Diffuse renal enlargement is an uncommon manifestation of lymphoma and may mimic primary renal disorders. We report a young woman who presented with acute kidney injury (AKI) and bilateral ballotable flank masses, initially suspected to represent polycystic kidney disease. Chest radiography demonstrated a large mediastinal mass, prompting cross‐sectional imaging that revealed bulky anterior mediastinal disease with widespread nodal and extranodal involvement. Imaging showed asymmetric bilateral renal enlargement, markedly greater on the left, with diffuse hypodense infiltrative lesions radiologically suspicious for lymphomatous involvement. Core biopsy of the mediastinal mass confirmed primary mediastinal large B‐cell lymphoma (PMBCL), and concurrent testing identified newly diagnosed human immunodeficiency virus infection. The patient developed anuric, dialysis‐dependent AKI and died before definitive rituximab‐based chemotherapy could be initiated. This case highlights an atypical and aggressive presentation of PMBCL with presumed diffuse renal involvement, emphasizing the need to consider infiltrative malignancy in patients with unexplained nephromegaly and AKI.
Introduction Myelodysplastic syndromes (MDS) may be overlooked in patients undergoing hemodialysis (HD) because anemia is commonly attributed to renal anemia and treated with erythropoiesis‐stimulating agents. MDS is also associated with an increased risk of bacterial infections due to neutropenia and qualitative immune dysfunction. We report recurrent invasive methicillin‐susceptible Staphylococcus aureus (MSSA) infections in a patient undergoing HD with concomitant MDS. Case Presentation The patient was a 76‐year‐old man undergoing HD for end‐stage kidney disease due to nephrosclerosis who was referred to our hospital because of persistent anemia despite high‐dose darbepoetin alfa therapy. He had a history of CHOP therapy for diffuse large B‐cell lymphoma, and his MDS was considered possibly therapy related. Bone marrow aspiration revealed trilineage dysplasia and 3.4% blasts without chromosomal abnormalities, leading to a diagnosis of MDS with multilineage dysplasia. Approximately 1 year later, he developed persistent fever. Blood cultures yielded MSSA, and imaging studies revealed septic pulmonary embolism and multiple cerebral infarctions. He improved after intravenous cefepime therapy. Twenty‐two months later, he developed fever and left shoulder pain. Contrast‐enhanced computed tomography revealed an abscess in the left subscapularis muscle, and MSSA was isolated from the drainage fluid after CT‐guided drainage. He improved with drainage and antibiotic therapy. In both episodes, the neutrophil count was preserved. Conclusion This case illustrates recurrent invasive MSSA infections in a non‐neutropenic HD patient with possibly therapy‐related MDS. HD‐related factors should be carefully evaluated as common causes of recurrent S. aureus infection, and MDS may represent an additional, unproven host factor. MDS should be considered in ESA‐resistant anemia in HD patients, particularly in those with a history of cytotoxic chemotherapy.
Piperacillin-tazobactam is a generally well-tolerated broad-spectrum antibacterial. Mild hypokalemia may occur with piperacillin-tazobactam therapy as a result of increased renal potassium losses. Severe hypokalemia is rare. We report here a case of very severe hypokalemia during piperacillin-tazobactam therapy, refractory to aggressive potassium replacement.
Background:Primary hyperoxaluria Type 1 is a rare inherited metabolic disorder caused by pathogenic variants in the AGXT gene. Because the disorder leads to excessive internal oxalate formation, progressive end-stage kidney disease (ESKD) may occur. While most affected individuals present during childhood, a subset is diagnosed only later in adult life, frequently after substantial renal deterioration. Delayed diagnosis increases the risk of recurrent oxalate nephropathy and graft dysfunction following kidney transplantation. Case Presentation:We report a 30-year-old woman with ESKD of unknown aetiology who underwent living-donor kidney transplantation. One year later, during a subsequent pregnancy, she developed progressive graft dysfunction. Kidney biopsy demonstrated extensive calcium oxalate crystal deposition, raising suspicion for an underlying metabolic disorder. Genetic testing subsequently confirmed a pathogenic AGXT mutation, establishing the diagnosis of adult-onset PH1. Urinary oxalate concentrations were within normal limits before and after transplantation, emphasizing the diagnostic challenge. Conclusion:This case highlights the importance of considering PH1 in adults with unexplained chronic or ESKD, even in the absence of classical features or elevated urinary oxalate excretion. Early genetic testing and careful assessment of family history are essential for timely diagnosis, enabling appropriate transplant planning, disease-specific therapy, and genetic counselling.
Background:Frequently relapsing nephrotic syndrome (FRNS) and steroid-dependent nephrotic syndrome (SDNS) are distinct phenotypes defined by relapse frequency and the temporal relationship of relapse to prednisolone therapy, respectively. Both remain therapeutic challenges despite the use of corticosteroid-sparing agents. Relapses may be triggered by intercurrent infections and can be complicated by significant edema, hypoalbuminemia, and infection risk, requiring prompt optimization of immunosuppressive and supportive therapy. Case Presentation:An 11-year-old boy with SDNS presented with a two-day history of bilateral periorbital swelling and facial puffiness following fever, rhinorrhea, and productive cough. He had experienced 11 previous relapses and was receiving ciclosporin 50 mg twice daily and enalapril 5 mg once daily with good adherence. Previous kidney biopsy showed minor glomerular change, and ciclosporin trough concentration was therapeutic. On admission, he was febrile (38.3°C) with leukocytosis, neutrophilia, thrombocytosis, marked hypoalbuminemia, significant proteinuria, and hematuria. Penicillin V was initiated for spontaneous bacterial peritonitis prophylaxis. Prednisolone was optimized from 40 mg once daily to 30 mg twice daily based on a body surface area of 1.17 m2. Progressive edema and weight gain required escalation to intravenous frusemide with 20% human albumin, resulting in marked clinical improvement. Proteinuria, hematuria, and ascites resolved, and he was discharged clinically stable with minimal residual edema. Conclusion:This case highlights several important therapeutic considerations in relapsing childhood nephrotic syndrome: recognition of SDNS as a subgroup of SSNS, accurate prednisolone dosing during relapse, careful assessment of edema and intravascular volume status before diuretic therapy, and individualized use of steroid-sparing agents and antimicrobial prophylaxis. In children receiving prolonged ciclosporin therapy, treatment should be regularly reviewed with blood pressure, renal function, and therapeutic drug monitoring in view of potential calcineurin inhibitor toxicity, and alternative steroid-sparing options such as levamisole may be considered where clinically appropriate.
