Rationale: Rare cases of euglycemic diabetic ketoacidosis (eu-DKA) have been reported after the administration of sodium-glucose cotransporter-2 (SGLT-2) inhibitors. No reports have described eu-DKA complicated by hypernatremia due to SGLT-2 inhibitors. Patient concerns: A 76-year-old woman with a 40-year history of type 2 diabetes mellitus (DM), for which metformin (1000 mg/day) and dapagliflozin (10 mg/day) were prescribed, presented with malaise, fever, and oliguria. On presentation, her white blood cell count (11,800/μL), serum creatinine (3.2 mg/dL), and C-reactive protein (54 mg/L) were abnormal. Bilateral pyeloureteritis and diffuse paralytic ileus were present. She received intravenous antibiotics and total parenteral nutrition, and was asked to fast. Her renal function and ileus briefly improved. Oral hypoglycemic agents, metformin and dapagliflozin, along with enteral feeding were reinstituted on day 3 of hospitalization. However, on day 6 of hospitalization, the patient developed an altered state of consciousness including confusion, lethargy, and stupor. Several laboratory abnormalities suggestive of ketoacidosis with euglycemia were noted. Diagnoses: The patient was diagnosed with eu-DKA accompanied by severe hypernatremia (corrected serum Na+ concentration, 163 mEq/L) and hypokalemia following dapagliflozin re-administration. Interventions: The patient was treated with indicated intravenous fluid therapy. Dapagliflozin use was discontinued. Outcomes: The patient's mental status and laboratory findings improved gradually, and she was discharged on maintenance doses of insulin and metformin on day 14 of hospitalization. Lessons: Acute illnesses such as diffuse paralytic ileus and urinary tract infection, and dietary restrictions or fasting in patients with DM can be considered potential predisposing factors for SGLT-2 inhibitor-associated eu-DKA. For patients with diabetes in the setting of acute morbidity, timely resumption of the SGLT-2 inhibitor therapy should be carefully determined. In addition, eu-DKA due to SGLT-2 inhibitor use may be accompanied by electrolyte disturbances such as hypernatremia and hypokalemia.

Rationale: Pituitary apoplexy (PA) and posterior reversible encephalopathy syndrome (PRES) are rare neurologic diseases that show acute neuro-ophthalmologic symptoms such as headache, decreased visual acuity, and altered consciousness. These diseases are rarely found in patients with end-stage renal disease (ESRD) on hemodialysis, and simultaneous occurrence of these 2 diseases has not been reported. Patient concerns: The patient was a 75-year-old man with a history of hypertension, diabetes mellitus, and non-functioning pituitary macroadenoma. He had been receiving hemodialysis for ESRD for 3 months before his presentation to the emergency room. The patient complained of headache, vomiting, and dizziness that started after the previous day's hemodialysis. The patient had voluntarily discontinued his antihypertensive medication 2 weeks before presentation and had high blood pressure with marked fluctuation during hemodialysis. Complete ptosis and ophthalmoplegia on the right side suggested 3rd, 4th, and 6th cranial nerve palsies. Diagnoses: Magnetic resonance imaging of the brain revealed a pituitary tumor, intratumoral hemorrhage within the sella, and symmetric vasogenic edema in the subcortical white matter in the parieto-occipital lobes. Based on these findings, the patient was diagnosed with PA and PRES. Interventions: Intravenous administration of hydrocortisone (50 mg every 6 hours after a bolus administration of 100 mg) was initiated. Although surgical decompression was recommended based on the PA score (5/10), the patient declined surgery. Outcomes: Headache and ocular palsy gradually improved after supportive management. The patient was discharged on the 14th day of hospitalization with no recurrence 5 months post-presentation. Current therapy includes antihypertensive agents, oral prednisolone (7.5 mg/day), and maintenance hemodialysis. Lessons: Neurologic abnormalities developed in a patient with ESRD on hemodialysis, suggesting the importance of prompt diagnosis and treatment in similar instances.

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Rationale: Renal hemosiderosis is a disease in which hemosiderin deposits in the renal cortex as a form of iron overload. However, cases of renal hemosiderosis due to intravascular hemolysis following mitral valve repair have been rarely reported. Patient concerns: We present the case of a 62-year-old woman who developed asymptomatic urinary abnormalities including microscopic hematuria and proteinuria due to renal hemosiderosis following a mitral valve repair surgery performed two years earlier. Diagnoses: A percutaneous renal biopsy showed no specific glomerular abnormality, tubular atrophy, or interstitial fibrosis but extensive deposition of hemosiderin in the proximal tubule. The patient was diagnosed with renal hemosiderosis and chronic intravascular hemolysis following mitral valve repair. Interventions: Our patient refused a mitral valve repeat surgery and hence was treated with oral iron preparations, N-acetylcysteine, and a β-receptor blocker. Outcomes: Moderate mitral regurgitation with the regurgitant blood striking against the annuloplasty ring was confirmed on follow-up echocardiography. After the 24-month follow-up period, hemolytic anemia persisted, but there was no significant decline of renal function. Lessons: For cases of chronic intravascular hemolysis accompanied with asymptomatic urinary abnormalities, a renal biopsy is required to exclude underlying kidney pathology and predict potential renal insufficiency.

Rationale: Systemic lupus erythematosus (SLE) is an autoimmune disease that involves multiple organs and causes various clinical manifestations. Cases of rhabdomyolysis as the initial presentation of SLE are rare, and there are no reported cases of SLE presenting hyponatremia-associated rhabdomyolysis as the first manifestation. Herein, we report a case of SLE with lupus nephritis in a patient with acute hyponatremia-associated rhabdomyolysis. Patient concerns: A 44-year-old woman was admitted with complaints of altered consciousness, myalgia, and red-brownish urine that first appeared three days prior. Peripheral blood tests revealed elevated creatine kinase (19,013 IU/L) and myoglobin (5099 U/L) levels and severe hyponatremia (111 mEq/L) with no azotemia. Urinalysis showed nephritic sediments. Diagnosis: Whole-body bone scintigraphy showed increased uptake of radiotracer in the both upper and lower extremities. Serological evaluation revealed the presence of anti-nuclear (speckled pattern, 1:640), anti-double stranded DNA, and anti-Smith antibodies and absence of anti-Jo-1 antibody. A kidney biopsy demonstrated mesangial proliferative (class II) lupus nephritis. Interventions: Fluid therapy, including intravenous administration of 3% NaCl, was initiated. After three consecutive days of intravenous methylprednisolone (1 g/d), oral prednisolone (1 mg/kg/d), mycophenolate mofetil, and hydroxychloroquine were administered. Outcomes: On day 28, the patient was discharged with marked resolution of SLE-associated symptoms and laboratory findings. Lupus reactivation was not present during the subsequent six-month follow-up. Lessons: Hyponatremia-associated rhabdomyolysis can be the first manifestation of SLE. Moreover, prompt fluid therapy and timely administration of immunosuppressive agents in SLE patients presenting with hyponatremia and rhabdomyolysis can significantly help alleviate disease activity and improve clinical outcomes.