Long-Term Indomethacin Treatment in a Chinese Child with Gitelman Syndrome: Case Report and Literature Review on its Efficacy and Tolerance.

BACKGROUND Gitelman syndrome (GS) is a rare inherited autosomal recessive salt-losing renal tubulopathy. Early-onset GS is difficult to differentiate from Bartter syndrome (BS). It has been reported in some cases that cyclooxygenase (COX) inhibitors, which pharmacologically reduce prostaglandin E2(PGE2) synthesis, are helpful for GS patients, especially in children, but the long-term therapeutic effect has not yet been revealed. CASE REPORT A 4-year-old boy was first brought to our hospital for the chief concern of short stature and growth retardation. Biochemical tests demonstrated severe hypokalemia, hyponatremia, and hypochloremic metabolic alkalosis. The patient's serum magnesium was normal. He was diagnosed with BS and treated with potassium supplementation and indomethacin and achieved stable serum potassium levels and slow catch-up growth. At 11.8 years of age, the patient showed hypomagnesemia and a genetic test confirmed that he had GS with compound heterozygous mutations in the SLC12A3 gene. At the age of 14.8 years, when indomethacin had been taken for nearly 10 years, the boy reported having chronic stomachache, while his renal function remained normal. After proton pump inhibitor and acid inhibitor therapy, the patient's symptoms were ameliorated, and he continued to take a low dose of indomethacin (37.5 mg/d divided tid) with good tolerance. CONCLUSIONS Early-onset GS in childhood can be initially misdiagnosed as BS, and gene detection can confirm the final diagnosis. COX inhibitors, such as indomethacin, might be tolerated by pediatric patients, and long-term therapy can improve the hypokalemia and growth retardation without significant adverse effects.

Primary aldosteronism without hypertension:A case report and review of the literature / Hyperaldostéronisme primaire sans hypertension artérielle : à propos d'un cas et revue de la littérature

We describe the case of a patient who presented with hyperaldosteronism without arterial hypertension. She had been referred for consultation for persistent severe hypokalaemia despite oral KCl supplementation. The absence of hypertension had been proven by repeated clinical measurements and by ABPM. Hyperaldosteronism had been demonstrated by hormonal assays and catheterization of the adrenal veins. Abdominal CT revealed a left adrenal adenoma. Finally, the anatomopathological examination of the surgical specimen confirmed the adenoma. After the intervention, serum potassium normalized. The clinical case is completed by a review of the literature of hyperaldosteronisms without arterial hypertension.

Nous décrivons le cas d'une patiente qui s'est présentée avec un hyperaldostéronisme sans hypertension artérielle. Elle a été adressée en consultation pour une hypokaliémie sévère persistante malgré une supplémentation orale en chlorure de potassium (KCl). L'absence d'hypertension a été prouvée par des mesures cliniques répétées et par mesure ambulatoire de la pression artérielle (MAPA). L'hyperaldostéronisme a été mis en évidence par des dosages hormonaux et un cathétérisme des veines surrénales. Le scanner abdominal a révélé un adénome surrénalien gauche. Enfin, l'examen anatomopathologique de la pièce opératoire a confirmé l'adénome. Après l'intervention, le potassium sérique s'est normalisé. Le cas clinique est complété par une revue de la littérature des hyperaldostéronismes sans hypertension artérielle.

Gitelman syndrome combined with diabetes mellitus: A case report and literature review.

RATIONALE: Gitelman syndrome (GS) is an uncommon autosomal recessive tubulopathy resulting from a functional deletion mutation in the SLC12A3 gene. Its onset is typically insidious and challenging to discern, and it is characterized by hypokalemia, metabolic alkalosis, and reduced urinary calcium excretion. There is limited literature on the diagnosis and management of GS in individuals with concomitant diabetes. PATIENT CONCERNS: A 36-year-old male patient with a longstanding history of diabetes exhibited suboptimal glycemic control. Additionally, he presented with concurrent findings of hypokalemia, hypomagnesemia, hypocalciuria, and metabolic alkalosis. DIAGNOSIS: Building upon the patient's clinical manifestations and extensive laboratory evaluations, we conducted thorough genetic testing, leading to the identification of a compound heterozygous mutation within the SLC12A3 gene. This definitive finding confirmed the diagnosis of GS. INTERVENTIONS: We have formulated a detailed medication regimen for patients, encompassing personalized selection of hypoglycemic medications and targeted electrolyte supplementation. OUTCOMES: Following 1 week of comprehensive therapeutic intervention, the patient's serum potassium level effectively normalized to 3.79 mmol/L, blood glucose parameters stabilized, and there was significant alleviation of clinical symptoms. LESSONS: GS has a hidden onset and requires early diagnosis and intervention based on patient related symptoms and laboratory indicators in clinical practice, and personalized medication plans need to be provided according to the specific situation of the patient.

