Clinical trials in oncology initially recruit heterogeneous populations, without catering for all types of variability. The target cohort is often not representative, leading to variability in pharmacokinetics (PK). To address enrollment challenges in clinical trials, physiologically based pharmacokinetic models (PBPK) models can be used as a guide in the absence of large clinical studies. These models require patient-specific systems data relevant to the handling of drugs in the body for each type of cancer, which are scarce.

This review explores system parameters affecting PK in cancer and highlights important gaps in data. Changes in drug-metabolizing enzymes (DMEs) and transporters have not been fully investigated in cancer. Their impaired expression can significantly affect capacity for drug elimination. Finally, the use of PBPK modeling for precision dosing in oncology is highlighted. Google Scholar and PubMed were mainly used for literature search, without date restriction.

Model-informed precision dosing is useful for dosing in sub-groups of cancer patients, which might not have been included in clinical trials. Systems parameters are not fully characterized in cancer cohorts, which are required in PBPK models. Generation of such data and application of cancer models in clinical practice should be encouraged.

Acute kidney injury (AKI) is a common complication in cancer patients and significantly impacts their treatment and prognosis. To better understand the epidemiology and clinical implications of AKI in hospitalised cancer patients, this study was designed to determine the incidence of AKI, identify risk factors for AKI and assess the impact of AKI on in-hospital outcomes.

Retrospective analysis of 68 379 cancer admissions in 2019. AKI incidence, risk factors (demographics, comorbidities and clinical characteristics), and impact on in-hospital mortality and length of stay were assessed. Logistic regression was employed to identify the risk factors for AKI. Survival analysis was conducted using the Cox proportional hazards model, with log-rank statistics used to assess survival outcome.

Of the 68 379 eligible cancer admissions, 7734 AKI cases were recognised with an incidence rate of 11.3%. The highest rates were observed in renal cancer (40.1%), ureter cancer (27.9%) and multiple myeloma (16.1%). Clinical risk factors such as age > 50 years, body mass index < 18.5 kg/m2, and hyperuricemia were significantly associated with hospital-acquired AKI compared to the non-AKI group (p < 0.001). In cases of severe community-acquired AKI, significant differences in hypertension, anaemia and leukocyte elevation were also observed (p < 0.001). The mortality rate was notably higher in AKI patients, especially in the severe AKI subgroup. The length of stay was markedly prolonged in patients with hospital-acquired and severe AKI, further underscoring the clinical burden of this complication.

Hospitalised cancer patients experience a high incidence of AKI. Identifying and mitigating risk factors may improve patient outcomes.

Reduced kidney function (or kidney dysfunction) is commonly an exclusion criterion for randomised controlled trials (RCTs) in cancer. Consequently, high quality evidence for anticancer drug dosing in reduced kidney function is limited and no internationally agreed guidelines exist to inform prescribing decisions in this population. A methodology for guideline development was applied which did not require availability of RCTs but used critical appraisal of existing observational literature and group consensus. An international multidisciplinary working group (n = 38) established consensus recommendations in two parts to form the International Consensus Guideline on Anticancer Drug Dosing in Kidney Dysfunction (ADDIKD). The approach enabled virtual participation worldwide. In Part 1 we developed a standardised approach for assessment and classification of kidney function in patients with cancer using global nephrology standards and working group expertise. Part 2 involved a comprehensive literature search of 59 anticancer drugs followed by a critical appraisal of the evidence certainty through the Grading of Recommendations Assessment, Development and Evaluation (GRADE) process and development of dosing recommendations in reduced kidney function. Key external stakeholders (n = 9) invited expert contributors (n = 25), and the working group participated in virtual interactive workshops to vote on the acceptability of these recommendations. The participants were provided with evaluation of the literature, and they engaged in several rounds of virtual discussion (involving robustness of the evidence behind recommendations and their real-world application) and anonymous consensus voting. Adapting the ADDIKD guideline development process to a virtual format enabled engagement with a very broad base of specialised international experts especially during the global pandemic. Combining GRADE methodology with consensus-building approaches was an effective method of producing recommendations (in an area lacking RCTs) by merging critical review of the literature with expert opinion and clinical practice.

Development of the ADDIKD guideline is funded by the Cancer Institute NSW as part of the NSW Government and received no funding from external commercial sources.

The kidney disease: Improving Global Outcomes (KDIGO) guideline recommends assessing kidney function using glomerular filtration rate (GFR) either through direct measurement or through estimation (eGFR) and describes a standardised classification of reduced kidney function. KDIGO guidelines have been adopted by most internal medicine specialities for the assessment and classification of kidney function, but not by cancer medicine. The development of the International Consensus Guideline on Anticancer Drug Dosing in Kidney Dysfunction (ADDIKD) aims to overcome the perceived challenges with KDIGO recommendations by describing their utility in patients with cancer. Two virtual, consensus building workshops were held consecutively, involving international, multidisciplinary participants (Part 1 of ADDIKD development). During these workshops, three consensus recommendations were agreed upon based on KDIGO's principles; to standardise kidney function assessment, classify kidney function, and determine a uniform approach to dose anticancer drugs in patients with reduced kidney function. Cancer clinicians attending the workshops identified issues regarding the adoption of KDIGO's recommendations. These issues were addressed by nephrologists, clinical pharmacologists, and other clinicians with extensive experience in the contemporary assessment of kidney function. The key concern for cancer specialists was a hesitancy to move away from the familiar and long-standing practice of using the Cockcroft-Gault equation to estimate creatinine clearance. The consensus building within the two multidisciplinary workshops allowed a thorough assessment of the evidence and clarified how directly measured GFR and eGFR, rather than creatinine clearance, could be optimally utilised in cancer care. The development of Part 1 of the ADDIKD guideline represents a standardised, contemporary approach to the assessment, classification, and utility of kidney function in the setting of cancer care and it harmonises with the approach used in other areas of medicine internationally.

