Hydrothorax is a possible complication of peritoneal dialysis due to migration of dialysate from the peritoneal cavity to the thoracic cavity through a congenital or acquired diaphragmatic defect that allows its passage. Diagnosis is clinical, supported by peritoneal CT and pleural fluid analysis. Therapy is given in the first instance by discontinuation of the peritoneal method, but sometimes an attempt may be made to reinstate it with appropriate changes in the prescription. We report here our experience about a case of hydrothorax during peritoneal dialysis reporting the most recent protocols for proper management.

Sodium–glucose cotransporter 2 (SGLT2) inhibitors are widely used in patients with kidney disease and have been shown to increase serum magnesium levels. Case reports have described their role in correcting hypomagnesemia; however, there is limited evidence regarding their efficacy in patients with renal magnesium wasting. Furthermore, data regarding their role in acute treatment and sustained efficacy to treat hypomagnesemia are lacking. We present a multicenter retrospective, observational case series from two U.S. medical centers describing five patients with refractory hypomagnesemia who experienced significant improvement following initiation of SGLT2 inhibitors. Patients 1–4 showed marked renal magnesium wasting with severe symptomatic hypomagnesemia which responded robustly to SGLT2 inhibitor therapy. Even though Patient 5 did not have renal magnesium wasting, hypomagnesemia still improved with the addition of an SGLT2 inhibitor. Furthermore, the addition of an SGLT2 inhibitor acutely improved the hypomagnesemia of Patients 1 and 2 in an inpatient setting, and Patients 3–5 demonstrated sustained improvement of hypomagnesemia across extended outpatient follow-up. The improvement of hypomagnesemia was irrespective of the diabetic status of the patient. All cases resulted in substantial reduction or cessation of magnesium (Mg) supplementation. These findings suggest a novel therapeutic application of SGLT2 inhibitors for managing intractable hypomagnesemia, both acutely and chronically, regardless of the diabetes being the primary culprit.

Cefepime is widely used in sepsis owing to its broad spectrum of activity with coverage against Pseudomonas. Though it is usually well-tolerated, in the presence of certain risk factors, renal impairment, high doses, and critical illness, it is associated with the development of neurotoxicity. Those most susceptible are at high risk for developing complications of their underlying illness and the clinical manifestations of cefepime-related neurotoxicity are nonspecific, with reduced level of consciousness, confusion, myoclonus, and seizures, thus a high index of suspicion is required to make a diagnosis. The management includes drug discontinuation, seizure prophylaxis in the right clinical setting, and hemodialysis in severe cases. This case reinforces the need to renally adjust medications in the setting of acute kidney injury to avoid uncommon complications while using common medications.

The cause of acute skeletal muscle damage, defined as rhabdomyolysis, is multifactorial. Medicines are prominent among the most important reasons. The clinical significance of rhabdomyolysis lies in the fact that it can cause acute kidney injury (AKI) in 10%-40% of patients. In this presented case, oxcarbazepine, which is a preferred drug in the treatment of epilepsy and also in neuropathic pain in clinical practice, triggered rhabdomyolysis and subsequently caused the development of AKI. Through this case report, we aimed to emphasize that some serious side effects should not be forgotten when prescribing drugs in clinical practice.

Thrombotic microangiopathy (TMA) is characterized by microvascular thrombosis, microangiopathic hemolytic anemia (MAHA), and thrombocytopenia. TMA can lead to acute kidney injury (AKI) due to the formation of thrombi within the renal microvasculature causing ischemic injury. AKI in the setting of TMA requires early recognition, comprehensive serologic evaluation, and timely intervention due to the risk of irreversible renal damage. Due to many potential causes, both hereditary and acquired, the workup of renal TMA includes analysis of ADAMTS13 activity, genetic testing, and antibody analysis to rule out extraneous etiologies. Ultimately, renal pathology is used to confirm the diagnosis. Recommended treatment of renal TMA is dependent on the underlying etiology and varies from therapeutic plasma exchange and anticomplement therapy to renal replacement therapy and supportive care. This case report highlights an underrecognized cause of renal TMA: hypertensive emergency. Pathological histology imaging of renal tubules can be used to diagnose renal TMA due to evidence of schistocytes and tubular necrosis. Diagnosing TMA can have life-saving consequences as delayed hemodialysis can be fatal. Renal pathological imaging should be an important diagnostic tool when presented with hypertension cases, especially those associated with the aforementioned symptoms. Blood pressure control is the primary focus for management of hypertensive emergency-associated TMA. We present a case of TMA-associated AKI in a hypertensive patient that had a characteristic onion-skin lesion seen on renal pathology.