Case report: Gitelman syndrome with diabetes: Confirmed by both hydrochlorothiazide test and genetic testing.

RATIONALE: Gitelman syndrome (GS) is an autosomal recessive tubulopathy caused by mutations of the SLC12A3 gene. It is characterized by hypokalemic metabolic alkalosis, hypomagnesemia and hypocalciuria. Hypokalemia, hypomagnesemia, and increased renin-angiotensin-aldosterone system (RAAS) activity can cause glucose metabolism dysfunction. The diagnosis of GS includes clinical diagnosis, genetic diagnosis and functional diagnosis. The gene diagnosis is the golden criterion while as functional diagnosis is of great value in differential diagnosis. The hydrochlorothiazide (HCT) test is helpful to distinguish GS from batter syndrome, but few cases have been reported to have HCT testing. PATIENT CONCERNS: A 51-year-old Chinese woman presented to emergency department because of intermittent fatigue for more than 10 years. DIAGNOSES: Laboratory test results showed hypokalemia, hypomagnesemia, hypocalciuria and metabolic alkalosis. The HCT test showed no response. Using next-generation and Sanger sequencing, we identified 2 heterozygous missense variants (c.533C > T:p.S178L and c.2582G > A:p.R861H) in the SLC12A3 gene. In addition, the patient was diagnosed with type 2 diabetes mellitus 7 years ago. Based on these findings, the patient was diagnosed with GS with type 2 diabetic mellitus (T2DM). INTERVENTIONS: She was given potassium and magnesium supplements, and dapagliflozin was used to control her blood glucose. OUTCOMES: After treatments, her fatigue symptoms were reduced, blood potassium and magnesium levels were increased, and blood glucose levels were well controlled. LESSONS: When GS is considered in patients with unexplained hypokalemia, the HCT test can be used for differential diagnosis, and genetic testing can be continued to confirm the diagnosis when conditions are available. GS patients often have abnormal glucose metabolism, which is mainly caused by hypokalemia, hypomagnesemia, and secondary activation of RAAS. When a patient is diagnosed with GS and type 2 diabetes, sodium-glucose cotransporter 2 inhibitors (SGLT2i) can be used to control the blood glucose level and assist in raising blood magnesium.

A case report of Gitelman syndrome in children.

RATIONALE: Giltelman syndrome (GS) is an autosomal recessive infectious disease, which is caused by the mutation of SLC12A3 gene encoding thiazide diuretic sensitive sodium chloride cotransporter located in the distal convoluted tubule of the kidney. PATIENT CONCERNS: A 7-year-old and 3-month-old male patient has poor appetite, slow growth in height and body weight since the age of 3, body weight: 16 kg (-3 standard deviation), height: 110 cm (-3 standard deviation), normal exercise ability and intelligence. One year ago, he was diagnosed with hypokalemia. After potassium supplement treatment, the blood potassium returned to normal. The patient developed abdominal pain, vomiting, limb weakness, and tetany 1 day before admission. DIAGNOSES: After admission examination, the patient was found to have hypokalemia (2.27-2.88 mmol/L), hypomagnesemia (0.47 mmol/L), hypophosphatemia (1.17 mmol/L), hypocalcemia (1.06 mmol/24 hours), and metabolic alkalosis (PH 7.60). The blood pressure is normal, and the concentration of aldosterone is 791.63 pg/mL. The adrenocorticotropic hormone and cortisol detected at 8 am are 4.95 pmol/L and 275.09 nmol/L, respectively. Twenty-four hours of urine potassium is 32.52 mmol. Gene sequencing results showed 2 pathogenic variants in the GS-related SLC12A3 gene, which are related to the phenotype of the subject. INTERVENTIONS: After admission, the patients were given potassium and magnesium supplements, as well as oral spironolactone. The symptoms of limb weakness and tetany were significantly relieved. After discharge, the patients continued to maintain treatment to keep the blood potassium at more than 3.0 mmol/L, and the blood magnesium at more than 0.6 mmol/L. OUTCOMES: Follow-up at 1 month after discharge, in the patient's self-description, he had no symptoms such as limb weakness and tetany, and his height was increased by 1 cm and the body weight increased by 1.5 kg. LESSONS: For patients with hypokalemia, hypomagnesemia, and metabolic alkalosis, the possibility of GS should be given priority. After the diagnosed by gene sequencing of SLC12A3 gene, potassium and magnesium supplementation could significantly improve symptoms.