Development of the ADDIKD guideline is funded by the Cancer Institute NSW as part of the NSW Government and received no funding from external commercial sources.

Patients with cancer are at increased risk of venous thromboembolism (VTE). Treatment of VTE remains challenging due to a significant risk of both VTE recurrence and bleeding compared with patients without underlying malignancy. Moreover, patients with cancer often present with several comorbidities such as tumor- or treatment-induced bone marrow failure, renal impairment, and extensive concomitant anticancer or supportive medication, resulting in potential drug-drug interactions. Further challenging circumstances include gastrointestinal (GI) disorders, in the context of a GI intraluminal tumor itself, GI surgery, or systemic therapy-induced GI toxicity. However, treatment options and study data in the management of cancer-associated thrombosis (CAT) have expanded over the last few years. As a result, it is becoming increasingly important to assess the patient's individual risk of bleeding and its comorbidities, and the patient's personal preferences. Prospectively, further therapeutic strategies such as factor XIa inhibitors are under clinical investigation. The aim of our narrative review is to summarize the current literature on therapy options for CAT, including common treatment situations encountered in the management of patients with cancer.

Chimeric antigen receptor (CAR)-T cell therapy is a novel therapy for the treatment of different hematologic malignancies. Besides its efficiency, CAR-T cell therapy is associated with significant toxicity, primarily manifested as cytokine release syndrome (CRS) and neurotoxicity. However, there are reports that CAR-T cell therapy is also nephrotoxic and this aspect has attracted less attention to date. In this review, we focus on the incidence and association between CAR-T cell therapy and kidney injury. Here, we describe risk factors, biomarkers, and potential reasons for acute kidney injury (AKI) and chronic kidney disease (CKD) related to CAR-T cell therapy to shed light on pathomechanisms leading to renal impairment as well as to the association of kidney failure with other side effects of CAR-T cell therapy. We also review the toxicity of different types of CAR-T cell products, the impact of nephrotoxicity on CAR-T cell therapy efficacy, and the safety of lymphodepletion in patients with baseline AKI or CKD.

Approximately 30% of the patients with cancer experience kidney complications, which hinder optimal cancer management, imposing a burden on patients' quality of life and the healthcare system. The etiology of kidney complications in patients with cancer is often attributed to oncological therapies. However, the direct impact of cancer on kidney health is underestimated. Our previous study demonstrated that metastatic lung cancer adversely alters the kidney and exacerbates chemotherapy-induced nephrotoxicity, indicating lung cancer-kidney crosstalk. The current study examines whether this phenomenon is specific to the employed cancer model. Female and male mice of various strains were injected with different cell lines of remote organ cancer, and their kidney tissues were analyzed for toxicity and fibrosis. The impact of cancer on the kidney varied by cancer type. Breast cancer and specific subtypes of lung cancer, including KRAS- and epidermal growth factor receptor (EGFR)-mutant cancer, pathologically altered kidney physiology and function in a manner dependent on the metastatic potential of the cell line. This was independent of mouse strain, sex, and cancer cell line origin. Moreover, tumor DNA was not detected in the renal tissue, excluding metastases to the kidney as a causative factor for the observed pathological alterations. Lewis lung carcinoma and B16 melanoma did not cause nephrotoxicity, regardless of the tumor size. Our results confirm cancer-kidney crosstalk in specific cancer types. In the era of precision medicine, further research is essential to identify at-risk oncology populations, enabling early detection and management of renal complications.NEW & NOTEWORTHY Patients with cancer frequently experience kidney complications, often attributed to antineoplastic therapies. This emphasis on therapy-induced nephrotoxicity has led to the underestimation of the impact of cancer on the kidney. Our study demonstrates that distant organ cancer is sufficient to induce nephrotoxicity, highlighting the existence of cancer-kidney crosstalk. Our findings underscore a gap in our understanding of renal complications in patients with cancer and provide a rationale for identifying the underlying mechanisms for the development of nephroprotective agents.

This study investigated the prevalence and risk factors of acute kidney injury (AKI) and chronic kidney disease (CKD) in cancer patients with the aim of providing guidance for clinical treatment of cancer patients.

A retrospective study was conducted on all cancer and hematological malignancy patients admitted to Xuanwu Hospital, Capital Medical University, from January 2018 to July 2023. The study population included patients aged 18-80 years with a confirmed cancer or malignancy diagnosis. Chi-square tests, Spearman's correlation, and logistic regression were used to evaluate the relationships between demographic factors, comorbidities, cancer types, antitumor drugs and the prevalence of AKI/CKD.

Among the 2438 participants, the prevalence rates of AKI and CKD were 3.69% and 7.88%, respectively. Patients with diabetes had higher prevalence of AKI/CKD than those without diabetes (OR = 1.66, 95% CI 1.01-2.68, p = 0.040; OR = 1.60, 95% CI 1.10-2.31, p = 0.012, respectively). In addition, a higher prevalence of CKD was observed in patients with hypertension (OR = 3.49, 95% CI 2.43-5.06, p < 0.001). Underweight patients were more likely to develop AKI (OR = 2.66, 95% CI 1.03-6.08, p = 0.029). Anthracyclines may contribute to a higher risk of AKI, and antimetabolites and immunomodulators may be associated with the development of CKD. Overall, patients with hematological malignancies had significantly higher rates of AKI/CKD than those with solid tumors. Among solid tumor patients, the prevalence of AKI/CKD was low in patients with lung and breast cancer.

AKI and CKD prevalence varies across cancer types, influenced by factors, such as diabetes, hypertension, body weight, and antitumor drugs. Tailored treatment plans are essential for improving cancer patient outcomes.

