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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

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.

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.

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.

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.

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.

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.

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.

Purpose Renal toxicities are common with angiogenesis multikinase inhibitors (AMKI), and can be limiting in phase I trials. Factors associated with such toxicities are poorly known. The aims of this exploratory study were to describe renovascular toxicities associated with AMKI, impact on drug development and to identify baseline parameters associated with the occurrence of renal toxicities in phase I trials. Methods Consecutive patients treated with AMKI in Gustave Roussy phase I unit between October 2005 and August 2013 were included. We retrospectively collected baseline characteristics and renovascular side effects. Associations were assessed in univariate and multivariate analyses. Results Overall, 168 patients were included: male 53.0 %, mean age 55.5 years old, history of hypertension 26.8 %, diabetes 6.0 %, atherosclerosis 13.6 %, stage 3 Chronic Kidney Disease (CKD, NKF-KDOQI) 17.2 %. Incidences of reno-vascular side effects were: hypertension 47.6 %, proteinuria 19.0 %, renal failure 11.9 % and thrombotic microangiopathy 10.1 %. Eighty percent of dose limiting toxicities (DLTs) were related to a renal toxicity. Multivariate analysis showed that onset of renal failure was associated with history of hypertension (p = 0.0003) and stage 3 CKD (p = 0.032). Conclusions A majority of the DLTs associated with AMKI in phase 1 trials are renal toxicities. Baseline hypertension and stage 3 CKD (NKF-KDOQI) might help to better identify patients at risk of AMKI-related renal toxicities.

Anaplastic lymphoma kinase 1 (ALK-1) is a member of the insulin receptor tyrosine kinase family. In clinical practice, three small molecule inhibitors of ALK-1 are used, namely crizotinib, ceritinib and alectinib. Several more agents are in active pre-clinical and clinical studies. Crizotinib is approved for the treatment of advanced ALK-positive non-small cell lung cancer (NSCLC). According to the package insert and published literature, treatment with crizotinib appears to be associated with kidney failure as well as an increased risk for the development and progression of renal cysts. In addition, this agent is associated with development of peripheral edema and rare electrolyte disorders. This review focuses on the adverse renal effects of Crizotinib in clinical practice.

Drug-induced nephrotoxicity (DIN) remains a current problem with economic and medical consequences. It affects all nephron segments. Recovery of renal function is based on the identification of risk factors, early diagnosis of renal disease, rapid (if possible) cessation of the causative agent and, in some cases, adjunctive therapy. Prevention is based on identification of early markers of DIN, correction of risk factors, initial assessment of renal function for adequate dosage adjustment and exclusion of other nephrotoxic factors. It has recently been proposed to standardize the phenotype of iatrogenic renal disease and, on the other hand, new markers of renal toxicity allowing early diagnosis and therefore better management of nephrotoxicity.

Expanded clinical experience with patients taking antiangiogenic compounds has come with increasing recognition of the renal adverse effects. Because renal histology is rarely sought in those patients, the renal consequences are underestimated. Antiangiogenic-treated-cancer patients, who had a renal biopsy for renal adverse effects from 2006 to 2013, were included in the current study. Clinical features and renal histologic findings were reviewed. Our cohort was 100 patients (58 women) with biopsy-proven kidney disease using anti-vascular endothelial growth factor (VEGF) therapy with a mean age of 59.8 years (range, 20–85 yr). Patients were referred for proteinuria, hypertension, and/or renal insufficiency. Kidney biopsy was performed 6.87 ± 7.18 months after the beginning of treatment. Seventy-three patients experienced renal thrombotic microangiopathy (TMA) and 27 patients had variable glomerulopathies, mainly minimal change disease and/or collapsing-like focal segmental glomerulosclerosis (MCN/cFSGS). MCN/cFSGS-like lesions developed mainly with tyrosine-kinase inhibitors, whereas TMA complicated anti-VEGF ligand. Thirty-one percent of TMA patients had proteinuria up to 1 g/24 h. Half of TMA cases are exclusively renal localized. Pathologic TMA features are intraglomerular exclusively. MCN/cFSGS glomeruli displayed a high abundance of KI-67, but synaptopodin was not detected. Conversely, TMA glomeruli exhibited a normal abundance of synaptopodin-like control, whereas KI-67 was absent. Median follow-up was 12 months (range, 1–80 mo). Fifty-four patients died due to cancer progression. Hypertension and proteinuria resolved following drug discontinuation and antihypertensive agents. No patient developed severe renal failure requiring dialysis. Drug continuation or reintroduction resulted in a more severe recurrence of TMA in 3 out of 4 patients requiring maintenance of anti-VEGF agents despite renal TMA. In conclusion, TMA and MCN/cFSGS are the most frequent forms of renal involvement under anti-VEGF therapy. Careful risk-benefit assessment for individual patients should take into account risk factors related to the host and the tumor.

