RENAL DISEASE IN SYSTEMIC LUPUS ERYTHEMATOUS: ALL THAT GLITTERS IS NOT GOLD

Patients with systemic lupus erythematosus may occasionally develop renal pathology from causes unrelated to the underlying disease. We describe one such case. This 22-year-old lady, with past history of arthritis, presented with dyspnea and fever. She had clinical signs consistent with systemic lupus erythematosus. Echocardiogram revealed valvular regurgitation. Antibiotics were started for probable infective endocarditis. She developed acute kidney injury. This was initially attributed to lupus nephritis, but subsequently renal histopathology revealed acute interstitial nephritis. Renal functions normalized with oral prednisolone. This case highlights the fact that a broader differential diagnosis must always be considered even if the diagnosis is clear.

Nilotinib-Induced Acute Interstitial Nephritis during the Treatment of Chronic Myeloid Leukemia

Tyrosine kinase inhibitors (TKIs) are targeted therapy drugs that selectively inhibit protein kinases. Nephrotoxicity associated with TKIs is uncommon. We report a case of a 39-year-old man with acute kidney injury that developed after nilotinib treatment for chronic myeloid leukemia (CML). The renal function of the patient decreased during treatment with nilotinib but improved when treatment was discontinued due to neutropenia. However, the renal function of the patient deteriorated again with the reintroduction of nilotinib for treatment. A renal biopsy revealed acute interstitial nephritis (AIN). The patient had no history of comorbidities and medication causing renal injury. Finally, we diagnosed the patient with nilotinib-induced AIN. After switching to imatinib mesylate, the renal function of the patient stabilized without further deterioration. Our case indicates that nilotinib can be a potential cause of renal dysfunction by inducing AIN when renal function deteriorates in patients treated with nilotinib.

Efficacy of Plasmapheresis in Nivolumab-Associated ANCA Glomerulonephritis: A Case Report and Pathophysiology Discussion

Immune checkpoint inhibitors (ICIs) have revolutionized solid organ and hematologic cancer treatments by improving overall prognoses. However, they can lead to overactivation of the immune system and several immune-related adverse events and sometimes affecting the renal system. Although acute interstitial nephritis is well described, we know little about ICI-associated glomerular injury. Herein, we report an exceptional case of renal ANCA positive-associated vasculitis (AAV) after nivolumab therapy. Three weeks after the last nivolumab injection, the patient presented with proteinuria at 1.73 g/g of creatininuria, hematuria, and acute kidney injury needing dialysis associated with lung hemorrhage; anti-neutrophil cytoplasmic antibody (ANCA titer ≥1,280 with myeloperoxidase specificity of 780 U/mL) was positive, and kidney biopsy confirmed glomerular injury with crescents. The patient underwent treatment with steroid pulses, rituximab, and plasmapheresis, resulting in an improvement of the renal function and lung hemorrhage and produced a negative ANCA titer. Despite the results of the PEXIVAS study and the absence of clear benefit of plasmapheresis demonstrated in idiopathic AAV, we suggest that drug-induced AAV may be effectively treated by plasmapheresis, steroids, and rituximab.

A case of tubulointerstitial nephritis and uveitis syndrome after suspected drug-induced acute interstitial nephritis

Distinguishing between late-onset TINU syndrome and drug-induced AIN remains difficult given that patients with TINU syndrome may develop uveitis long after the onset of AIN. Therefore, ophthalmic examination is required not only upon diagnosis but also continuously or when eye symptoms, and relapse of urinary findings are observed.