Kidney complications associated with anticancer drug therapy have greatly increased recently. We aimed to investigate the real-world clinical outcomes of anticancer drug therapy-associated renal complications in Japan using the national kidney biopsy database, Japan Renal Biopsy Registry (J-RBR).

From 2018 to 2021, 449 cases from 49 facilities identified as 'drug-induced' histopathology in the J-RBR were screened, of which a total of 135 were confirmed as anticancer drug-related cases and included in the analysis. Overall survival rates were estimated using the Kaplan-Meier method and compared by logrank test. The Cox regression model was used to evaluate the association between variables and deaths.

The most common primary sites of malignancies were the lung (33.3%), followed by gastrointestinal (16.3%) and gynaecological (11.1%) cancers. Tubulointerstitial nephritis (TIN; 47.4%) and thrombotic microangiopathy (TMA; 35.6%) were the most frequent diagnoses. All immunoglobulin A nephropathy, minimal change disease and crescentic glomerulonephritis (CrGN) cases were immune checkpoint inhibitor related. All CrGN cases were anti-neutrophil cytoplasmic antibody negative. Antibiotics were most frequently used concomitantly with anticancer drugs in TMA cases among subgroups (TMA versus others: 62.5 versus 27.5%; P < .001). Among TMA cases, the serum lactate dehydrogenase level tended to be higher in cytotoxic agent-associated TMA (CTx-TMA) than in other TMAs, but was not significant between groups (415.5 versus 219.0 U/l; P = .06). Overall survival was worse in CTx-TMA than in other TMAs (P = .007). The Cox model demonstrated proton pump inhibitor (PPI) use (hazard ratio 2.49, P = .001) as a significant prognostic factor, as well as the presence of metastasis and serum albumin level.

Our registry analysis highlighted various presentations of biopsy-proven kidney complications associated with anticancer drug therapy. Clinicians should be aware of worse outcomes associated with CTx-TMA and the prognostic role of PPI use.

Clinical trials play a pivotal role in advancing treatments for people with cancer, but often struggle with low enrollment. Unnecessarily including kidney function eligibility criteria when a trial's interventions do not have any potential kidney effects may contribute to this problem by needlessly limiting the pool of eligible patients, adding complexity to the patient screening process, and raising issues of inequitable access to trials. For these reasons, we applied custom natural language processing to assess renal function eligibility criteria, and the appropriateness of these exclusions, within phase 3 urologic oncology trials.

We accessed all phase 3 urologic oncology trials registered on ClinicalTrials.gov from 2007 to 2021. We used a custom natural language processing script to extract kidney function requirements (e.g., creatinine, GFR) from trial free-text records. For each trial, we manually coded whether any trial intervention affected renal function or was renally excreted. Additionally, we recorded the formula used to calculate GFR in each trial.

Of 850 trials, 299 (35%) listed kidney function eligibility restrictions, and 432 (51%) tested an intervention with possible renal effects. Of the 299 trials with kidney function exclusions, 124 (41%) tested interventions with no kidney effects.

There is a major disconnect in urologic oncology clinical trials between renal function exclusions and potential harm to the kidneys from the tested interventions. Standardizing eligibility criteria and restricting enrollment based on renal function only when necessary has the potential to increase the success, access, and applicability of clinical trials.

Onco-nephrology is an emerging subspecialty aiming to better understand and prevent renal events in cancer patients. We assessed patients' knowledge about (1) oncological/hematological treatments induced renal toxicity and (2) kidney protective measures.

Adult patients receiving systemic anti-tumor treatments in multiple day hospital units in France answered a self-administered questionnaire about their knowledge and expectations related to treatment-associated renal toxicity.

In total, 621 questionnaires were collected in 8 units from November 2021 to January 2022. Among respondents, 84.5% were treated for a solid tumor. Overall, 34.3% (n = 208) patients reported they had some knowledge about potential renal adverse events related to their anticancer treatment, and 38.5% (n = 234) about kidney protection measures. Their referring oncologist or hematologist represented the commonest source of knowledge (67.8%). Sufficient hydration was cited as a kidney protection measure by 93.2% (n = 218) of patients declaring some knowledge about renal toxicity; prevention of nausea/vomiting by 52.6% (n = 123). Consumption of still and alkaline water was chosen by respectively 64.4% (n = 400) and 16.8% (n = 104) of participants to correct dehydration. A majority of patients expressed strong interest for receiving more information about renal toxicity and prevention: median Likert scale score was 10/10 (Q1-Q3, 5-10), with online resources mentioned as the most desired source of information.

One-third of patients declared they had some knowledge about potential renal toxicity of their oncologic treatment and the ways to prevent them, especially regarding hydration. However, a majority expressed interest for dedicated information, which conducted to the elaboration of free online educational sheets for patients.

Onconephrology is a growing discipline that aims to improve the management of patients with cancer and kidney disease. If kidney histology is an essential key, the anatomopathological data remain weak although essential to this complex management.

Patients with active cancer who had a kidney biopsy (KB) between 2014 and 2020 were included, and their clinicobiological and histological data were analyzed retrospectively.

Our cohort consisted of 154 patients (83 women) with a mean age of 58 years. One hundred twelve patients presented with proteinuria, 95 with acute kidney injury, and 59 with arterial hypertension. Histologically, interstitial fibrosis was found in 74% of KBs, tubular atrophy in 55.1%, arteriolar hyalinosis in 58.4%, and fibrous endarteritis in 54.4%. Regarding the main acute lesions, thrombotic microangiopathy (TMA) was found in 29.9% of biopsies, acute tubular necrosis (ATN) in 51.3%, and acute interstitial nephritis in 24.8%. The etiological diagnosis most often made was the nephrotoxicity of anticancer drugs (87 patients), followed by a pre-renal (15 patients) and kidney disease unrelated to cancer (13 patients). Sixty-seven patients presented with at least 2 associated diagnoses reflecting the complexity of kidney damage in cancer. Different clusters were found, highlighting that immunotherapy and anti-VEGF were the most commonly involved drugs.