A Case of Hypokalemia Caused by Left Native Renal Artery Stenosis in a Kidney Transplant Recipient.

A 39-year-old woman with end-stage renal failure of unknown origin was on peritoneal dialysis for 10 years. One year ago, she underwent ABO-incompatible living-donor kidney transplantation from her husband. After the kidney transplantation, her serum creatinine level remained around 0.7 mg/dL, but her serum potassium level remained low at around 3.5 mEq/L despite potassium supplementation and spironolactone. The patient's plasma renin activity (PRA) and plasma aldosterone concentration (PAC) were markedly elevated (20 ng/mL/h and 868 pg/mL, respectively). A CT angiogram of the abdomen performed 1 year previously suggested stenosis of the left native renal artery, which was considered responsible for the hypokalemia. Renal venous sampling was done on both the native kidneys and the transplanted kidney. Since renin secretion from the left native kidney was significantly elevated, a laparoscopic left nephrectomy was performed. Postoperatively, the renin-angiotensin-aldosterone system was markedly improved (PRA: 6.4 ng/mL/h, PAC: 147.3 pg/mL), and the serum potassium levels also improved. Pathological examination of the removed kidney showed many atubular glomeruli and hyperplasia of the juxtaglomerular apparatus (JGA) in residual glomeruli. In addition, renin staining showed strong positivity in the JGA of these glomeruli. Here, we report a case of hypokalemia caused by left native renal artery stenosis in a kidney transplant recipient. This valuable case study provides histological confirmation of maintained renin secretion in an abandoned native kidney after kidney transplantation.

Efficacy of Potassium Supplementation in Hypokalemic Patients Receiving Peritoneal Dialysis: A Randomized Controlled Trial.

RATIONALE & OBJECTIVE: Hypokalemia is a common electrolyte abnormality in patients on peritoneal dialysis (PD) and has been associated with increased risks of peritonitis and death. Whether correction of hypokalemia improves these outcomes is unknown. STUDY DESIGN: Multicenter, open-label, prospective, randomized controlled trial. SETTING & PARTICIPANTS: Adult (aged ≥18 years) PD patients with hypokalemia (defined as at least 3 values or an average value <3.5 mEq/L in the past 6 months). Randomization was stratified according to center and residual urine output (≤100 or >100 mL/day). INTERVENTIONS: Random assignment to either protocol-based potassium supplementation (titratable dose of oral potassium chloride to maintain serum potassium of 4-5 mEq/L) or conventional potassium supplementation (reactive supplementation when serum potassium is <3.5 mEq/L) over 52 weeks. Treatment groups were compared using intention-to-treat analyses implemented using Cox proportional hazards regression. OUTCOME: The primary outcome was time from randomization to first peritonitis episode (any organism). Secondary outcomes were all-cause mortality, cardiovascular mortality, hospitalization, and conversion to hemodialysis. RESULTS: A total of 167 patients with time-averaged serum potassium concentrations of 3.33 ± 0.28 mEq/L were enrolled from 6 PD centers: 85 were assigned to receive protocol-based treatment, and 82 were assigned to conventional treatment. The median follow-up time was 401 (IQR, 315-417) days. During the study period, serum potassium levels in the protocol-based treatment group increased to 4.36 ± 0.70 mEq/L compared with 3.57 ± 0.65 mEq/L in the group treated conventionally (mean difference, 0.66 [95% CI, 0.53-0.79] mEq/L; P < 0.001). The median time to first peritonitis episode was significantly longer in the protocol-based group (223 [IQR, 147-247] vs 133 [IQR, 41-197] days, P = 0.03). Compared with conventional treatment, the protocol-based group had a significantly lower hazard of peritonitis (HR, 0.47 [95% CI, 0.24-0.93]) but did not differ significantly with respect to any of the secondary outcomes. Asymptomatic hyperkalemia (>6 mEq/L) without characteristic electrocardiographic changes occurred in 3 patients (4%) in the protocol-based treatment group. LIMITATIONS: Not double-masked. CONCLUSIONS: Compared with reactive potassium supplementation when the serum potassium level falls below 3.5 mEq/L, protocol-based oral potassium treatment to maintain a serum potassium concentration in the range of 4-5 mEq/L may reduce the risk of peritonitis in patients receiving PD who have hypokalemia. TRIAL REGISTRATION: Registered at the Thai Clinical Trials Registry with study number TCTR20190725004.

