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Erdheim-Chester disease (ECD) is a rare non-Langerhans cell histiocytosis that frequently infiltrates the peri-kidney space ("hairy kidney" appearance), kidney pelvis and proximal ureters, leading to obstructive uropathy. Here, we analyzed the clinical characteristics, imaging findings and long-term kidney outcome of a large multicenter cohort comprising 195 consecutive patients with ECD. Retroperitoneal peri-kidney or peri-ureteral involvement was detected at diagnosis in 147 patients. Of them, 70 had hydronephrosis (bilateral in 47), and 16 with kidney atrophy (unilateral in 14). Kidney vascular peduncle infiltration was found in 60 patients, and kidney artery stenosis in 31. The estimated glomerular filtration rate (eGFR) at diagnosis was significantly lower in patients with than in those without peri-kidney involvement (median 74 vs. 98 mL/min/1.73 m

Systemic AA amyloidosis is associated with systemic inflammatory processes such as autoimmune disorders or chronic infections. In addition, AA amyloidosis can develop in a localized or systemic form in patients with malignant neoplastic disorders, and usually involves kidneys impacting renal function. Among solid tumors, renal cell carcinoma (RCC) appears to be responsible for one-quarter to half of all cancers associated with amyloidosis. Among other solid cancers, various clinical presentations and pathological types of lung cancer and basal cell carcinoma skin were reported with AA amyloidosis more often than isolated case reports on other cancers with AA amyloidosis. Symptoms from kidney involvement rather than from the tumor per se were the presenting manifestations in cases of RCC associated with AA amyloidosis. Among hematological malignancies, clonal B cell/plasma cell dyscrasias such as monoclonal gammopathy and lymphoma were noted to be associated with AA amyloidosis. In addition, AA amyloidosis was reported in a substantial number of cases treated with immune checkpoint inhibitors such as pembrolizumab and nivolumab. The mechanism of association of cancer and AA amyloidosis seems to be mediated by the immune response exacerbated from the tumor and its microenvironment or immune therapy. The mainstay of treatment consists of therapy directed against the underlying malignancy or careful withdrawal of the offending agent. This review will discuss this rare but highly morbid clinical condition.

Systemic mastocytosis (SM) is a disorder of excessive mast cell accumulation in tissues due to a somatic gain-of-function mutation, commonly in the KIT gene, which prevents apoptosis of mast cells. Whereas bone marrow, skin, lymph nodes, spleen, and gastrointestinal tract are commonly involved, kidneys are rarely involved directly by SM. However, there are increasing reports of indirect kidney involvement in patients with SM. Novel anti-neoplastic agents to treat advanced forms of SM include non-specific tyrosine kinase inhibitors, which are reported to be associated with kidney dysfunction in some patients. SM is also associated with immune-mediated glomerulonephritis (GN) like mesangioproliferative GN, membranous nephropathy, and diffuse proliferative GN. Kidney injury, in the form of monoclonal deposition disease and primary light chain amyloidosis, is reported in SM associated with plasma cell dyscrasia. In this narrative review, we discuss the various ways kidneys (and the urinary tract) are involved in patients with SM.

Genetic renal phosphate leak is one of the rare disorders in recurrent stone formers with absorptive hypercalciuria. Diagnosis and appropriate management may change the life of patients. To provide answers on how and when to make the diagnosis of genetic renal phosphate leak and how medical management prevents the recurrences and changes patients' life, we conducted a retrospective study including nine patients with recurrent nephrolithiasis and a confirmed genetic mutation of a phosphate transporter between 2008 and 2019 in our multidisciplinary center at the Pitié Salpetriere Hospital, Paris, France. We compared the number and the annual rate of urological intervention before and after the diagnosis and management using the Wilcoxon test. A qualitative survey was done to evaluate the quality of life of patients. A total of 9 patients were included in this study. Patient baseline characteristics and elements supporting the diagnosis are described. We showed an effective decrease in urological intervention number (p = 0.0078) and annual rate (p = 0.0117) after the diagnosis and the appropriate management, and an improvement in the patients' quality of life. The diagnosis and the appropriate management of genetic renal phosphate leak disorder improve the quality of life by preventing stone recurrence and decreasing the number of surgical intervention.