During onconephrology practice, kidney toxicity of treatments is the most common etiology. Several mechanisms can be involved, underscoring the importance of kidney biopsy and the complexity of its management. Chronic histological lesions were very common.

The population with kidney failure is at increased risk of cancer and associated mortality. Relative survival can provide insight into the excess mortality, directly or indirectly, attributed to cancer in the population with kidney failure.

We estimated relative survival for people all ages receiving dialysis (n = 4089) and kidney transplant recipients (n = 3253) with de novo cancer, and for the general population with cancer in Australia and New Zealand (n = 3 043 166) over the years 1980-2019. The entire general population was the reference group for background mortality, adjusted for sex, age, calendar year and country. We used Poisson regression to quantify excess mortality ratios.

Five-year relative survival for all-site cancer was markedly lower than that for the general population for people receiving dialysis [0.25, 95% confidence interval (CI) 0.23-0.26] and kidney transplant recipients (0.55, 95% CI 0.53-0.57). In dialysis, excess mortality was more than double (2.16, 95% CI 2.08-2.25) that of the general population with cancer and for kidney transplant recipients 1.34 times higher (95% CI 1.27-2.41). There was no difference in excess mortality from lung cancer between people with kidney failure and the general population with cancer. Comparatively, there was a significant survival deficit for people with kidney failure, compared with the general population with cancer, for melanoma, breast cancer and prostate cancers.

Decreased cancer survival in kidney failure may reflect differences in multi-morbidity burden, reduced access to treatment, or greater harm from or reduced efficacy of treatments. Our findings support research aimed at investigating these hypotheses.

A substantial majority of patients diagnosed with metastatic breast cancer consists of individuals 65-year-old or above. Emerging treatment approaches, which utilize genomics-guided therapy and innovative biomarkers, are currently in development. Given the numerous choices in the metastatic context, it is necessary to adopt a personalized approach to decision-making for these patients.

The authors provide a comprehensive analysis of the existing literature on the use of systemic anticancer treatments in older women, specifically those aged 65 and above, who have metastatic breast cancer, focusing on the reported effectiveness and adverse effects of these treatments in this population.

The evidence to treat older patients with metastatic breast cancer primarily relies on subgroup analyses, whose interpretation should be approached with caution. In several clinical trials subgroup analysis, it has been observed that this population seem to have comparable benefits and toxicities to younger patients, but real-world data have showed older women exhibit worse rates of survival compared to younger women. Multiple factors are likely involved in this, but we postulate this is related to lower rates of guideline concordant, and factors such as comorbidity, lack of social supports, malnutrition, and geriatric factors like frailty and/or vulnerability. This underscores the importance of a broader assessment for patients with a geriatric perspective and involvement of multi-disciplinary team.

Drugs targeting angiogenesis and immunotherapy have transformed outcomes in renal cancer but may contribute to progressive kidney disease.

We linked healthcare databases in the West of Scotland (spanning 2010-2020) to identify adults with renal cancer who received one or both classes of drugs. Over two years following initiation, estimated glomerular filtration rate (eGFR) slope was modelled using linear mixed-effects models. Additional renal outcomes used competing risk regression considering the competing risk of death.

Amongst 357 adults (62.5% male; median age 63.0 years, IQI 55.0-71.0), there was no significant change in eGFR (annual eGFR change +1.03 mL/min/1.73 m²/year, 95%CI -1.64 to +3.70), nor in subgroups of patients who had nephrectomy, metastatic cancer or an eGFR < 60 mL/min/1.73 m² prior to systemic therapy. A ≥ 40% decline in eGFR occurred in 82 people (23.0%) within one year of starting systemic therapy and was associated with pre-existing diabetes (subhazard ratio 1.89, 95%CI 1.05-3.41).

Anti-angiogenic and immune therapy had no substantial impact on the average change in eGFR but people with diabetes are at higher risk of clinically significant renal events. With appropriate monitoring, more widespread use of these agents in patients with renal impairment may be warranted.

Approximately 30% of cancer patients experience kidney complications, which hinder optimal cancer management, imposing a burden on patients' quality of life and the healthcare system. The etiology of kidney complications in cancer patients is often attributed to nephrotoxic oncological therapies. However, the direct impact of cancer on kidney health is underestimated, as most nephrotoxic oncological therapies have been studied in animal models that do not have cancer. Our previous study demonstrated that advanced lung cancer adversely alters kidney physiology and function, and exacerbates chemotherapy-induced nephrotoxicity, indicating lung cancer-kidney crosstalk. This study examines whether this phenomenon is specific to the employed cancer model. Female and male mice of various strains were injected with different cell lines representing human and mouse lung cancer, breast cancer, and melanoma, and their kidney tissues were analyzed for toxicity and fibrosis. The impact of cancer on the kidney varied by cancer type. Breast cancer and specific subtypes of lung cancer, including KRAS- and EGFR-mutant cancer, pathologically altered kidney physiology and function in a manner dependent on the metastatic potential of the cell line. This was independent of mouse strain, sex, and cancer cell line origin. Moreover, tumor DNA was not detected in the renal tissue, excluding metastases to the kidney as a causative factor for the observed pathological alterations. Lewis lung carcinoma and B16 melanoma did not cause nephrotoxicity, regardless of the tumor size. Our results confirm cancer-kidney crosstalk in specific cancer types and highlight gaps in understanding the risk of renal complications in cancer patients. In the era of precision medicine, further research is essential to identify at-risk oncology populations, enabling early detection and management of renal complications.