We herein present a case of bilateral serous retinal detachment (SRD) as a presenting sign of nephrotic syndrome (NS). A 48-year-old man complained of decreased vision related to bilateral SRD. Laboratory tests revealed NS (serum albumin, 17 g/L: proteinuria, 15.40 g over 24 hours). Following treatment for edema with a diuretic, the bilateral SRD resolved completely, with a full recovery of the patient's vision. A kidney biopsy disclosed glomerular and vascular amyloid deposits; the amyloid stained strongly with anti-λ antiserum. Therefore, a diagnosis of AL amyloidosis was made. The sudden appearance of SRD should raise suspicion of a diagnosis of NS. Prompt recognition of this symptom is important for early treatment and restoration of the visual function.

Summary Background and objectives Renal infarction is an arterial vascular event that may cause irreversible damage to kidney tissues. This study describes the clinical characteristics of patients with renal infarction according to underlying mechanism of vascular injury. Design, setting, participants, & measurements This study retrospectively identified 94 patients with renal infarction diagnosed between 1989 and 2011 with the aim of highlighting potential correlations between demographic, clinical, and biologic characteristics and the etiology of renal infarction. Four groups were identified: renal infarction of cardiac origin (cardiac group, n=23), renal infarction associated with renal artery injury (renal injury group, n=29), renal infarction associated with hypercoagulability disorders (hypercoagulable group, n=15), and apparently idiopathic renal infarction (idiopathic group, n=27). Results Clinical symptoms included abdominal and/or flank pain in 96.8% of cases; 46 patients had uncontrolled hypertension at diagnosis. Laboratory findings included increase of lactate dehydrogenase level (90.5%), increase in C-reactive protein level (77.6%), and renal impairment (40.4%). Compared with renal injury group patients, this study found that cardiac group patients were older (relative risk for 1 year increase=1.21, P=0.001) and displayed a lower diastolic BP (relative risk per 1 mmHg=0.94, P=0.05). Patients in the hypercoagulable group had a significantly lower diastolic BP (relative risk=0.86, P=0.005). Patients in the idiopathic group were older (relative risk=1.13, P=0.01) and less frequently men (relative risk=0.11, P=0.02). Seven patients required hemodialysis at the first evaluation, and zero patients died during the first 30 days. Conclusions This study suggests that the clinical and biologic characteristics of patients can provide valuable information about the causal mechanism involved in renal infarction occurrence.

Recent advances in immune checkpoint inhibitor (ICPI) development have led to major improvements in oncology patient outcomes. Cytotoxic T-lymphocyte antigen 4 (CTLA-4) and programmed cell death protein 1 (PD-1) are two essential immune checkpoint receptors. Ipilimumab and tremelimumab (anti-CTLA-4-blocking antibodies) and pembrolizumab and nivolumab (antibodies targeting PD-1 receptors) have already been approved by US Food and Drug Administration in several malignancies. Two different forms of ICPI-induced renal damage have been identified, including acute (granulomatous) tubulointerstitial nephritis and immune complex glomerulonephritis. The observed acute renal damage can be reversed upon ICPI drug discontinuation and renal function can recover back to normal following the introduction of systemic corticosteroid treatment. Any delay in treating this complication could result in definitive and irreversible renal injury.

