatment option should include consideration of the drug causing the electrolyte disturbance, the patient's risk factor profile, and the severity of symptoms as they present in the individual patient. Healthcare providers should be aware of hyponatremia as a potential side effect of ASMs, the signs and symptoms of hyponatremia, the different treatment options available, and the potential complications associated with rapid correction of hyponatremia.

Old woman with Sheehan's syndrome suffered severe hyponatremia following percutaneous coronary intervention: a case report and review of literature.

Glucocorticoid deficiency can lead to hypoglycemia, hypotension, and electrolyte disorders. Acute glucocorticoid deficiency under stress is very dangerous. Here, we present a case study of an elderly patient diagnosed with Sheehan's syndrome, manifesting secondary adrenal insufficiency and secondary hypothyroidism, managed with daily prednisone and levothyroxine therapy. She was admitted to our hospital due to acute non-ST segment elevation myocardial infarction. The patient developed nausea and limb twitching post-percutaneous coronary intervention, with subsequent diagnosis of hyponatremia. Despite initial intravenous sodium supplementation failed to rectify the condition, and consciousness disturbances ensued. However, administration of 50 mg hydrocortisone alongside 6.25 mg sodium chloride rapidly ameliorated symptoms and elevated blood sodium levels. Glucocorticoid deficiency emerged as the primary etiology of hyponatremia in this context, exacerbated by procedural stress during percutaneous coronary intervention. Contrast agent contributed to blood sodium dilution. Consequently, glucocorticoid supplementation emerges as imperative, emphasizing the necessity of stress-dose administration of glucocorticoid before the procedure. Consideration of shorter intervention durations and reduced contrast agent dosages may mitigate severe hyponatremia risks. Moreover, it is crucial for this patient to receive interdisciplinary endocrinologist management. In addition, Sheehan's syndrome may pose a risk for coronary atherosclerotic disease.

The Effect of Thiazide Diuretics on Urinary Prostaglandin E2 Excretion and Serum Sodium in the General Population.

CONTEXT: Thiazide-induced hyponatremia is one of the most common forms of hyponatremia, but its pathogenesis is incompletely understood. Recent clinical data suggest links with prostaglandin E2 (PGE2) and a single nucleotide polymorphism (SNP) in the prostaglandin transporter gene (SLCO2A1), but it is unknown if these findings also apply to the general population. OBJECTIVE: To study the associations between serum sodium, thiazide diuretics, urinary excretions of PGE2 and its metabolite (PGEM), and the rs34550074 SNP in SLCO2A1 in the general population. DESIGN: Prospective population-based cohort study (Rotterdam Study). SETTING: General population. PARTICIPANTS: 2,178 participants (65% female, age 64 ± 8 years). INTERVENTION(S): None. MAIN OUTCOME MEASURE(S): Serum sodium levels. RESULTS: Higher urinary PGE2 excretion was associated with lower serum sodium: difference in serum sodium for each two-fold higher PGE2 -0.19 mmol/l (95%CI -0.31 to -0.06), PGEM -0.29 mmol/l (95%CI -0.41 to -0.17). This association was stronger in thiazide users (per two-fold higher PGE2 -0.73 vs. -0.12 mmol/l and PGEM -0.6 vs. -0.25 mmol/l, p for interaction < 0.05 for both). A propensity score matching analysis of thiazide vs. non-thiazide users yielded similar results. The SNP rs34550074 was not associated with lower serum sodium or higher urinary PGE2 or PGEM excretion in thiazide or non-thiazide users. CONCLUSIONS: Serum sodium is lower in people with higher urinary PGE2 and PGEM excretion and this association is stronger in thiazide users. This suggests that PGE2-mediated water reabsorption regulates serum sodium, which is relevant for the pathogenesis of hyponatremia in general and thiazide-induced hyponatremia in specific.

Exertional hyponatremia among active component members of the U.S. Armed Forces, 2008-2023.