Nephrotic syndrome (NS) can occur as a paraneoplastic disorder in association with various types of carcinoma. However, paraneoplastic nephrotic syndrome (PNS) is often misdiagnosed as idiopathic nephrotic syndrome or as an adverse effect of oncology treatment, leading to delayed diagnosis and suboptimal treatment. The characteristics of NS associated with solid malignancies are not yet elucidated. We systematically summarized the clinical data for 128 cases of NS combined with solid malignancies with the aim of informing the clinical management of PNS.

We searched the PubMed database for articles published from the date of inception through to October 2023 using the following keywords: "cancer" or "malignant neoplasms" or "neoplasia" or "tumors" and "nephrotic syndrome", "nephrotic" or "syndrome, nephrotic". All data were extracted from case reports and case series, and the extraction included a method for identifying individual-level patient data.

A literature search yielded 105 cases of PNS and 23 of NS induced by cancer therapy. The median age at diagnosis was 60 years, with a male to female ratio of 1.8:1. In patients with PNS, manifestations of NS occurred before, concomitantly with, or after diagnosis of the tumor (in 36%, 30%, and 34% of cases, respectively). Membranous nephropathy (49%) was the most prevalent renal pathology and found particularly in patients with lung, colorectal, or breast carcinoma. Regardless of whether treatment was for cancer alone or in combination with NS, the likelihood of remission was high.

The pathological type of NS may be associated with specific malignancies in patients with PNS. Prompt identification of PNS coupled with suitable therapeutic intervention has a significant impact on the outcome for patients.

Nephroprotection is a set of recommendations that aim to prevent the risks of acute and/or chronic renal failure and to limit the progression of renal failure towards an end stage. Nephroprotection is not limited to nephrology and applies to all patients at risk of renal failure. Cancer patients are particularly at risk of developing intrinsic and extrinsic renal failure, as well as the toxicity of specific treatments. However, they are poorly included in nephroprotection studies. Thus, current guidelines have not been adapted to these pathologies and oncology-specific comorbidities, such as malnutrition or prognosis, are often not taken into account. In this article, we review the established recommendations by transposing them to the cancer patient as a whole. In addition to the reminder of hygiene and dietary rules to control blood pressure and diabetes, we discuss the importance of therapeutic education, iatrogeny and treatment options to control renal failure in this context. The lack of clearly established data in cancer confirms the needs to strengthen links between oncologists, hematologists and nephrologists and reinforces the emergence of onco-nephrology as a new discipline.

Hypertension is the leading risk factor for cardiovascular disease (CVD). Although cancer has recently been increasingly recognized as a novel risk factor for CVD events, little is known about whether co-morbid cancer in individuals with hypertension could further increase the risk of CVD events. We sought to determine the association between the cancer history and the risk of CVD in individuals with hypertension. We retrospectively analyzed a large cohort of 747,620 individuals diagnosed with hypertension from January 2005 through May 2022 using the JMDC Claims Database. Composite CVD events, including myocardial infarction (MI), angina pectoris (AP), stroke, heart failure (HF), and atrial fibrillation (AF), were recorded, and a Cox proportional hazard regression was done to estimate hazard ratios (HR) based on the history of cancer and chemotherapy. 26,531 individuals had a history of cancer. During the mean follow-up period of 1269 ± 962 days, 67,154 composite CVD events were recorded. Compared with individuals without a cancer history, cancer survivors had a higher risk of developing composite CVD events (HR: 1.21, 95% confidence interval [CI]: 1.17-1.26). The HRs (95% CIs) associated with cancer history for MI, AP, stroke, HF, and AF were 1.07 (0.90-1.27), 1.13 (1.06-1.20), 1.14 (1.06-1.24), 1.31 (1.25-1.38), and 1.22 (1.10-1.35), respectively. Lastly, individuals who had received chemotherapy for cancer had a particularly higher risk of developing CVD compared to those who did not undergo chemotherapy. A history of cancer was associated with a greater risk of developing CVD among individuals with hypertension.

Cancer is among the leading cause of death worldwide. Chemotherapy is commonly used in cancer management and among the challenges in managing cancer patients is renal insufficiency (RI), which can be due to cancer or anticancer treatment and can be potentiated by different factors. Data regarding the prevalence of RI and associated factors in Tanzania is scanty. This study aims to assess the prevalence of RI and associated factors among selected cancer patients on chemotherapy.

This analytical cross-sectional study was conducted at Ocean Road Cancer Institute (ORCI) in Dar es Salaam, Tanzania, from March to May 2023. The study included cancer patients on chemotherapy. Data was collected using semi-structured questionnaires whereby socio-demographics, clinical and laboratory data were recorded. Data was analyzed by using STATA version 15. Categorical data was presented as frequencies and percentages, and continuous data was summarized using means. A modified Poisson regression model was used to assess factors associated with RI. The p-values ≤ 0.05 was considered statistically significant.

Out of 354 patients, the majority (76.6%) were female. The enrolled patients' mean age was 53 ± 13.19 years. The proportion of cancer patients with RI was 62.2% with most (60%) having stage 2 and stage 3 (37.7%). Age, hypertension (HTN), human immunodeficiency virus (HIV), diabetes mellitus (DM) and non-steroidal anti-inflammatory drugs (NSAIDs) use were significantly associated with increased risk of RI (p ≤ 0.05).

This study showed that RI is common among cancer patients on chemotherapy. Age, HTN, DM, HIV and NSAIDS use were associated with RI. Close monitoring of kidney function is necessary for cancer patients with other factors associated with RI. Use of creatinine clearance (CrCl) rather than serum creatinine in estimating kidney function is important.