Hypokalemic Paralysis Due to Primary Sjögren's Syndrome: Case Series.

BACKGROUND: Sjögren's syndrome (SS) is autoimmune disorder charaterized by exocrine glandular involvement and extra-glandular manifestations. Associations between hypokalemic paralysis and SS have not been emphasized enough. Present study evaluates hypokalemic paralysis as presenting feature in PSS. METHODS: A retrospective cross-sectional study from 2015 to 2020 was conducted to evaluate the clinical phenotype of primary Sjögren's syndrome (PSS) who presented to us with hypokalemic paralysis. RESULTS: Data of 13 patients were evaluated. All were female patients and mean age was 38 years. 61.5% (n= 8) had more than one episode of hypokalemic paralysis; 61.5% (n= 8) patients had oral dryness and 69% (n= 9) had dryness of eyes. 23% (n= 3) patients had inflammatory arthritis and 1 patient had Raynaud's phenomenon, myopathy respectively. 1 patient had chronic constipation and hypothyroidism was present in 61.5% (n= 8) patients. Other co-morbidity included hypertension, renal calculi and situs inversus present in 15%, 15% and 7% respectively. The mean ESR at presentation was 64 mm/hr; average serum potassium level was 2.04meq/dl and distal renal tubular acidosis was present in all patients. Paralysis was completely recovered in all patients after supplementation with potassium. CONCLUSION: The renal involvement in PSS can uncommonly present as hypokalemic paralysis in the absence of significant sicca symptoms or may precede sicca symptoms. A high index of suspicion for PSS should be kept in all patients with hypokalemic paralysis. This phenotype may represent a distinct subset. Serum electrolytes should be regularly monitored in all patients with SS.

Hypokalaemic quadriparesis in a patient with urinary diversion through Indiana pouch.

A man in his 20s, a patient with chronic kidney disease with a baseline estimated glomerular filtration rate of 33 mL/min/1.73 m2, who had an Indiana pouch continent urinary diversion procedure done at 6 years of age for bladder exstrophy, presented to the emergency room with sudden-onset progressive quadriparesis over 6 hours with power 1/5 in all the limbs with preserved reflexes. He was fully conscious and oriented, with stable vital signs. On evaluation, he had severe hypokalaemia and severe metabolic acidosis (both high anion gap and non-anion gap acidosis). Imaging studies showed bilateral gross hydroureteronephrosis, and renal and pouch calculi. Hypokalaemia was promptly treated with intravenous potassium chloride and acidosis with emergency haemodialysis. The patient had a complete motor recovery following intravenous potassium correction and was discharged with oral potassium and bicarbonate supplements. Here, the Indiana pouch, its metabolic and electrolyte complications, and its treatment are discussed.

Refractory familial hypokalaemic periodic paralysis leading to cardiovascular compromise.

Familial hypokalaemic periodic paralysis (FHPP) is a rare neuromuscular disorder that is classified under periodic paralysis (PP), which is characterised by episodes of muscle weakness. Common triggers include intense exercise, fasting or consumption of carbohydrate-rich meals. Hypokalaemic PP has an incidence of 1 in 100 000; despite the temporal association, cardiac manifestations are exceedingly rare. We present a case of FHPP, a channelopathy presenting with severe refractory hypokalaemia. The challenges with our patient were maintaining potassium levels within normal ranges and initiating a close follow-up plan. Due to the lack of clinical guidance in our case, many aspects of care, including surveillance, medications and genetic testing, remain unaddressed. Medical management includes aggressive correction with supplements, potassium-sparing diuretics and carbonic anhydrase inhibitors. Severe cases of dysrhythmias, especially ventricular fibrillation, require electrophysiology evaluation and possible implantation of a defibrillator to prevent sudden cardiac death.