Lung cancer is the leading cause of cancer-related mortality and approximately 5% of non–small-cell lung cancer (NSCLC) patients are positive for anaplastic lymphoma kinase (ALK) gene rearrangement or fusion with echinoderm microtubule-associated protein-like 4. ALK inhibitors are the mainstay treatment for patients with NSCLC harboring a rearrangement of the ALK gene or the ROS1 oncogenes. With the recent publication of pivotal trials leading to the approval of these compounds in different indications, their toxicity profile warrants an update. Several ALK-1 inhibitors are used in clinical practice, including crizotinib, ceritinib and alectinib. According to the package insert and published literature, treatment with several ALK-1 inhibitors appears to be associated with the development of peripheral edema and rare electrolyte disorders, kidney failure, proteinuria and an increased risk for the development and progression of renal cysts. This review introduces the different types of ALK inhibitors, focusing on their detailed kidney-related side effects in clinical practice.

Immune checkpoint inhibitors (CPIs) have recently become a cornerstone for the treatment of different advanced cancers. These drugs have the ability to reactivate the immune system against tumour cells but can also trigger a myriad of side effects, termed immune-related adverse events (irAEs). Although there are numerous reports of CPI-related endocrinopathies, hypercalcaemia as a suspected irAE is not well documented. The mechanisms of CPI hypercalcaemia are not clearly established. However, in our review, four distinct causes emerged: endocrine disease-related, sarcoid-like granuloma, humoral hypercalcaemia due to parathyroid-related hormone and hyperprogressive disease following CPI initiation. Prompt recognition of hypercalcaemia and the institution of therapy can be lifesaving, affording the opportunity to address the underlying aetiology. In this review we discuss the incidence, diagnosis and management of immune-related hypercalcaemia in oncological patients receiving CPI agents.

Immune checkpoint inhibition had a major clinical success in clinical oncology and impacted the treatment paradigm in many cancers. Immune related adverse events are well-described toxicities that are closely associated with CPI therapies and can involve any organ in the body. Renal toxicity is multifocal. In addition to the predominant tubulointerstitial involvement, immunotherapy can lead to a variety of glomerular damage and electrolyte disorders. Suggested mechanisms include direct renal interstitium lymphocyte infiltration, renal immune complex deposition, microangiopathic endothelial disease, or cytokine release leading to podocytopathy. Immunotherapy in the renal transplant patient raises the question of the rejection occurrence. Current recommendations for diagnosis and management of renal effects are not optimal because of the limited data available and understanding of their pathophysiology.

Resume L’avenement des nouvelles molecules en oncologie, notamment les therapies ciblees, a entraine une amelioration de la survie des patients par rapport a la chimiotherapie standard. Les toxicites renales de ces agents anticancereux sont de plus en plus reconnues et sont variables selon la cible therapeutique visee. Cet article passe en revue la toxicite renale associee aux therapies ciblees anticancereuses dirigees contre Epidermal growth factor receptor, Human epidermal growth factor-2, B-rapidly accelerated fibrosarcoma, Mitogen-activated protein kinase, Anaplastic lymphoma kinase, Programmed cell death-1/programmed cell death ligand-1, Cytotoxic T lymphocyte antigen-4 et Vascular endothelial growth factor/receptor. Le diagnostic et la prise en charge precoces de ces evenements indesirables renaux sont essentiels pour le clinicien en charge de ces patients.

Hypercalciuria is the main risk factor for recurrent calcium urolithiasis. The goal of our study is to determinate how useful an oral calcium load test is for stone formers to classify different forms of hypercalciuria in pathogenetic categories defined as renal or absorptive according to the current knowledge. Between June 2013 and February 2016, a prospective study was carried out on 117 documented recurrent hypercalciuric stone formers undergoing an oral calcium load test modified from the original description by Pak. After 2 days of calcium-restricted diet, urine and blood were analyzed at baseline and 120 min after receiving orally 1 g of calcium. Total and ionized calcium, parathyroid hormone from serum and urine calcium and creatinine were assessed in order to divide patients in three groups as previously described: resorptive, absorptive, and renal hypercalciuria. This allowed the identification of 19, 39, 34 and 33 patients with normocalcemic primary hyperparathyroidism (NPHPT), renal hypercalciuria aka renal calcium leak (RCL), absorptive hypercalciuria (AH) and unidentified cause, respectively. Patients with NPHPT (who required parathyroidectomy) experienced a lower PTH decrease (41.41 ± 12.82 vs. 54.06 ± 13.84% p 0.01), higher beta-crosslaps, as well as lower TmP/GFR and distal third radius bone mineral density. RCL resulted in increased fasting urine calcium-to-creatinine ratio (Uca/Cr), i.e., 0.37 mmol/mmol), without hyperparathyroidism. AH was diagnosed by the presence of ΔUCa/Cr 0.60 mmol/mmol between baseline and 120 min without any other anomaly. For all remaining patients, results were inconclusive due to the lack of sufficient increase in serum calcium or because the cause of lithogenesis could not be clearly identified. The oral calcium load test is useful in nearly 80% of patients by identifying the different forms of hypercalciuria causing urolithiasis and by guiding treatment, including parathyroid surgery.

