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

2021 ◽  
Vol 36 (2) ◽  
pp. 153-160.
Author(s):  
Min Jeong Kim

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.

2018 ◽  
Vol 8 (3) ◽  
pp. 257-259
Author(s):  
Hafsa Hassan Khan ◽  
Muhammad Abdur Rahim ◽  
Mehruba Alam Ananna ◽  
Tufayel Ahmed Chowdhury ◽  
Sarwar Iqbal

Rifampicin is one of the most effective anti-tubercular agents. Among its rare adverse effects, acute interstitial nephritis (AIN) is noteworthy. Here, we describe the case history of a 55-year-old female with tubercular lymphadenitis who developed rifampicin induced AIN upon re-exposure and recovered satisfactorily without requiring steroids. Rifampicin induced AIN should be kept in mind when patients present with acute kidney injury as prompt diagnosis and discontinuation of the drug has excellent prognosis.Birdem Med J 2018; 8(3): 257-259


2020 ◽  
Vol 9 (4) ◽  
pp. e35-e35
Author(s):  
John David Chetwood ◽  
Lin Lin Myat ◽  
Helen Lammi ◽  
Mani Panat ◽  
James Hughes

We report a case of acute kidney injury (AKI) secondary to immune-mediated acute interstitial nephritis (AIN), with supporting diagnostic results and a successful response to treatment. This entity is gaining increasing recognition with the burgeoning use of immunotherapy agents in oncology. The timeline for the development of AIN from the initiation of immunotherapy varies, and may range in severity from asymptomatic to severe, organ-threatening and with life threatening consequences. Renal biopsy should be performed to confirm the diagnosis due to the potential impact of discontinuation of immunotherapy on cancer survival. Re-challenge with immunotherapy is reasonable once renal function recovers.


2020 ◽  
Vol 8 ◽  
pp. 232470962093245
Author(s):  
Faisal Inayat ◽  
Syed Rizwan A. Bokhari ◽  
Lisa Roberts ◽  
Raquel M. Rosen

Acute interstitial nephritis is a well-known cause of acute kidney injury, but its association with cocaine use is extremely rare. In this article, we chronicle the case of a patient who developed acute interstitial nephritis secondary to cocaine insufflation. Furthermore, we conducted a systematic literature search of MEDLINE, Cochrane, Embase, and Scopus databases regarding cocaine-induced acute interstitial nephritis. A comprehensive review of the search results yielded a total of 7 case reports only. The data on patient characteristics, clinical features, biochemical profiles, treatment, and outcomes were collected and analyzed. This paper illustrates that acute interstitial nephritis may be added to the list of differentials in patients with acute kidney injury and a history of cocaine use. The therapeutic approach for cocaine-related kidney disease may be different than other etiologies responsible for acute renal insult. Prompt recognition of this entity is crucial because such patients may ultimately develop severe deterioration in renal function.


2021 ◽  
Vol 9 ◽  
pp. 232470962110016
Author(s):  
B. K. Anupama ◽  
Parth Sampat ◽  
Harvir S. Gambhir

We report the case of a 71-year-old female who was incidentally found to have nonoliguric acute kidney injury on a routine workup for new-onset visual hallucination. Further history revealed inadvertent usage of nitrofurantoin for 3 months for an anticipated urological procedure. Renal biopsy demonstrated acute granulomatous interstitial nephritis. The renal function significantly improved following discontinuation of nitrofurantoin and corticosteroid administration. We highlight a rare association of nitrofurantoin with acute granulomatous interstitial nephritis through this case report.


2020 ◽  
Vol 5 (7) ◽  
pp. 1068-1070 ◽  
Author(s):  
Benjamin Lazarus ◽  
Matthew R.P. Davies ◽  
Jason A. Trubiano ◽  
Rebecca Pellicano

2020 ◽  
Vol 4 (3) ◽  
pp. 100-104
Author(s):  
Filipa Cardoso ◽  
Rui Barata ◽  
David Navarro ◽  
Marco Mendes ◽  
Mário Góis ◽  
...  