Although all patients with cancer-associated thrombosis (CAT) have a high morbidity and mortality risk, certain groups of patients are particularly vulnerable. This may expose the patient to an increased risk of thrombotic recurrence or bleeding (or both), as the benefit-risk ratio of anticoagulant treatment may be modified. Treatment thus needs to be chosen with care. Such vulnerable groups include older patients, patients with renal impairment or thrombocytopenia, and underweight and obese patients. However, these patient groups are poorly represented in clinical trials, limiting the available data on which treatment decisions can be based. Meta-analysis of data from randomised clinical trials suggests that the relative treatment effect of direct oral factor Xa inhibitors (DXIs) and low molecular weight heparin (LMWH) with respect to major bleeding could be affected by advanced age. No evidence was obtained for a change in the relative risk-benefit profile of DXIs compared to LMWH in patients with renal impairment or of low body weight. The available, albeit limited, data do not support restricting the use of DXIs in patients with TAC on the basis of renal impairment or low body weight. In older patients, age is not itself a critical factor for choice of treatment, but frailty is such a factor. Patients over 70 years of age with CAT should undergo a systematic frailty evaluation before choosing treatment and modifiable bleeding risk factors should be addressed. In patients with renal impairment, creatine clearance should be assessed and monitored regularly thereafter. In patients with an eGFR less than 30mL/min/1.72m2, the anticoagulant treatment may need to be adapted. Similarly, platelet count should be assessed prior to treatment and monitored regularly. In patients with grade 3-4, thrombocytopenia (less than 50,000platelets/μL) treatment with a LMWH at a reduced dose should be considered. For patients with CAT and low body weight, standard anticoagulant treatment recommendations are appropriate, whereas in obese patients, apixaban may be preferred.

Renal injury is common in cancer patients and its etiology is multifactorial. Different patterns of renal histological lesions have been described in relation to oncologic treatments, notably acute tubular necrosis and tubulointerstitial nephritis, but also thrombotic microangiopathy (TMA).

We report a case of TMA secondary to capecitabine in an 82-year-old woman diagnosed with localized colon adenocarcinoma.

The patient, with previous normal kidney function, presented with renal impairment during the fourth cycle of chemotherapy. After potential nephrotoxic factors were ruled out, capecitabine was discontinued and a kidney biopsy was performed, which displayed TMA lesions. An improvement in renal function was observed after definitive cessation of cytotoxic chemotherapy. Although rare, renal toxicity in the form of TMA may be associated with the use of cytotoxic agents such as gemcitabine, but there is no reported evidence of its association to capecitabine. Early withdrawal of the drug and nephrology consultation is necessary to prevent irreversible damage.

We describe, to our knowledge, the first case reported in the literature regarding the possible association of TMA and capecitabine.

Despite recent advances in the management of urothelial cancer (UC), cisplatin-based combination chemotherapy regimens remain critical. However, their use can be complicated in patients with chronic kidney disease (CKD), which is not uncommon in UC patients. Based on the Galsky criteria for cisplatin ineligibility, most patients with CKD will be excluded from receiving cisplatin-based chemotherapy altogether. For patients with borderline kidney function, several strategies - such as the use of split-dose cisplatin, dose reductions, or extra hydration - may facilitate the use of cisplatin, but these need to be prospectively validated. This review highlights the critical need for a multidisciplinary team, including onco-nephrologists, to help manage renal complications and optimize delivery of cancer care in complex UC patients with CKD.

Patients with renal insufficiency, usually defined as those with creatinine clearance < 40 mL/min, were excluded from pivotal clinical trials, especially in studies involving nivolumab therapy in patients with renal cell carcinoma (RCC). The aim of the study is to evaluate the efficacy and safety of nivolumab in patients with metastatic RCC (mRCC) stratified according to creatinine clearance.

Data from mRCC patients treated with nivolumab were retrospectively analyzed. Patients were classified into two categories according to their estimated glomerular filtration rate (eGFR); the first category (C1) included patients with eGFR < 40 mL/min/1.73 m2 and the second category (C2) included those with eGFR ≥ 40 mL/min/1.73 m2.

Of the 95 patients enrolled, 1. group included 26 patients (27.4%) and 2. group included 69 patients (72.6%). None of the pts in category 1 were on hemodialysis. Overall incidence of adverse events was not statistically different between the two groups (P = .469). The overall response rate ORR was 50% in the first group and 42.0% in the second group (P = .486). Median overall survival (OS) was longer with 23.3 months in the 2. group versus 11 months in the 1. group (P = .415).

Renal insufficiency is a common problem in patients with advanced renal cancer since they often undergo nephrectomy and their renal function may also worsen while receiving tyrosine kinase inhibitor therapy. We found that there is no significant difference in the safety and efficacy of nivolumab treatment between two groups. Nivolumab appears to be a safe and effective agent in patients with renal impairment.

Platinum-based chemotherapy, a widely used backbone of systemic cytotoxic anticancer treatment, is associated with nephrotoxicity. Currently, renal function is generally assessed prior to each administration of cisplatin or carboplatin, but there is no guideline regarding the frequency of renal function determination.

The primary objective was to determine the median time to a clinically relevant dosage adjustment (>10%) due to change in renal function in patients treated with cisplatin and carboplatin. Secondly, variables influencing changes in renal function were assessed.

We conducted a retrospective analysis of serial renal function assessments in platinum-treated patients with cancer in two academic medical centers, using a query to extract data from the electronic health records between 2017 and 2019.

In total, 512 patients receiving cisplatin and 628 patients receiving carboplatin were included. In total, 15% of all cisplatin-treated patients were found to have a renal function less than 60 mL/min at least once during treatment, with a median time to renal function decline of 67 days (range 5-96 days), which did not differ between treatment regimens. For carboplatin 21% of patients were found to have had a dosage variation of more than 10% at least once during treatment, with a median time-to-event period of 64 days (range 5-100 days).