The term capillary leak syndrome (CLS) describes the manifestations associated with an increased capillary permeability to proteins leading to an escape of plasma from the blood circulatory system to surrounding tissues, muscle, organs, or body cavities. This results clinically in the typical triad of hypotension, edema, and elevated hematocrit. The more severe cases of CLS may present with cardiovascular collapse, shock, and death. The most classic form of this pathology is represented by the idiopathic systemic CLS (SCLS) also called Clarkson's disease, but capillary leaks are also described as adverse drug reactions foremost among which are anticancer drugs. This review will focus on oncologic drugs such as gemcitabine, therapeutic growth factors or cytokines, and monoclonal antibodies (mAbs) that appear now as the strongest candidates for anticancer drug-induced CLS.

International audience

Coronavirus disease 2019 (COVID-19) is an ongoing pandemic that to date has spread to >100 countries. Acute kidney injury is not uncommon with this disease. The most common kidney biopsy finding is acute tubular injury. Glomerular diseases such as collapsing glomerulopathy and vasculitis, and thrombotic microangiopathy have been reported. Viral inclusion particles with distinctive spikes in the tubular epithelium and podocytes, and endothelial cells of the glomerular capillary loops, have been visualized by electron microscopy by some but disputed by others as non-viral structures. Interstitial infiltrates have not commonly been described in the published kidney biopsy series from patients with COVID-19. Medications used to treat COVID-19 can lead to interstitial nephritis, but very few have been reported. In summary, interstitial kidney disease is a rare finding in COVID-19.

BackgroundRenal biopsy is the cornerstone of systemic lupus erythematosus (SLE) nephritis and antiphospholipid syndrome (APS) nephropathy management. However, transcutaneous renal biopsy (TCRB) is hampered by the antithrombotic treatment frequently prescribed for those diseases. Transjugular renal biopsy (TJRB) offers an attractive alternative for patients at increased risk of bleeding. The primary objective of the study was to describe the safety profile and diagnostic performance of TJRB in SLE and APS patients.MethodsAll SLE and/or APS patients who underwent a renal biopsy in our department (between January 2004 and October 2016) were retrospectively reviewed. Major complications were death, haemostasis nephrectomy, renal artery embolization, red blood cell transfusion, sepsis and vascular thrombosis; macroscopic haematuria, symptomatic perirenal/retroperitoneal bleeding and renal arteriovenous fistula without artery embolization were considered as minor complications.ResultsTwo hundred and fifty-six TJRBs—119 without antithrombotics (untreated), 69 under aspirin and 68 on anticoagulants and 54 TCRBs without antithrombotics—were analysed. Their major and minor complication rates, respectively, did not differ significantly for the four groups: 0 and 8% for untreated TJRBs, 1 and 6% for aspirin-treated, 6 and 10% for anticoagulant-treated and 2 and 2% for TCRBs. The number of glomeruli sampled and the biopsy contribution to establishing a histological diagnosis was similar for the four groups.ConclusionsTJRBs obtained from SLE and APS patients taking antithrombotics had diagnostic yields and safety profiles similar to those of untreated TCRBs. Thus, TJRB should be considered for SLE and APS patients at risk of bleeding.

Background Despite new therapeutics, the prognosis for pancreatic cancer remains poor. Pancreatic surgery is a therapeutic option in non-metastatic forms. The consequences for renal function are poorly described. Methods Patients who underwent surgery for pancreatic cancer between 1 January 2010 and 1 January 2017 and who experienced kidney biopsy in the Pitié-Salpêtrière Hospital were analysed. Results Two hundred and ninety-four patients had pancreatic surgery during the period of analysis and five of them had a kidney biopsy (mean ± SD 20 months ±13.6 months after surgery) during the post-operative follow-up. Among these patients, three exhibited oxalate nephropathy (ON), indicating that the prevalence of ON in patients with pancreatectomy is at least 1%. ON may be insidious, with chronic renal failure without urinary abnormalities. All patients had a high oxalate-to-creatinine ratio in urine sample. Renal function improved after specific management of ON in two patients. Pancreaticoduodenectomy may represent a higher risk of ON than left pancreatectomy. Conclusion Although rare and underestimated, ON appears to be a real risk after pancreatic resection. Early detection may preserve renal function.