Thrombotic microangiopathy (TMA) reflects a syndrome of endothelial injury characterised by microangiopathic haemolytic anaemia (nonimmune), thrombocytopenia, and often end-organ dysfunction. TMA disorders are well-recognised in kidney transplant recipients, often due to an underlying genetic predisposition related to complement dysregulation, or de novo due to infection, immunosuppression toxicity, or antibody-mediated rejection. In pregnancy, TMA disorders are most commonly due to severe pre-eclampsia or HELLP, but may also be due to thrombotic thrombocytopenic purpura (TTP) or complement-mediated (atypical) haemolytic uremic syndrome (aHUS). Complement dysregulation is being recognised as playing a role in the development of preeclampsia and HELLP syndrome in addition to aHUS. Due to overlapping clinical and laboratory features, diagnosis can be difficult and delays in treatment can be life-threatening for both mother and fetus. This report describes a 32 year-old female who had two successive wanted pregnancies. The first pregnancy was terminated at 22 weeks gestation due to presumed severe preeclampsia and fetal growth restriction in the context of known chronic kidney failure due to reflux nephropathy. A living-related kidney transplant was performed to improve the chances of pregnancy resulting in a live birth. A subsequent pregnancy was complicated by progressive kidney impairment and hypertension at 22 weeks gestation. Kidney biopsy showed TMA, but the etiology was unclear. This report highlights the diagnostic dilemma of TMA in a pregnant kidney transplant recipient and a role for the anti-C5 terminal complement blockade monoclonal antibody eculizumab, in pregnancy-associated TMA, especially at a peri-viable gestation.

Peritonitis is the major complication of peritoneal dialysis (PD) patients. Staphylococcus is the leading causative organism of PD-related peritonitis. However, there were more reports of unusual organisms causing peritonitis. Clinical features, management, and outcome of peritonitis from unusual organisms are important information. We reported herein a 72-year-old female patient who presented with fever, abdominal pain, and cloudy dialysate for 3 days. Upon admission, ceftazidime and vancomycin were given intraperitoneally. A preliminary report of blood and PD fluid culture showed the presence of Gram-positive bacilli. Her clinical status improved 48 hours after the commencement of the antibiotics. Subsequently, culture reports of blood and PD fluid showed Lysinibacillus sphaericus which was susceptible to vancomycin at a minimal inhibitory concentration of less than 0.25 μg/mL. The patient was given intraperitoneal vancomycin for a total of 14 days. Then, the PD effluent was clear, and its cell count was below 100 cells/mm3 in 3 days. The patient did not have a recurrence of peritonitis after antibiotic discontinuation. The possibility of this organism infection is environmental contamination related to the patient's gardening activities.

Hypercalcemia is a common and potentially serious electrolyte abnormality that is often observed in patients with chronic kidney disease (CKD). When malignancy is considered, parathyroid hormone-related protein (PTHrP) levels are often measured. PTHrP is produced by cancer cells and mimics the effects of parathyroid hormone (PTH) to elevate serum calcium concentrations. The amino and carboxy termini of PTHrP are of functional relevance. C-terminal PTHrP levels accumulate with CKD and can be elevated in normocalcemic CKD patients who lack malignancy. The existence of amino (N)-terminal and carboxy (C)-terminal PTHrP assays and how their concentrations are impacted by CKD are reviewed herein. The case of a patient on maintenance hemodialysis who developed prolonged hypercalcemia with elevated PTHrP concentrations is presented. The workup revealed suppressed intact PTH, low 25-hydroxyvitamin D, and 1,25-dihydroxyvitamin D levels. The initial PTHrP assay returned elevated. However, it was unappreciated that it was the C-terminal assay and the patient underwent an unnecessary search for malignancy. A subsequent N-terminal PTHrP assay returned within the normal range. Many commercial labs run the C-terminal PTHrP assay as their first-line test. This can lead to inaccurate differential diagnoses in hypercalcemic patients with CKD. We emphasize the need to specifically request N-terminal PTHrP assays in patients with advanced kidney disease when humoral hypercalcemia of malignancy is suspected.

PD-1/PD-L1 inhibitors such as pembrolizumab have radically improved the prognosis for many patients with advanced malignancies. Although revolutionary, its use can be complicated and limited by various immune-related adverse effects. Effective management depends on early recognition and prompt intervention. Herein, we describe a unique syndrome of hypercalcemia, with associated acute renal injury and hypoxic respiratory failure that was responsive to corticosteroids suggestive of immunotoxicity from pembrolizumab.

Beer potomania is one of the less common causes of hyponatremia that we encounter. Patients usually have a recent history of binge drinking along with poor diet. The low solute content in alcoholic beverages limits daily urine output, and ingestion of extra fluid will cause dilutional hyponatremia as a result. Blindly providing intravenous fluid without an underlying cause of the hyponatremia can be detrimental, such as in patients with beer potomania. In our case, a patient presented to the emergency department due to poor oral intake from jaw pain and was found to be hyponatremic from alcohol intake. He initially received 2 liters of fluid, which caused overcorrection of his sodium, requiring more free water to lower his sodium as a result.