Maxime Ilzkovitz

Immune checkpoint inhibitors (ICIs) improve survival in multiple malignancies but may induce immune-related adverse events (irAEs), including immune-related bronchiolitis (IRB). Radiologic patterns frequently overlap with infectious diseases, particularly tuberculosis (TB), whose reactivation risk may be increased by ICIs via disruption of granuloma integrity. Differentiation between IRB and TB is challenging, especially in patients from endemic areas. We report the case of a 53-year-old Turkish man with metastatic clear-cell renal cell carcinoma, who underwent right nephrectomy followed by nivolumab plus ipilimumab. Four months after treatment, he developed fatigue, dyspnea, productive cough, and weight loss. Chest CT scan showed centrilobular nodules with a tree-in-bud pattern. QuantiFERON® testing was positive. Bronchoalveolar lavage showed lymphocyte predominance with no infectious or neoplastic cells. Transbronchial biopsy demonstrated non-caseating granulomas. PCR for Mycobacterium tuberculosis was negative, and cultures were pending. Given the overlap between IRB and TB, empirical quadruple anti-TB therapy and inhaled corticosteroids were initiated and immunotherapy was temporarily discontinued. After 2 months, given negative mycobacterial cultures and significant hepatotoxicity, isoniazid was discontinued, rifampicin was carefully reintroduced under close monitoring, and the total anti-TB treatment duration was shortened to 4 months. The patient subsequently showed gradual improvement in respiratory symptoms, biomarkers, and radiologic findings. This case illustrates the challenge of distinguishing IRB from TB in ICI-treated patients. Empirical anti-TB therapy may be warranted in high-risk settings despite absent microbiological confirmation but carries toxicity and complicates oncologic management. Pre-treatment latent TB screening and multidisciplinary decision-making are essential to balance infection control with cancer therapy.

Temozolomide (TMZ), an alkylating agent used in glioblastoma multiforme and anaplastic astrocytoma treatment, is generally associated with side effects like myelosuppression and nausea. This case report describes a rare occurrence of nephrogenic diabetes insipidus (NDI) in a 45-year-old male with grade IV astrocytoma undergoing TMZ therapy. Following TMZ discontinuation due to haematological toxicity, the patient developed significant polyuria and hypernatremia. Central diabetes insipidus was initially suspected, but limited improvement with desmopressin and normal endocrine investigations suggested renal involvement. The diagnosis of partial NDI was made and linked to TMZ-induced acute tubulointerstitial nephropathy (ATN). Despite symptom onset coinciding with TMZ administration, recovery was delayed after discontinuation, implicating possible lasting tubular damage. Although the precise pathogenesis remains uncertain, it may involve TMZ-induced renal tubule inflammation, affecting aquaporin-2 expression and water retention. In this case, management of NDI included adequate intravenous hydration, oral fluid restriction, and progressive resolution of polyuria without the need for diuretic or non-steroidal anti-inflammatory drug. This case emphasizes the need for vigilance regarding renal complications, particularly NDI, in patients receiving TMZ, warranting careful monitoring of electrolytes, renal function and diuresis to ensure prompt identification and management of this rare but serious side effect.

Introduction: This case highlights the diagnostic complexity of pulmonary granulomatosis in oncology patients, especially when treated with targeted therapy. Case report: We report the case of a 46-year-old female with metastatic HER2-mutated breast cancer who had received multiple lines of HER2-targeted therapies. The patient presented with suspected lung and mediastinal lymph node progression, despite a good response at other affected sites. A lymph node biopsy revealed non-necrotizing pulmonary granulomas, with negative microbiological testing. Further evaluations showed highly elevated anti-PR3 autoantibodies, while angiotensin-converting enzyme (ACE) and calcium levels remained within the normal range. Pulmonary function tests confirmed a restrictive syndrome. Nasal fibroscopy identified chronic sinusitis with massive nasal polyposis, without renal or cutaneous involvement. High-dose corticosteroid therapy was initiated, leading to a favourable response. Based on the clinical presentation, radiological findings, and pathological features, we concluded that the granulomatosis was related to HER2-targeted therapy. Conclusion: This case highlights that both an underlying malignancy and specific drugs—such as HER2-targeted therapy—can occasionally contribute to granuloma formation.

This case report addresses the association between ulcerative colitis and ANCA vasculitis-associated alveolar hemorrhage. A 20-year-old African woman with a history of ulcerative colitis with high PR3-ANCAs titer presented to the emergency department for chest pain, dyspnea, and hemoptysis in January 2022. A thoracic CT scan and bronchoalveolar lavage were compatible with alveolar hemorrhage. This case emphasizes the pathogenic kinetics of high ANCA titer in ulcerative colitis.

This case report addresses segmental arterial mediolysis (SAM), a rare non-inflammatory vasculopathy. A 51-year-old man presented at the emergency department for epigastric and left upper quadrant pain. He had a history of arterial hypertension and had recently received methylprednisolone for knee pain. Blood tests revealed elevated C-reactive protein levels at 40 mg/l and lactate dehydrogenase levels at 496 IU/ml. Abdominal computerized tomography showed arterial thickening, arterial dilatations, and dissections of the splenic and renal arteries, leading to organ ischemia. This case emphasizes the importance of considering SAM in cases of unexplained abdominal pain or suspected arteriopathy.

Kidney stone disease represents a rare cause of chronic kidney disease (2–3%) but has severe clinical consequences. Type 1 renal tubular acidosis is a strong lithogenic condition mainly related to primary Sjögren syndrome. This study aimed to illustrate an unusual presentation of Sjögren syndrome to improve the knowledge about rare kidney stone diseases, and to provide clues for the diagnostic approach in this specific condition. We report the case of a 35-year-old Indian woman with severe nephrocalcinosis and chronic kidney disease with tubular proteinuria who presented for metabolic assessment. We found advanced chronic kidney disease, low serum bicarbonate, permanent alkaline urine with pH at ~7.1, and severe hypocitraturia corresponding to type 1 renal tubular acidosis. The erythrocyte sedimentation rate was high. Serological screening for HAV, HBV, HCV, HIV, EBV was negative and complement was normal. Autoimmune screening showed antinuclear antibodies (>1/1.280) with anti-SSA, anti-SSA/Ro52 and anti-SSB antibodies. Genetic testing excluded an inherited cause of renal tubular acidosis. A renal biopsy showed moderate chronic tubulo-interstitial nephritis without any glomerular involvement. Primary Sjögren syndrome with significant renal involvement was considered, and corticosteroids were then subsequently initiated in combination with potassium citrate with vitamin D substitution. Only partial improvement was observed in electrolytes disturbance. After 15 months, her renal function remained stable. In conclusion, nephrocalcinosis could be the first manifestation of severely impacting diseases such as primary Sjögren syndrome. Chronic kidney disease, bilateral nephrocalcinosis, and metabolic acidosis can be linked through type 1 renal tubular acidosis. Therefore, autoimmune screening for Sjögren syndrome should be considered in such cases.