We present a case of a young man with a new-onset supraventricular arrhythmia accompanied by polyuria and natriuresis with subsequent renal salt-wasting causing hypovolemic hyponatremia. Resolution of the electrolyte imbalance occurred only after successful atrial flutter ablation.

Bartter syndrome is a genetic disorder characterised by chloride-unresponsive metabolic alkalosis, hypokalaemia, hypomagnesaemia and hypercalciuria. While it commonly presents antenatally or in early infancy, sometimes, drugs can induce a state similar to Bartter syndrome in any age group, called acquired Bartter syndrome. Polymyxins and aminoglycosides are the most commonly implicated drugs. Polymyxin B and polymyxin E (popularly known as colistin) are the two chemically similar polymyxins that are commonly used clinically. While colistin is frequently associated with nephrotoxicity, polymyxin B is generally considered less nephrotoxic. This difference is due to the way these two drugs are handled by the kidneys. In this case report, we discuss a middle-aged male who developed Bartter syndrome due to polymyxin B, which resolved on discontinuation of the drug, and re-appeared after its re-introduction later. This case exemplifies the nephrotoxicity caused by polymyxin B and the need for vigilance when using this drug.

This case describes a rare occurrence of high anion gap metabolic acidosis due to chronic acetaminophen (paracetamol) usage, which can be confirmed by measuring 5-oxoproline (pyroglutamate), an organic acid metabolite. As acetaminophen is an extremely common drug prescribed in both inpatient and outpatient settings, a high degree of clinical suspicion is required to isolate it as the aetiology for metabolic acidosis. Management includes discontinuation of acetaminophen use and at times the supplementation of oral bicarbonate. Metabolic acidosis due to a high anion gap is commonly described by the mnemonic \'MUDPILES\' in daily practice. A newer mnemonic, \'GOLD MARK\' is proposed to be a more inclusive tool to assist in determining the cause of high anion gap metabolic acidosis, especially with such cases being reported.

Bartter syndrome (BS) is a rare genetic tubulopathy affecting the loop of Henle leading to salt wasting. It is commonly seen in utero or in the early neonatal period. Rare cases of acquired BS are reported in association with infections like tuberculosis, granulomatous conditions like sarcoidosis, autoimmune diseases and drugs. The mainstay of management includes potassium, calcium and magnesium supplementation. We report the case of a woman in her 50s with a history of type 2 diabetes mellitus for the last 10 years, who presented with diabetic foot ulcers and generalised weakness with ECG changes suggestive of hypokalaemia. She had severe hypokalaemia with high urine potassium excretion and hypochloraemic metabolic alkalosis. She poorly responded to intravenously administered potassium supplements and had persistent hypokalaemia. On further evaluation of the persistent hypokalaemia, a diagnosis of idiopathic Bartter-like phenotype was made. She responded well to tablet indomethacin and is presently asymptomatic and is being maintained on tablet indomethacin after 6 months of follow-up.

A patient in her 50s presented with altered mental status and shortness of breath at 4600 m elevation. After descent to the base of the mountain, the patient became comatose. She was found to have bilateral pulmonary infiltrates and a serum sodium of 102 mEq/L. She was rapidly corrected to 131 mEq/L in 1 day. Initial MRI showed intensities in bilateral hippocampi, temporal cortex and insula. A repeat MRI 17 days post injury showed worsened intensities in the bilateral occipital lobes. On admission to acute rehabilitation, the patient presented with blindness, agitation, hallucinations and an inability to follow commands. Midway through her rehabilitation course, antioxidant supplementations were started with significant improvement in function. Rapid correction of hyponatraemia may cause central pontine myelinolysis or extrapontine myelinolysis (EPM). In some cases of hypoxic brain injury, delayed post-hypoxic leucoencephalopathy (DPHL) may occur. Treatment options for both disorders are generally supportive. This report represents the only documented interdisciplinary approach to treatment of a patient with DPHL and EPM. Antioxidant supplementation may be beneficial as a treatment option for both EPM and DPHL.