Several specialists in medicine use local anesthetics. In patients with kidney disease, these agents are used during catheter insertions for hemodialysis and peritoneal dialysis, arteriovenous fistula and graft procedures, kidney transplantation, parathyroidectomy, kidney biopsies, and dental and skin procedures. Patients on chronic hemodialysis use a topical application prior to use of needles for arteriovenous fistula cannulation before starting dialysis. They are also used to manage acute and chronic pain conditions, in regional nerve blockade and in multi-modal enhanced recovery protocols. Despite their frequent use by both physicians and patients, data on the use of local anesthetics in patients with kidney impairment are not well reported. This review will summarize the use of local anesthetics in chronic kidney disease, describe their pharmacology and the impact of lower estimated glomerular filtration rate on their pharmacokinetics, and suggest dose regulation in those with kidney dysfunction.

International audience; The use of inhibitors of vascular endothelial growth factor (VEGF)/vascular endothelial growth factor receptor 2 (VEGFR2) signaling for the treatment of cancer has increased over the last decade. This signaling pathway plays a fundamental role in angiogenesis and also in kidney physiology. The emergence of anti-angiogenic therapies has led to adverse nephrotoxic effects, despite improving the outcomes of patients. In this review, we will present the different anti-angiogenic therapies targeting the VEGFR pathway in association with the incidence of renal manifestations during their use. In addition, we will discuss, in detail, the pathophysiological mechanisms of frequent renal diseases such as hypertension, proteinuria, renal dysfunction, and electrolyte disorders. Finally, we will outline the cellular damage described following these therapies.

Rationale & Objective Due to extensive comorbid conditions, coronavirus disease 2019 (COVID-19) has a poor prognosis in people receiving maintenance hemodialysis. In this article, we describe our experience with 200 maintenance hemodialysis patients in a hemodialysis center that used universal reverse transcriptase-polymerase chain reaction testing, including 38 COVID-19–positive patients. Study Design Descriptive observational cohort, including the time line of patient diagnoses along with contextual events including precautions, testing, screening algorithms, clinical diagnostics and therapy, and the clinical course of COVID-19–infected patients and their final outcomes. Setting & Participants 200 patients within a single hemodialysis center with 2 dialysis clinics in Paris. Results Among 200 maintenance hemodialysis patients, 38 (19%) had COVID-19 diagnosed; of these, 15 (39.5%) were admitted to the hospital, including 4 who required intensive care unit (ICU) care. There were 8 (21%) deaths. The most common symptom was fever, followed by dry cough, fatigue, and dyspnea. All COVID-19–infected patients had lymphopenia and an increase in C-reactive protein levels. Median time from the onset of respiratory symptoms to ICU admission was 1 to 2 days. Durations of non-ICU hospitalizations and ICU stays were 7 and 13 days, respectively. Limitations Retrospective study, single hemodialysis center. Conclusions Dialysis patients are a highly susceptible population and hemodialysis centers are a high-risk area in a COVID-19 epidemic. "Unexplained" lymphopenia and/or an increase in C-reactive protein level should lead physicians to the diagnosis of COVID-19 and should, when possible, be followed by diagnostic testing with universal reverse transcriptase-polymerase chain reaction, as well as the reinforcement of contamination barrier measures.

Nephrotic range proteinuria has been reported during the course of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and coronavirus disease (COVID-19). However, the pathological mechanisms underlying this manifestation are unknown. In this article, we present two cases of collapsing glomerulopathy (CG) associated with acute tubular necrosis during the course of COVID-19, and review the literature for similar reports. In our two cases, as in the 14 cases reported so far, the patients were of African ancestry. The 14 patients assessed had an APOL1 high-risk genotype. At the end of the reported period, two patients had died and five patients were still requiring dialysis. The 16 cases detailed in the present report strongly argue in favour of a causal link between SARS-CoV-2 infection and the occurrence of CG in patients homozygous for APOL1 high-risk genotype for which the term COVID-associated nephropathy (COVIDAN) can be put forward.

