CD163 detection in immune check-point inhibitors-related acute interstitial nephritis.

Background: Acute interstitial nephritis (AIN) is the most common renal immune-related adverse event after immune check-point inhibitors (ICI). We hypothesized that alternatively activated macrophages (CD163-M) could be involved in ICI-AIN and wished to evaluate the use of their soluble urinary form (us)CD163 as a non-invasive diagnostic marker.

Methods: CD163-M infiltrates were evaluated by both immune-histochemistry and multiplex immunofluorescence and imaging.

Abcc6 deficiency prevents rhabdomyolysis-induced acute kidney injury.

Rhabdomyolysis is a risk factor for acute kidney injury, transition towards chronic kidney disease, and death. The role of calcium phosphate deposits in the mechanisms of rhabdomyolysis-induced acute kidney injury (RAKI) is still unclear. Better insight of the role calcium in RAKI could lead to new therapeutic avenues.

Are serum C3 levels or kidney C3 deposits useful markers for predicting outcomes in patients with ANCA-associated vasculitis?

Introduction: Complement activation emerged as a key actor of anti-neutrophil cytoplasmic antibodies-associated vasculitis (AAV). Whether serum levels of C3 (sC3) or C3 kidney deposition may help to refine the prognosis of AAV remains elusive.

Methods: Retrospective multicentric study that included 154 patients with a first flare of AAV and sC3 (n = 143) or C3 kidney staining (n = 95) available at diagnosis.

[Nephropathy associated with monoclonal immunoglobulins: From clonal expansion B to renal toxicity of pathological immunoglobulins].

Germinal center regulation pathways are often involved in lymphomagenesis and myelomagenesis. Most of the lymphomas (and multiple myeloma) derive from post-germinal center B-cells that have undergone somatic hypermutation and class switch recombination. Hence, B-cell clonal expansion can be responsible for the presence of a monoclonal component (immunoglobulin) of variable titer which, owing to physicochemical properties, can provoke pathologically defined entities of diseases.

Ibrutinib does not prevent kidney fibrosis following acute and chronic injury.

Recent studies suggested that ibrutinib, a Bruton tyrosine kinase (BTK) inhibitor, developed for the treatment of chronic lymphocytic leukemia, may prevent NLRP3 inflammasome activation in macrophages, IL-1β secretion and subsequent development of inflammation and organ fibrosis. The role of NLRP3 has been underlined in the various causes of acute kidney injury (AKI), a pathology characterized by high morbimortality and risk of transition toward chronic kidney disease (CKD). We therefore hypothesized that the BTK-inhibitor ibrutinib could be a candidate drug for AKI treatment.

Kidney Involvement in Patients With Chronic Myelomonocytic Leukemia or BCR-ABL-Negative Myeloproliferative Neoplasms.

Introduction: The identification of specific molecular signatures and the development of new targeted drugs have changed the paradigm of onco-nephrology, now allowing a multiscale approach of kidney involvement related to hematologic malignancies relying on combined hematologic and molecular assessments. In this study, we aimed to refine the spectrum of kidney disorders associated with chronic myelomonocytic leukemia (CMML) or BCR-ABL-negative myeloproliferative neoplasms (MPNs), 2 very rare conditions scarcely described.

Methods: Case series.

[Lyme nephritis in humans: Physio-pathological bases and spectrum of kidney lesions].

Known in less than half a century, borreliosis, or Lyme disease, is a zoonosis caused by the tick bite. It is the most common vector disease in Europe and the United States. Borrelia burgdorferi sensu lato, the bacterium in question, is fitted with a "cunning device" that allows it to trick the immune system and implant the infection chronically.