Several types of nephrological side-effects can occur during treatment with targeted therapy: high blood pressure, proteinuria, thrombotic microangiopathy, kidney failure, etc. Screening and treatment for high blood pressure, proteinuria and kidney failure are recommended during treatment with molecular targeted therapy (mainly for anti-VEGF). If BP is greater than 140/90mmHg on two measurements, it must be treated before the start of treatment. Self-measurement or ambulatory measurement of blood pressure is recommended. All antihypertensive drugs may be used apart from those, which interfere with cytochrome P450 (verapamil and diltiazem). Specialist advice (cardiology or nephrology) is recommended in the event of uncontroled hypertension. It is essential to monitor proteinuria with a urine strip test: if proteinuria is less than 2+ (grade 1), maintain treatment with molecular targeted therapy; if proteinuria is greater or equal to 2+ (grade2 or 3, confirmed by weight assay), specialist advice is required. Persisting proteinuria of grade2 or 3 requires nephrological monitoring. Thrombotic microangiopathy must be investigated in the event of hypertension greater than grade2 and/or proteinuria greater than 2+.

Blocking integrin binding to fibronectin by a monoclonal antibody directed to integrin receptors induces apoptosis of proliferating endothelial cells. We report a case of grade 2 proteinuria, occurred fifteen days after the first administration of an anti-integrin monoclonal antibody associated to standard doses of carboplatin/paclitaxel and to a single dose of zoledronic acid in a patient treated in first line setting for a metastatic non small cell lung cancer. Kidney biopsy revealed a tubular damage probably associated to minimal change glomerulonephritis. Even if this patient did not receive any further dose of zoledronic acid, proteinuria reoccurred, although at a lower level when the investigational drug was reintroduced at the same dose. Renal function remained normal. The patient received two further cycles with lower doses, without recurrence of proteinuria. These findings suggest that this type of integrin antibody may induce transient urinary excretion of protein in a dose dependent manner without adversely affecting renal function.

The introduction of lenalidomide into the therapeutic arsenal of hematologic malignancies has represented an important step forward in the management of multiple myeloma. However, its use is associated with several toxicities including kidney injury. The present review examines the drug's pharmacokinetics, discusses the main adverse renal effects that are associated with lenalidomide treatment, and makes recommendations for dosage adjustment in patients with underlying renal impairment.

• A frequent and expensive problem. Ninety percent of contrast media nephrotoxicity (CMN) occur in patients with pre-existing kidney failure. Its aggravation may require early chronic dialysis. • Preventive measures. CMN prophylaxis is important in these patients. Pre- and post-hydration, with infusion of isotonic saline solution or sodium bicarbonate, and reduction of contrast medium (CM) volume to the strict minimum are essential for preventing CMinduced kidney failure. • The interest of prophylactic hemodialysis and hemofiltration. An interesting approach in preventing CMN is the early elimination of the CM with dialysis techniques. Preventive hemodialysis does not reduce the risk of CMN, but hemofiltration has shown significant efficacy in a population of patients with kidney failure. • The interest of immediate hemodialysis in chronic hemodialysis patients. Although nephrotoxicity is no longer a problem in patients undergoing chronic hemodialysis, CM, especially in highdose injections, may be responsible for fluid and electrolyte abnormalities and/or volemic expansion. No data yet justify a conclusion that a hemodialysis session immediately after injection of a CM in chronic dialysis patients might be helpful.

Background Adefovir (ADV), an orally administered nucleotide analogue active against hepadnaviruses, retroviruses and herpes viruses was shown to be effective in HIV-infected patients, but the prevalence of nephrotoxicity with doses of 60-120 mg/day was considered unacceptable. Recently, lower doses of ADV were shown to be effective for the treatment of HIV-1 patients with chronic lamivudine (LAM)-resistant hepatitis B. Methods In a cohort of 35 patients infected with both HIV-1 and LAM-resistant hepatitis B virus, we investigated the renal tolerance of a once-daily dose of ADV 10 mg over 52 weeks. Their mean baseline creatinine clearance was within the normal range (105 +/- 3 ml/min/1.73 m(2)). No patient had significant changes in renal function or electrolyte balance secondary to ADV treatment. Results Transient increases in serum creatinine, which resolved by the end of the study were noted in two patients and three developed proteinuria, which was felt to be unrelated to ADV treatment. The cohort's mean serum phosphate level, 2.45 +/- 0.09 mg/dl at baseline, did not change significantly under treatment (2.66 +/- 0.12 mg/dl at week 52, P = NS). Conclusions Our study shows that ADV dosed at 10 mg/day for the treatment of LAM-resistant chronic hepatitis B in patients co-infected with HIV is not associated with renal tubular dysfunction or a significant change in renal function.