Purpose We investigated the activities of an ImmunoTOX board, an academic, multidisciplinary group of oncologists and organ specialists that adopts a real-life, case-by-case approach in the management of patients with immune-related adverse events (irAEs). Experimental design The ImmunoTOX assessment board was set up in 2016 at Gustave Roussy in France. It meets every 2 weeks to discuss the case-by-case management of patients presenting with irAEs. Here, we describe the ImmunoTOX board's activities between 2016 and 2019. Results Over study period, 398 requests (concerning 356 patients) were submitted to the ImmunoTOX board. Most of the requests concerned the putative causal link between immunotherapy and the irAE (n = 148, 37%), followed by possible retreatment after temporary withdrawal because of an adverse event (n = 109, 27%), the clinical management of complex situations (n = 100, 25%) and the initiation of immunotherapy in patients with pre-existing comorbidities (n = 41, 10%). The ImmunoTOX board discerned 273 irAEs. The five organ systems most frequently involved by irAEs were lung (n = 58, 21%), gastrointestinal tract (n = 36, 13%), liver or biliary tract (n = 33, 12%), musculoskeletal system (n = 27, 10%), and nervous system (n = 23, 8%). The time to occurrence was shorter for severe irAEs (grade III and VI) than for mild irAEs (grades I and II), with medians of 47 and 91 days, respectively (p = 0.0216). Conclusion The main medical needs in the management of irAEs involved the lung organ. Severe irAEs were expected to occur earlier than mild irAEs. This real-life study can help to better estimate medical needs and therefore help to assess the management of irAEs.

International audience; Objective : Expanded clinical experience with patients treated by pembrolizumab has accumulated. However, renal toxicities associated with this anti-programmed cell death 1 agent are poorly described because kidney histology is rarely sought. As a nephrology referral centre, we aimed to describe the clinic-biological and histopathological characteristics of pembrolizumab-related nephropathy and its response to treatment.Methods : We conducted a monocentric large case series study, including all pembrolizumab-treated cancer patients presenting a renal toxicity addressed to our centre from 2015 to 2017.Results : A total of 12 patients (7 men) out of 676 pembrolizumab-treated patients (incidence 1.77%) were included (median age 69.75 years). Patients were referred for acute kidney injury (n = 10) and/or proteinuria (n = 2). A kidney biopsy was performed in all patients, with a median duration of use of 9 months (range 1-24 months) after the beginning of treatment. Biopsy showed that four patients had acute interstitial nephritis (AIN), whereas five had acute tubular injury (ATI) alone, one had minimal change disease (MCD) and ATI, and one had MCD alone. Pembrolizumab withdrawal coupled with corticosteroid therapy was the most effective treatment for kidney function recovery. Drug reintroduction resulted in a more severe recurrence of AIN in one patient who required maintenance of pembrolizumab. Two patients died of cancer progression with one of them developing severe renal failure requiring dialysis.Conclusion : In our series, ATI, AIN and MCD are the most frequent forms of kidney involvement under pembrolizumab therapy. Kidney dysfunction is usually isolated but can be severe. Use of corticosteroids in case of AIN improves the glomerular filtration rate.

[This corrects the article DOI: 10.1093/ckj/sfab121.].

The introduction of novel molecularly targeted therapies in the last 2 decades has significantly improved the patient survival compared to standard conventional chemotherapies. However, this improvement has been accompanied by a whole new spectrum of kidney adverse events. Although known as "targeted," many of these agents lack specificity and selectivity, and they have a tendency to inhibit multiple targets including those in the kidneys. Early detection and correct management of kidney toxicities is crucial to preserve kidney functions. The knowledge of these toxicities helps guide optimal and continued utilization of these potent therapies. The incidence, severity, and pattern of nephrotoxicity may vary depending on the respective target of the drug. Here, we review the mechanism of action, clinical findings of kidney adverse events, and their proposed management strategies.