Exertional hyponatremia, or exercise-associated hyponatremia, occurs within 24 hours after physical activity due to a serum, plasma, or blood sodium concentration (Na+) below the normal reference range of 135 mEq/L. If not detected early and managed properly, hyponatremia can be fatal. From 2008 to 2023, 1,812 cases of exertional hyponatremia were diagnosed among U.S. active component service members (ACSMs), with an overall incidence rate of 8.3 cases per 100,000 person-years (p-yrs). In 2023 there were 153 cases of exertional hyponatremia diagnosed among ACSMs, resulting in a crude incidence rate of 11.7 per 100,000 p-yrs. Female service members, those older than 40, non-Hispanic Black service members, Marine Corps members, recruits, those in combat-specific occupations, and ACSMs stationed in the Northeast U.S. region had higher incidence rates of exertional hyponatremia diagnoses than their respective counterparts. During the surveillance period, annual rates of incident exertional hyponatremia diagnoses peaked in 2010 (12.8 per 100,000 p-yrs) and then decreased to a low of 5.3 cases per 100,000 p-yrs in 2013. Thereafter the incidence rate fluctuated but has increased from 6.2 per 100,000 p-yrs in 2017 to its second-highest level in 2023. Service members and their supervisors should be aware of the dangers of excessive fluid consumption and prescribed limits for consumption during prolonged physical activity including field training exercises, personal fitness training, or recreational activities, particularly in hot, humid weather.

Status seizures as a secondary effect from the "squash drinking syndrome" in an infant.

Abstract: The "hypotonic drink syndrome" is characterized by loss of appetite, normal activity levels and, in some cases, intestinal disturbances in children with an intake of more than 30% of the recommended daily calories in the form of non-dairy drinks. Diarrhea and growth retardation are possible complications due to the amount of nonnutritive calorie intake ("empty calories") contained in this type of hypotonic beverages.We present the case of an 11-month-old boy who suffered a "Squash drinking syndrome" requiring admission to the pediatric intensive care unit because of a status seizure secondary to a severe hyponatremia (118 mmol/L) due to massive ingestion of hypotonic drinks, such as squash. The seizure did not subside until sodium levels reached 123 mmol/L with hypertonic saline (3%). Neurological, renal, digestive, endocrine and metabolic problems were all ruled out and normal sodium levels were maintained with dietary recommendations and a restriction of hypotonic fluid intake. Conclusions: To prevent these situations it is important to be aware of this entity and to know how to identify the possible complications that may appear after excessive ingestion of hypotonic drinks, as in the case of our patient, ranging from lack of appetite, growth failure and diarrhea, to a status seizure.

Case Report: Chorea as a Rare Manifestation of Secondary Adrenal Insufficiency.

The word "chorea" comes from the Latin word "choreus," which means dancing movement. Chorea is defined as a hyperkinetic movement disorder characterized by uncontrolled, unintended, jerky, brief, irregular, random movements involving the limbs or facial muscles. Here, we discuss the case of a 48-year-old male with hypothyroidism for two years, which is well-controlled with medication. He presented with behavioral disturbances for the past seven months and choreiform movements affecting all four limbs, his tongue, and his face for the past six months. Investigations revealed hyponatremia and low serum osmolality. An MRI of the brain showed the empty sella sign. Further investigations revealed low levels of adrenocorticotropic hormone (ACTH), prolactin, and testosterone. Considering the diagnosis of chorea with euvolemic hyponatremia due to secondary adrenal insufficiency, the patient was started on tetrabenazine, trihexyphenidyl, oral hydrocortisone, and gradual correction of sodium level. The patient's condition improved during the hospital stay, and he continues to do well in routine follow-ups.

Hyponatremia as a predictor of cognitive deterioration in hospitalized post-stroke patients.