Thrombotic microangiopathy (TMA) is a complication that can develop directly from certain malignancies, but more often results from anticancer therapy. Currently, the incidence of cancer drug–induced TMA during the last few decades is >15%, primarily due to the introduction of anti–vascular endothelial growth factor (VEGF) agents. It is important for clinicians to understand the potential causes of cancer drug–induced TMA to facilitate successful diagnosis and treatment. In general, cancer drug–induced TMA can be classified into 2 types. Type I cancer drug–induced TMA includes chemotherapy regimens (ie, mitomycin C) that can potentially promote long-term kidney injury, as well as increased morbidity and mortality. Type II cancer drug–induced TMA includes anti-VEGF agents that are not typically associated with cumulative dose–dependent cell damage. In addition, functional recovery of kidney function often occurs after drug interruption, assuming a type I agent was not given prior to or during therapy. There are no randomized controlled trials to provide physician guidance in the management of TMA. However, previously accumulated information and research suggest that endothelial cell damage has an underlying immunologic basis. Based on this, the emerging trend includes the use of immunosuppressive agents if a refractory or relapsing clinical course that does not respond to plasmapheresis and steroids is observed.

Pemetrexed belongs to a new generation of multitargeted antifolate cytotoxic agents. It is increasingly used as first-line treatment in combination with cisplatin, and as second-line treatment or maintenance monotherapy mainly in metastatic non-small cell lung cancer and in malignant mesothelioma. It is increasingly used as first-line treatment in combination with cisplatin in lung adenocarcinoma, and as second-line treatment or maintenance monotherapy in patients mainly controlled by the first-line to progression or poor tolerance. In mesothelioma, pemetrexed is indicated only in first-line with a platinum salt. The main side effect of pemetrexed is myelosuppression, which may be prevented by folinic acid supplementation. This review focuses on the progressive and cumulative emerging renal toxicity of pemetrexed, affecting five to ten percent of "long-term" pemetrexed-treated patients.

Expanded clinical experience with the antivascular endothelial growth factor (VEGF) agents has come with increasing recognition of their renal adverse effects. Although renal histology is rarely sought in antiangiogenic-treated cancer patients, kidney damage related to anti-VEGF is now established. Its manifestations include hypertension, proteinuria, and mainly glomerular thrombotic microangiopathy. Then, in nephrology practice, should we continue to perform kidney biopsy, and what should be done with the anti-VEGF agents in case of renal toxicity?

Although radical nephrectomy is still practiced in many patients with large renal tumors, oncology and nephrology arguments for kidney-sparing approach for small renal masses has taken over this first. Indeed, partial nephrectomy provides equivalent oncologic results while preserving renal function and thereby limit morbidity and cardiovascular mortality related to chronic kidney disease. In addition, patients who develop kidney cancer often have medical comorbidities that may affect renal function, such as diabetes and hypertension. Histological examination of renal tissue adjacent to the tumor showed significant pathological changes in the majority of patients. For elderly patients or patients with comorbidities, active surveillance allows kidney-sparing approach with extremely low rates of progression and metastasis of cancer disease. Despite these significant advances in understanding for the treatment of small renal masses, partial nephrectomy remains underused. Better management must take into account the preservation of renal function in order to increase overall survival. A strategy for the systematic evaluation of renal function in patients with CR, with multidisciplinary staff (nephrologist urologist and oncologist), is therefore highly desirable.