Chronic hypernatraemia is a rare clinical entity. In the younger population, hypernatraemia is often a consequence of failure to generate thirst in response to osmotic stimuli.We report the case of a male patient admitted with severe hypernatraemia (plasma sodium 175 mmol/L) on return from holidays. His urine was maximally concentrated at 894 mOsm/kg-suggestive of normal vasopressin reserve. MRI of the brain showed a large extra-axial cyst, with preservation of the posterior pituitary bright spot. Formal osmoregulatory studies demonstrated normal osmoregulated vasopressin secretion and normal thirst, but no appropriate drinking behaviour.This patient illustrates a unique pathophysiological disconnect between thirst appreciation and the central drive to drink, in the context of normal osmoregulatory function. It is likely that this disconnect is related to the patient\'s large intracranial cyst.The management challenge is to maintain appropriate fluid intake in order to prevent recurrent severe hypernatraemia.

We present a case of a man in his 70s who presented with worsening rectal and back pain associated with weight loss, dyspnoea and brownish discolouration of urine. Physical examination noted abdominal distention and epigastric tenderness. Laboratory investigations revealed acute kidney injury, hyperkalaemia, hyperphosphataemia and hyperuricaemia. Contrast CT of the abdomen/pelvis showed multiple, low-density masses throughout the liver, suspicious for metastatic disease. Oesophagogastroduodenoscopy demonstrated a large, fungating, infiltrative and ulcerated mass in the gastric body and lesser curvature of the stomach. Surgical pathology confirmed invasive moderately differentiated gastric adenocarcinoma. He met both the laboratory and clinical criteria for spontaneous tumour lysis syndrome (STLS) as per the Cairo-Bishop criteria. He was managed with aggressive fluid hydration, rasburicase and allopurinol, resulting in improvement in his renal function and laboratory findings. STLS of solid organ tumours, especially gastric adenocarcinoma, is rare and requires early detection with timely management to ensure favourable outcomes.

Here, we present a case of an older man presenting with worsening confusion. Laboratory tests showed serum sodium of 120 mmol/L with severe hypothyroidism and renal salt wasting that improved with treatment of hypothyroidism, normalising the serum sodium.

Lactic acidosis is a rare but serious side effect in individuals receiving nucleoside reverse transcriptase inhibitors. An underweight woman with HIV was admitted to our hospital because of nausea and diffuse myalgia. Her antiretroviral regimen had been changed to tenofovir disoproxil fumarate (TDF)/emtricitabine and darunavir/cobicistat 3 months prior, after which her renal function had gradually declined. After admission, she was diagnosed with lactic acidosis, and a liver biopsy suggested mitochondrial damage. Her plasma tenofovir levels were elevated at the onset of lactic acidosis. We hypothesise that the patient\'s low body weight, combined with the addition of cobicistat, induced renal dysfunction and led to elevated plasma tenofovir concentrations, resulting in mitochondrial damage and lactic acidosis. Careful monitoring of renal function and lactic acidosis is required during use of TDF-containing regimens for underweight HIV patients, particularly when combined with cobicistat.

Metformin-associated lactic acidosis (MALA) is a serious condition with high mortality. This case describes a man in the mid-60s with diabetes mellitus type 2 treated with metformin developing MALA 4 days after coronary stenting for non-ST-elevation myocardial infarction. He presented acutely with severe abdominal pain, a lactate of 19 mmol/L and pH 6.74. Despite treatment for MALA, he went into refractory cardiac arrest and was connected to venoarterial extracorporeal membrane oxygenation (VA-ECMO). He suffered a massive haemothorax due to perforation of the right atrial appendage. It was repaired through a sternotomy while being given massive blood transfusions. The following days, he was on VA-ECMO and double continuous venovenous haemodialysis (CVVHD). He survived with only mild paresis of the left hand. VA-ECMO should be considered a rescue therapy alongside treatment with CVVHD in case of cardiac arrest due to severe MALA.