A 73-year-old male diagnosed with metastasized malignant melanoma was started on combined therapy with dabrafenib and trametinib, but soon admitted with gastrointestinal intolerance. Blood tests revealed toxic hepatitis and acute kidney injury. Renal duplex Doppler ultrasound ruled out urinary and vascular obstruction and apart from a positive antinuclear antibody, other tests for acute kidney injury assessment were unremarkable. Urinary sediment microscopy showed dysmorphic red blood cells, in addition to yellow-pigmented casts. Kidney biopsy revealed signs of acute tubular necrosis and acute interstitial nephritis. Kidney function declined further, prompting the need for urgent hemodialysis. Treatment with dabrafenib and trametinib was stopped and corticosteroids were initiated, with a rapid beneficial effect on both the kidney function and liver toxicity. Hemodialysis was stopped after four sessions with a full recovery after 2 months of corticosteroids, with the dose being slowly tapered. Unfortunately, the patient died a few months later due to melanoma progression. Dual therapy with the combination of a B-Raf proto-oncogene inhibitor with a mitogen-activated protein kinase kinase inhibitor improves response rates and has been recently approved by the U.S. Food and Drug Administration, and while dermatologic toxicity is a common adverse effect, the association with acute renal failure has seldom been reported. To the best of our knowledge, there are only two published case reports of acute kidney injury in patients treated with combination of dabrafenib and trametinib and only one of them is biopsy proven. Further studies evaluating the incidence of acute kidney injury with the combination of B-Raf proto-oncogene and mitogen-activated protein kinase kinase inhibitors are warranted, and may provide new insights into the mechanisms underlying renal toxicity.


2019 ◽  
Vol 3 (7) ◽  
pp. 1084-1091 ◽  
Author(s):  
Adrian G. Minson ◽  
Katherine Cummins ◽  
Lucy Fox ◽  
Ben Costello ◽  
David Yeung ◽  
...  

Abstract Although second-generation tyrosine kinase inhibitors (TKIs) show superiority in achieving deep molecular responses in chronic myeloid leukemia in chronic phase (CML-CP) compared with imatinib, the differing adverse effect (AE) profiles need consideration when deciding the best drug for individual patients. Long-term data from randomized trials of nilotinib demonstrate an increased risk of vascular AEs (VAEs) compared with other TKIs, although the natural history of these events in response to dose modifications or cessation has not been fully characterized. We retrospectively reviewed the incidence of nilotinib-associated AEs in 220 patients with CML-CP at 17 Australian institutions. Overall, AEs of any grade were reported in 95 patients (43%) and prompted nilotinib cessation in 46 (21%). VAEs occurred in 26 patients (12%), with an incidence of 4.1 events per 100 patient-years. Multivariate analysis identified age (P = .022) and dyslipidemia (P = .007) as independent variables for their development. There was 1 fatal first VAE, whereas the remaining patients either continued nilotinib (14 patients) or stopped it immediately (11 patients). Recurrent VAEs were associated with ongoing therapy in 7 of 14 who continued (with 2 fatal VAEs) vs 1 of 11 who discontinued (P = .04). Nineteen of the 23 evaluable patients surviving a VAE ultimately stopped nilotinib, of whom 14 received an alternative TKI. Dose reduction or cessation because of VAEs did not adversely affect maintenance of major molecular response. These findings demonstrate that in contrast to other AEs, VAEs are ideally managed with nilotinib cessation because of the increased risk of additional events with its ongoing use.


2011 ◽  
Vol 2011 ◽  
pp. 1-4 ◽  
Author(s):  
Farheen Shah-Khan ◽  
Marc H. Scheetz ◽  
Cybele Ghossein

Vancomycin (VAN) has been associated with acute kidney injury (AKI) since it has been put into clinical use in the 1950's. Early reports of AKI were likely linked to the impurities of the VAN preparation. With the advent of the more purified forms of VAN, the incidence of AKI related to VAN were limited to acute interstitial nephritis (AIN) or as a potentiating agent to other nephrotoxins such as Aminoglycosides. VAN as the sole etiologic factor for nephrotoxic acute tubular necrosis (ATN) has not been described. Here, we report a case of biopsy-proven ATN resulting from VAN.


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