Difficulties in the management of hypokalemia in a pregnant patient with Gitelman syndrome.

Gitelman syndrome (GS) is a rare renal disorder, and little is known about its impact on pregnancy. We report the successful outcome of pregnancy in a patient with GS that was managed with aggressive oral and intravenous potassium supplementation.

A Rapidly Progressive Case of Ectopic Adrenocorticotropic Hormone (ACTH) Syndrome.

BACKGROUND Adrenocorticotropic hormone (ACTH)-dependent Cushing's syndrome (CS) secondary to an ectopic source is an uncommon condition, accounting for 4-5% of all cases of CS. Refractory hypokalemia can be the presenting feature in patients with ectopic ACTH syndrome (EAS), and is seen in up to 80% of cases. EAS can be rapidly progressive and life-threatening without timely diagnosis and intervention. CASE REPORT We present a case of a 74-year-old White woman who first presented with hypokalemia, refractory to treatment with potassium supplementation and spironolactone. She progressively developed generalized weakness, recurrent falls, bleeding peptic ulcer disease, worsening congestive heart failure, and osteoporotic fracture. A laboratory workup showed hypokalemia, hypernatremia, and primary metabolic alkalosis with respiratory acidosis. Hormonal evaluation showed elevated ACTH, DHEA-S, 24-h urinary free cortisol, and unsuppressed cortisol following an 8 mg dexamethasone suppression test, suggestive of ACTH-dependent CS. CT chest, abdomen, and pelvis, and FDG/PET CT scan showed a 1.4 cm right lung nodule and bilateral adrenal enlargement, confirming the diagnosis of EAS, with a 1.4-cm lung nodule being the likely source of ectopic ACTH secretion. Due to the patient's advanced age, comorbid conditions, and inability to attend to further evaluation and treatment, her family decided to pursue palliative and hospice care. CONCLUSIONS This case illustrates that EAS is a challenging condition and requires a multidisciplinary approach in diagnosis and management, which can be very difficult in resource-limited areas. In addition, a delay in diagnosis and management often results in rapid deterioration of clinical status.

Antenatal Bartter syndrome: a new compound heterozygous mutation in exon 2 of KCNJ1 gene.

A 30+6/7-week infant was born by vaginal delivery to a 21-year-old primigravida with pregnancy complicated by polyhydramnios. The infant developed polyuria and significant weight loss in the first 2 weeks of life despite appropriate fluid management. He developed hyponatraemia, hypochloraemia, transient hyperkalaemia and prerenal azotaemia with metabolic acidosis. On further evaluation, he had elevated plasma renin and aldosterone levels. Bartter syndrome was considered in the differential diagnosis. Bartter syndrome gene panel revealed a rare compound heterozygous mutation in exon 2 of the KCNJ1 gene (Lys186Glu/Thr71Met), suggesting antenatal Bartter syndrome (type 2). The infant developed late-onset hypokalaemia and metabolic alkalosis by week 4 of life. He regained birth weight by week 3 of life but failed to thrive (10-20 g/kg/day) despite high caloric intake (140 kcal/kg/day). His electrolyte abnormalities gradually improved, and he was discharged home without the need for electrolyte supplements or medications.

Caffeine-induced hypokalemia: a case report.

BACKGROUND: With an increase in the global popularity of coffee, caffeine is one of the most consumed ingredients of modern times. However, the consumption of massive amounts of caffeine can lead to severe hypokalemia. CASE PRESENTATION: A 29-year-old man without a specific past medical history was admitted to our hospital with recurrent episodes of sudden and severe lower-extremity weakness. Laboratory tests revealed low serum potassium concentration (2.6-2.9 mmol/L) and low urine osmolality (100-130 mOsm/kgH2O) in three such prior episodes. Urinary potassium/urinary creatinine ratio was 12 and 16 mmol/gCr, respectively. The patient was not under medication with laxatives, diuretics, or herbal remedies. Through an in-depth interview, we found that the patient consumed large amounts of caffeine-containing beverages daily, which included > 15 cups of coffee, soda, and various kinds of tea. After the cessation of coffee intake and concomitant intravenous potassium replacement, the symptoms rapidly resolved, and the serum potassium level normalized. CONCLUSIONS: An increased intracellular shift of potassium and increased loss of potassium in urine due to the diuretic action have been suggested to be the causes of caffeine-induced hypokalemia. In cases of recurring hypokalemia of unknown cause, high caffeine intake should be considered.