Thrombotic microangiopathy (TMA) is a group of disorders characterized by mechanical hemolytic anemia with thrombocytopenia and an ischemic organic lesion of variable and potentially fatal importance affecting mostly the kidneys and the brain with histologically a disseminated and occlusive microvasculopathy. The incidence of TMA represents 15% of acute kidney failure in oncological setting, largely due to the introduction of anti-angiogenic agents over the past decade. It may be more rarely related to cancer itself. The iatrogenic TMA can be classified into 2 types: The type I, secondary to chemotherapy (mitomycinC, gemcitabine), exposes to a chronic dose-dependent renal injury as well as an increase in morbidity and mortality; iatrogenic type II, secondary to anti-angiogenic agents', results in a dose-independent renal involvement and renal functional recovery is usual when the drug is discontinued. There is no randomized controlled trial to establish EBM-type management in TMA support. However, complement activation pathways and regulatory factors analyses allowed us to understand the mechanisms of endothelial lesions. As a result, the current trend includes the use of immunosuppressive agents in recurrent or plasmapheresis-refractory MAT.

Acute kidney injury (AKI) is a growing problem with untoward economic and medical consequences. Anticancer drug toxicity remains an important and increasing cause of AKI. Importantly, drug-induced AKI affects all nephron segments-vasculature, glomerulus, tubules, and interstitium. Recent studies have increased insight into the subcellular mechanisms of drug-induced AKI that include direct cellular toxicity and immune-mediated effects. Identification of patients with high-risk cancer before drug exposure may allow prevention or at least a reduction in the development and severity of nephrotoxicity. Recognition of drug-induced AKI and rapid discontinuation (or dose reduction) of the offending agents, when appropriate, are critical to maximizing kidney function recovery. Preventive measures require understanding patient and drug-related risk factors coupled with correcting risk factors, assessing baseline kidney function before initiation of therapy, adjusting the drug dosage and avoiding use of nephrotoxic drug combinations.

The epidermal growth factor receptor (EGFR) is implicated in various malignancies. The past decade has seen the development and widespread use of EGFR inhibitors for the successful treatment of such cancers. Available EGFR inhibitors include small molecule tyrosine-kinase inhibitors and monoclonal antibodies. Class-related renal adverse events result in dual toxicity including tubular/electrolyte disorders and glomerulopathies. Tubular injury is common and mainly due to monoclonal antibodies while glomerulopathy is rare and related to various anti-EGFR agents. The exact pathogenesis of anti-EGFR agents associated with kidney disorders remains to be elucidated.

Anaplastic lymphoma kinase 1 (ALK 1) is a member of the insulin receptor tyrosine kinase family. Crizotinib is a small molecule inhibitor available for clinical use, which is found within the ALK family of drugs. Several other ALK 1 inhibitors are currently being evaluated in preclinical and clinical trials. Crizotinib is approved for the treatment of advanced ALK positive non-small cell lung cancer (NSCLC). However, this drug is associated with various renal adverse effects. Treatment with crizotinib appears to be associated with pseudo- and true acute kidney injury. Peripheral edema and rare electrolyte disorders are also described with this ALK inhibitor. Finally, crizotinib also appears to increase the risk for the development and progression of renal cysts. This review focuses on the mechanism of action, clinical indications, pharmacology, and adverse renal effects of crizotinib.

The advent of new molecules oncology including targeted therapies, has resulted in improved patient survival over standard chemotherapy. The renal toxicities of these anticancer agents are more and more recognized and vary according to the targeted therapeutic target. This article reviews the renal toxicity associated with targeted anticancer therapies directed against Epidermal growth factor receptor, Human epidermal growth factor-2, B-rapidly accelerated fibrosarcoma, Mitogen-activated protein kinase, Anaplastic lymphoma kinase, Programmed cell death-1/programmed cell death ligand-1, Cytotoxic T lymphocyte antigen-4 and Vascular endothelial growth factor/receptor. The early diagnosis and management of these renal adverse events is essential for the clinician who cares for such patients.

Immune checkpoint inhibition had a major clinical success in clinical oncology and impacted the treatment paradigm in many cancers. Immune related adverse events are well-described toxicities that are closely associated with CPI therapies and can involve any organ in the body. Renal toxicity is multifocal. In addition to the predominant tubulointerstitial involvement, immunotherapy can lead to a variety of glomerular damage and electrolyte disorders. Suggested mechanisms include direct renal interstitium lymphocyte infiltration, renal immune complex deposition, microangiopathic endothelial disease, or cytokine release leading to podocytopathy. Immunotherapy in the renal transplant patient raises the question of the rejection occurrence. Current recommendations for diagnosis and management of renal effects are not optimal because of the limited data available and understanding of their pathophysiology.