PURPOSE: Evidence is scarce regarding the association between hyponatremia and alterations in cognitive function among hospitalized older patients. We aimed to investigate the associations between hyponatremia and the baseline cognitive status, as well as the improvement in cognitive function, in hospitalized post-stroke patients. METHODS: This retrospective cohort study included consecutive hospitalized post-stroke patients. Serum sodium concentrations were extracted from medical records based on blood tests performed within 24 h of admission, with hyponatremia defined as a serum sodium concentration < 135 mEq/L. The main outcomes included admission and discharge scores for cognitive levels, assessed through the cognitive domain of the Functional Independence Measure (FIM-cognition), as well as the score changes observed during the hospitalization period. Multivariate linear regression analyses were used to determine the association between hyponatremia and outcomes of interest, adjusted for potential confounders. RESULTS: Data from 955 patients (mean age 73.2 years; 53.6 % men) were included in the analysis. The median baseline blood sodium level was 139 [137, 141], and 84 patients (8.8 %) exhibited hyponatremia. After full adjustment for confounders, the baseline hyponatremia was significantly and negatively associated with FIM-cognition values at admission (ß = -0.009, p = 0.016), discharge (ß = -0.038, p = 0.043), and the gain during hospital stay (ß = -0.040, p = 0.011). CONCLUSION: Baseline hyponatremia has demonstrated a correlation with decline in cognitive level over the course of rehabilitation in individuals after stroke. Assessing hyponatremia at the outset proves to be a pivotal prognostic indicator.

A Case Report of an Ultrasound-Guided Popliteal Sciatic Nerve Block: An Asset for Emergency Lower Limb Debridement in a High-Risk Patient.

Severe sepsis, a syndrome characterized by systemic inflammation and acute organ dysfunction in response to infection, is a major healthcare problem affecting all age groups throughout the world. Sepsis-associated encephalopathy (SAE) is a common but poorly understood neurological complication of sepsis. It is characterized by diffuse brain dysfunction secondary to infection elsewhere in the body without overt central nervous system (CNS) infection. Such cases commonly present for emergency surgical management with inadequate fasting hours, limited time for preparation, and preoperative optimization. Regional blocks become the savior in such cases where both general and central neuraxial anesthesia become perilous. Here, we present a 70-year-old male, with a case of necrotizing fascitis of the left lower limb with septic encephalopathy, with compromised cardiac or respiratory function and deranged laboratory investigations. The patient was admitted for emergency lower limb debridement, and ultrasound-guided left lower limb popliteal sciatic nerve block along with an adductor canal block was chosen as the plan of anesthesia management.

Pseudohypoaldosteronism and acquired renal aldosterone resistance with hyperkalemic type IV renal tubular acidosis in 2 cats.

This report describes the diagnosis and treatment of aldosterone resistance (AR) and acquired hyperkalemic type IV renal tubular acidosis (RTA) in 2 cats comparable to acquired pseudohypoaldosteronism in people. One cat developed AR from chronic kidney disease after an acute kidney injury and was treated with furosemide per os, which resolved the hyperkalemic RTA. The second cat developed transient AR secondary to a bacterial urinary tract infection associated with urethral catheterization, and treatment with antibiotics resolved the hyperkalemic RTA.

Case report: Secondary failure to tolvaptan in a patient with SCLC and paraneoplastic SIADH.

The syndrome of inappropriate antidiuretic hormone secretion (SIADH) is frequent in lung cancer patients. Here, we report a case with persistent hyponatremia, which suggested malignant SIADH and facilitated an early diagnosis of small cell lung cancer (SCLC). A combined radio-chemotherapy led to a partial remission and resolution of SIADH. An early relapse was indicated by reoccurring severe hyponatremia and increased copeptin levels, which were used as surrogate markers for the antidiuretic hormone (ADH). As palliative immunochemotherapy, together with fluid restriction and solute substitution, were unable to control hyponatremia, treatment with the ADH V2-receptor antagonist tolvaptan was initiated. Over time, the dose of tolvaptan needed to be increased, paralleled by a well-documented exponential increase of copeptin levels. In summary and conclusion, this is a rare case of a secondary failure to tolvaptan with unique documentary evidence of increasing copeptin levels. This observation supports the hypothesis that exceedingly high ADH levels may lead to competitive displacement of tolvaptan from the V2 receptor.