Hypokalaemic periodic paralysis secondary to subclinical hyperthyroidism: an uncommon cause of acute muscle paralysis.

Hypokalaemic periodic paralysis secondary to subclinical hyperthyroidism is an uncommon clinical phenomenon characterised by lower limb paralysis secondary to hypokalaemia in the background of subclinical hyperthyroidism. In this article, we report a patient who presented with progressive lower limb muscle weakness secondary to hypokalaemia that was refractory to potassium replacement therapy. He has no diarrhoea, no reduced appetite and was not taking any medication that can cause potassium wasting. Although he was clinically euthyroid, his thyroid function test revealed subclinical hyperthyroidism. His 24-hour urine potassium level was normal, which makes a rapid transcellular shift of potassium secondary to subclinical hyperthyroidism as the possible cause. He was successfully treated with potassium supplements, non-selective beta-blockers and anti-thyroid medication. This case report aimed to share an uncommon case of hypokalaemic periodic paralysis secondary to subclinical hyperthyroidism, which to our knowledge, only a few has been reported in the literature.

Diagnosis and outpatient management of Gitelman syndrome from the first trimester of pregnancy.

A 32-year-old woman presented with an incidental finding of hypokalaemia on routine bloods at 9 weeks of a second pregnancy, on a background of lifelong salt craving. Her previous pregnancy was uncomplicated. She had no previous significant medical or family history. Venous blood gases showed a hypokalaemic, normochloraemic metabolic alkalosis. Urinary potassium was elevated. Escalating doses of oral supplementation of potassium, magnesium, sodium and potassium-sparing diuretics were required through the course of pregnancy, in response to regular electrolyte monitoring. These were later weaned and completely stopped post partum. Delivery was uneventful with no maternal or neonatal complications. Genetic testing performed post partum showed heterogenous mutation of SCL12A3 gene.

Hypokalaemic paralysis and metabolic alkalosis in a patient with Sjögren syndrome: a case report and literature review.

BACKGROUND: Acquired Gitelman syndrome is a very rare disorder reported in association with autoimmune disorders, mostly Sjögren syndrome. It is characterized by the presence of hypokalaemic metabolic alkalosis, hypocalciuria, hypomagnesaemia and hyper-reninaemia, in the absence of typical genetic mutations associated with inherited Gitelman syndrome. CASE PRESENTATION: A 20 year old woman who was previously diagnosed with primary Sjögren syndrome and autoimmune thyroiditis presented with two week history of lower limb weakness and salt craving. Examination revealed upper limb and lower limb muscle weakness with muscle power of 3/5 on MRC scale and diminished deep tendon reflexes. On evaluation, she had hypokalaemia with high trans-tubular potassium gradient, metabolic alkalosis and hypocalciuria, features suggestive of Gitelman syndrome. New onset hypokalaemic alkalosis in a previously normokalaemic patient with Sjögren syndrome strongly favored a diagnosis of acquired Gitelman syndrome. Daily potassium supplementation and spironolactone resulted in complete clinical recovery. CONCLUSIONS: Acquired Gitelman syndrome associated with Sjögren syndrome is rare. It should be considered as a differential diagnosis during evaluation of acute paralysis and hypokalaemic metabolic alkalosis in patients with autoimmune disorders, especially Sjögren syndrome.

Hypokalemia-Induced Rhabdomyolysis Caused by Adrenal Tumor-Related Primary Aldosteronism: A Report of 2 Cases.