Background Castleman disease (CD), or angiofollicular lymph-node hyperplasia, is an atypical lymphoproliferative disorder with heterogeneous clinical manifestations. Renal involvement in CD has been described in only single-case reports, which have included various types of renal diseases. Methods Nineteen patients with histologically documented CD and renal biopsies available were included. Clinical features and renal histological findings were reviewed, and the available samples were immunolabelled with anti-vascular endothelial growth factor (VEGF) antibody. Results Nineteen CD cases were identified: 89% were multicentric, and 84% were of the plasma-cell or mixed type. Four cases (21%) were associated with human immunodeficiency virus (HIV) infection. Among HIV-negative patients, two main patterns of renal involvement were found: (i) a small-vessel lesions group (SVL) (60%) with endotheliosis and glomerular double contours in all patients and with superimposed glomerular/arteriolar thrombi or mesangiolysis in most; and (ii) AA amyloidosis (20%). Renal histology was more heterogeneous among HIV-positive patients. Decreases in glomerular VEGF were observed only in some patients with SVL, whereas VEGF staining was normal in all other histological groups. Interestingly, glomerular VEGF loss associated with SVL was correlated with plasma C-reactive protein levels, a marker of CD activity. Conclusions Small-vessel lesions are the most frequent renal involvement in CD, whereas loss of glomerular VEGF is correlated with CD activity and could have a role in SVL pathophysiology.

Developments in the knowledge of molecular biology of cancer over the past 20 years have been identified. Angiogenesis is playing a key role in the physiopathology of cancer evolution. Several strategies have been developed to target angiogenesis for the treatment of metastatic RCC. These include inhibition of VEGF receptors (inhibition of the tyrosine kinase activity) or binding to the VEGF protein. Several additional kinases inhibitions including PDGF receptors are also targeted. Anti-angiogenic drugs recently marketed or still under clinical development, may interact with the kidneys. Clinical and pathological, and mechanisms of their renal toxicity are presented in this article.

Nephrotoxicity is an inherent adverse effect of certain anticancer drugs. Anti neoplasic drugs have a narrow therapeutic index and the amount of drug necessary to produce a significant reduction in tumour burden usually produces significant nephrotoxicity. The dosage used in clinical trials represents often the maximum tolerated doses determined during phase I drug evaluation. Greater toxicity is acceptable during curative therapy than during palliative therapy. But cancer patients often exhibit excretory reduced organ function. Modulation of pharmacokinetics and pharmacodynamics of these drugs in cancer patients is therefore necessary in order to improve tolerance. Patients with malignancies are particularly vulnerable to development of renal abnormalities. Conversely, patients with renal abnormalities who have undergone kidney transplantation are at high risk for malignancy. Clinical syndromes of renal involvement are diverse and sometimes insidious. Despite the recent advances in understanding the mechanism of anticancer drug nephrotoxicity, prevention still relies on drug dosage decrease and active screening for renal abnormalities as part of the usual biological work up in patients treated with anticancer drugs.

Bilateral renal cortical necrosis (BRCN) is an uncommon cause of acute renal failure. Kidney biopsy, arteriography, and contrast-enhanced computed tomography (CT) are usually used to diagnose BRCN. However, these methods can have potentially serious side effects. We report two cases in which magnetic resonance imaging (MRI) evidenced characteristic features of BRCN, which were confirmed by histological findings and arteriography and correlated with clinical evolution. In the first case report, the diagnosis of a massive and complete cortical necrosis variety was suggested on MRI that showed a thin rim of low signal intensity along border of kidneys. It was confirmed on kidney biopsy, and the renal function did not recover. The second case is an incomplete form with cortical patchy areas of low signal intensity. In these two patients, MRI helped to establish an early diagnosis of BRCN with characteristic representative findings, without the potential nephrotoxic effects of iodinated contrast that has to be used in CT and arteriography. Kidney biopsy, besides the risks of complications, provides only a parceled analysis of the renal tissue and therefore does not allow any conclusion as to the extension of cortical necrosis. MRI may be of great help for the diagnosis and follow-up of acute renal cortical necrosis.