Dose adjustments during platinum-based chemotherapy resulting from renal function decline occur after a median time of ≥64 days. Our data provide substantiated guidance to recommend renal function assessment during platinum-based chemotherapy in clinically stable patients to once every 3 weeks.

Cancer and kidney disease disproportionately impact Black patients. The CKD-EPI2021 equation was developed to estimate glomerular filtration rate (eGFR) without using race. We assessed the impact of using CKD-EPI2021 instead of CKD-EPI2009 or Cockcroft-Gault (CG) on dosing and eligibility of anticancer drugs in Black and non-Black patients. Utilizing the National Cancer Institute Theradex database, deindexed eGFR (mL/min) was calculated for 3931 patients (8.6 % Black) using CKD-EPI2021, CKD-EPI2009, and CG. Dosing simulations based on each eGFR were performed for ten anticancer drugs with kidney function-based eligibility or dosing cutoffs. eGFR differences using CKD-EPI2021 versus CKD-EPI2009 varied between Black and non-Black patients (p < 0.001); on average, Black patients had 10.3 mL/min lower eGFR and non-Black patients had 4.2 mL/min higher eGFR using CKD-EPI2021. This corresponded to a difference in relative odds of cisplatin ineligibility using CKD-EPI2021 versus CKD-EPI2009; Black patients had 48 % higher odds of ineligibility and non-Black patients had 27 % lower odds of ineligibility using CKD-EPI2021 (p < 0.001). When using CKD-EPI2021 versus CG, eGFR differences were similar between Black and non-Black patients (p = 0.679) and relative difference in odds of cisplatin ineligibility did not vary. Using CKD-EPI2021 versus CKD-EPI2009 differentially impacts Black versus non-Black cancer patients; Black patients have lower calculated eGFR and are less likely to receive full doses of drug using CKD-EPI2021. From the historical default of CG, adopting CKD-EPI2021 would not disparately impact patients based on race, but would result in Black patients being less likely to receive full doses of drug than if CKD-EPI2009 were used.

Due to the presence of other comorbidities and multi-therapeutic modalities in breast cancer, renally cleared chemotherapeutic regimens may cause nephrotoxicity. The aim of this retrospective study is to compare the chemotherapy types and outcomes in breast cancer patients with or without chronic renal disease.

We retrospectively enrolled 62 female patients with breast cancer and underlying late stages (stage 3b, 4, and 5) of chronic kidney disease (CKD) treated from 2000 to 2017. They were propensity score-matched 1:1 with patients in our database with breast cancer and normal renal function (total n = 124).

The main subtype of breast cancer was luminal A and relatively few patients with renal impairment received chemotherapy and anti-Her-2 treatment. The breast cancer patients with late-stage CKD had a slightly higher recurrent rate, especially at the locally advanced stage. The 5-year overall survival was 90.1 and 71.2% for patients without and with late-stage CKD, but the breast cancer-related mortality rate was 88.9 and 24.1%, respectively. In multivariate analyses, dose-reduced chemotherapy was an independent negative predictor of 5-year recurrence-free survival and late-stage CKD was associated with lower 5-year overall survival rate.

Breast cancer patients with late-stage CKD may receive insufficient therapeutic modalities. Although the recurrence-free survival rate did not differ significantly by the status of CKD, patients with breast cancer and late-stage CKD had shorter overall survival time but a lower breast cancer-related mortality rate, indicated that the mortality was related to underlying disease.

This review outlines the most up-to-date metastatic melanoma treatment recommendations and relevant risks for patients with solid organ transplants, patients with renal dysfunction, and patients with preexisting autoimmune conditions. These specific treatment populations were excluded from the original clinical trials, which studied immune checkpoint inhibitors and BRAF/MEK inhibitors in the advanced melanoma setting. We have synthesized the current body of literature, mainly case series and retrospective analyses, to reflect the evidence for the treatment of these special patient populations at present.

Bone metastases are frequently observed in advanced cancer, and bone modifying agents are used to prevent or treat skeletal-related events. Zoledronic acid is contraindicated in patients with severe renal impairment (Ccr < 30 mL/min), but it is not completely known whether denosumab can be used in them. We aimed to determine the association between renal function and hypocalcemia development during denosumab treatment.

We included patients with solid cancer and bone metastases who started denosumab treatment between April 2017 and March 2019. They were classified into four groups based on creatinine clearance (Ccr; mL/min): normal (Ccr ≥ 80), mild (50 ≤ Ccr ˂80), moderate (30 ≤ Ccr ˂50), and severe (Ccr ˂30). Hypocalcemia was evaluated using the Common Terminology Criteria for Adverse Events (v5.0) based on the albumin-adjusted serum calcium levels; its incidence (stratified by renal function) and risk factors were investigated using a Chi-square test and logistic regression analysis.

Of 524 patients (age: 69 ± 11 years; 303 men), 153 had a normal renal function and 222, 117, and 32 had mild, moderate, and severe renal dysfunction. The albumin-adjusted serum calcium level was higher than the measured (total) calcium level in most patients. The incidence of grade ≥ 1 hypocalcemia was 32.0% in the normal group and 37.4%, 29.9%, and 62.5% in the mild, moderate, and severe renal dysfunction groups, respectively. It was, therefore, higher in the severe renal dysfunction groups than in the normal group (P = 0.002). The incidence of grade ≥ 3 hypocalcemia did not differ significantly among the groups. Pre-treatment low serum calcium levels and severe renal dysfunction were risk factors for hypocalcemia.

Evaluating denosumab-induced hypocalcemia required albumin adjustment, and its incidence was high among patients with severe renal dysfunction. Reduced serum calcium levels and severely impaired renal function were associated with an elevated hypocalcemia risk.