BACKGROUND Primary aldosteronism, also known as Conn's syndrome, is a clinical condition caused by excessive production of aldosterone. The classic presenting signs of primary aldosteronism are hypertension and hypokalemia. However, rhabdomyolysis induced by severe hypokalemia is a rare manifestation of primary aldosteronism. There were only a few cases presented in the English literature over the last 4 decades. CASE REPORT We present 2 cases, a 53-year-old man and a 46-year-old man, with severe hypokalemia-induced rhabdomyolysis caused by adrenal tumor-related primary aldosteronism. Both of these patients were under medical treatment with oral anti-hypertension drug for hypertension, but were poorly controlled. They both presented to the Emergency Department with muscle weakness and pain. Laboratory testing showed elevated creatinine phosphokinase (CPK) and low serum potassium levels. Hypokalemia-induced rhabdomyolysis was suspected. A further endocrine survey showed low PRA (plasma renin activity) and high aldosterone levels, finding which are compatible with primary aldosteronism. Computed tomography (CT) was arranged for further evaluation, and adrenal tumors were found in both cases. Both patients underwent robotic-assisted laparoscopic adrenalectomy. In both cases, there was no recurrence of hypokalemia without potassium supplementation, and their hypertension was under better control at further follow-up visits. CONCLUSIONS Hypokalemic rhabdomyolysis is a rare manifestation of primary aldosteronism. It might be difficult to making a diagnosis when rhabdomyolysis and severe hypokalemia are the first manifestations in patients with primary aldosteronism. The use of diuretics for hypertension treatment might be a risk factor for extremely low potassium levels, which can induce rhabdomyolysis in patients with primary aldosteronism.

Glyphosate poisoning - a case report.

Glyphosate is the most commonly used broad-spectrum, non-selective herbicide in the world. The toxicity is supposed to be due to uncoupling of oxidative phosphorylation and the surfactant polyoxyethylene amine (POEA)- mediated cardiotoxicity. Clinical features of this herbicide poisoning are varied, ranging from asymptomatic to even death. There is no antidote and aggressive supportive therapy is the mainstay of treatment for glyphosate poisoning. We present a 69-year-old female patient with suicidal consumption of around 500 ml of Glycel®. Initially, gastric lavage was done and intravenous fluids were given. Within two hours of presentation, the patient developed respiratory distress needing intubation, hypotension needing vasopressor support, and severe lactic acidosis. She also developed acute respiratory distress syndrome, hypokalemia, hypernatremia, and aspiration pneumonia. Our patient was critically ill with multiple poor prognostic factors, but with timely aggressive supportive management, the patient gradually recovered.

Hypokalemia in peritoneal dialysis patients in Thailand: the pivotal role of low potassium intake.

OBJECTIVE: Hypokalemia is highly prevalent in chronic peritoneal dialysis (PD) patients worldwide, particularly in Thailand. This study aims to investigate the major determinants of hypokalemia in Thai PD patients. METHODS: A cross-sectional study was performed in chronic PD patients at 4 PD centers in Bangkok, Thailand. Hypokalemia was defined if the average serum potassium level during the last 3 consecutive visits was < 3.5 mEq/L. Patients and/or their caregivers were asked to perform a 3-day dietary food record and take pre- and post-meal pictures following the instructed protocol. Daily dietary nutrients, including potassium, were estimated by a single dietician using INMUCAL-N software. Total potassium excretion was determined by 24-h PD effluents and urine collection. Intracellular and extracellular water values (ICW and ECW, respectively) were measured by electrical bioimpedance assay (BIA) to indirectly explore the role of intracellular potassium shift in hypokalemia. RESULTS: Among 60 eligible PD patients, 19 (31%) had hypokalemia. Hypokalemic patients had significantly lower dietary potassium intake (24.4 ± 11.1 vs. 30.5 ± 9.4 mEq/day, p = 0.031) and lower total potassium excretion (28.5 ± 8.4 vs. 36.7 ± 11.2 mEq/day, p = 0.006) compared to normokalemic patients. Both groups had comparable values of ICW and ECW. On logistic regression, there was no significant correlation between hypokalemia and daily PD exchange volume, total Kt/Vurea, residual renal function, concurrent medications (insulin, diuretics, renin-angiotensin-aldosterone inhibitor, and beta-blockers) or ICW. Low dietary potassium was an independent risk factor for hypokalemia. CONCLUSION: Low dietary potassium intake, rather than increased potassium excretion or intracellular shift, is the major contributing factor of hypokalemia in Thai chronic PD patients. Dietary intervention or potassium supplement protocol should be implemented.