Acute kidney injury (AKI) and chronic kidney disease (CKD) are common in cancer patients. AKI is a brutal and reversible condition which makes it hard to manage from a pharmacological perspective when patients are receiving anticancer regimens and other supportive care drugs, such as anticoagulants, analgesics and other drugs. In contrast to CKD, which is a slow progressive disease, there is no clear guidance on how to manage and/or modify the dosage of drugs during AKI. Indeed, the slow progression of CKD allows physicians to monitor the renal function by using the glomerular filtration rate. Consequently, publications have explored the management of drugs in cancer patients with CKD, which is currently not the same for AKI. There are no recommendations or suggestions on how to manage drug doses in case of AKI in cancer patients. This commentary explores the different options to manage drugs (anticancer drugs, anticoagulants, and other supportive care drugs) during AKI in cancer patients.

Although all patients with cancer-associated thrombosis (CAT) have a high morbidity and mortality risk, certain groups of patients are particularly vulnerable. This may expose the patient to an increased risk of thrombotic recurrence or bleeding (or both), as the benefit-risk ratio of anticoagulant treatment may be modified. Treatment thus needs to be chosen with care. Such vulnerable groups include older patients, patients with renal impairment or thrombocytopenia, and underweight and obese patients. However, these patient groups are poorly represented in clinical trials, limiting the available data, on which treatment decisions can be based. Meta-analysis of data from randomised clinical trials suggests that the relative treatment effect of direct oral factor Xa inhibitors (DXIs) and low molecular weight heparin (LMWH) with respect to major bleeding could be affected by advanced age. No evidence was obtained for a change in the relative risk-benefit profile of DXIs compared to LMWH in patients with renal impairment or of low body weight. The available, albeit limited, data do not support restricting the use of DXIs in patients with CAT on the basis of renal impairment or low body weight. In older patients, age is not itself a critical factor for choice of treatment, but frailty is such a factor. Patients over 70 years of age with CAT should undergo a systematic frailty evaluation before choosing treatment and modifiable bleeding risk factors should be addressed. In patients with renal impairment, creatine clearance should be assessed and monitored regularly thereafter. In patients with an eGFR<30mL/min/1.72m2, the anticoagulant treatment may need to be adapted. Similarly, platelet count should be assessed prior to treatment and monitored regularly. In patients with grade 3-4, thrombocytopenia (<50,000 platelets/μL) treatment with a LMWH at a reduced dose should be considered. For patients with CAT and low body weight, standard anticoagulant treatment recommendations are appropriate, whereas in obese patients, apixaban may be preferred.

The association between mildly decreased renal function and cardiovascular (CV) outcomes in cancer patients remains unestablished.

We sought to explore this association in asymptomatic self-referred healthy adults.

We followed 25, 274 adults, aged 40-79 years, who were screened in preventive healthcare settings. Participants were free of CV disease or cancer at baseline. The estimated glomerular filtration rate (eGFR) was calculated according to the CKD Epidemiology Collaboration equation and categorized into groups [≤59, 60-69, 70-79, 80-89, 90-99, ≥100 (ml/min/1.73 m²)]. The outcome included a composite of death, acute coronary syndrome, or stroke, examined using a Cox model with cancer as a time-dependent variable.

Mean age at baseline was 50 ± 8 years and 7973 (32%) were women. During a median follow-up of 6 years (interquartile range: 3-11), 1879 (7.4%) participants were diagnosed with cancer, of them 504 (27%) develop the composite outcome and 82 (4%) presented with CV events. Multivariable time-dependent analysis showed an increased risk of 1.6, 1.4, and 1.8 for the composite outcome among individuals with eGFR of 90-99 [95% confidence interval (CI): 1.2-2.1 P = 0.01], 80-89 (95% CI: 1.1-1.9, P = 0.01) and 70-79 (95% CI: 1.4-2.3, P < 0.001), respectively. The association between eGFR and the composite outcome was modified by cancer with 2.7-2.9 greater risk among cancer patients with eGFR of 90-99 and 80-89 but not among individuals free from cancer ( Pinteraction < 0.001).

Patients with mild renal impairment are at high risk for CV events and all-cause mortality following cancer diagnosis. eGFR evaluation should be considered in the CV risk assessment of cancer patients.

To investigate the risk of acute kidney injury (AKI) in patients with cancer following the initiation of proton pump inhibitors (PPIs) and potassium-competitive acid blocker (PCAB), considering sex and anti-cancer drug use. We conducted a self-controlled case-series study using the Japan Medical Data Center claims data from 12422 patients with cancer who were prescribed PPIs or PCAB between January 2017 and December 2019. Considering the timing of PPI or PCAB, control period (days -120 to -1), risk period 1 (days 0 to +30), and risk period 2 (days +31 to +365) were defined. To assess the incidence rate ratio (IRR) and 95% confidence interval (CI) as the risk ratio, we adjusted for anti-cancer drugs to assess the risk of AKI. Additionally, we also examined sex differences to identify the risk of AKI. AKI was observed in risk period 1 [2.05 (1.12-3.72), p = 0.0192], but a slight reduction was noted in risk period 2 [0.60 (0.36-1.00), p = 0.0481]. A sex-specific increase in the risk of AKI was observed only in males during risk period 1 [2.18 (1.10-4.32), p = 0.0260], with a reduction in risk period 2 [0.48 (0.26-0.89), p = 0.0200]. We identified an increased risk of AKI in patients with cancer starting PPIs or PCAB particularly in males within 30 d after PPI or PCAB initiation, emphasizing the need for vigilant monitoring and management of AKI in this patient population.

To provide an integrated approach for deprescribing practice in oncology setting.

The data on deprescribing in oncology settings has been retrieved from the PubMed, Scopus and Google Scholar. We used "deprescribing," "potentially inappropriate medication" and "cancer" as a keyword for the conducting general search. The articles relevant to guidelines or tools used to deprescribe in cancer care were included.

The nature of cancer, its treatment strategies, adverse effects of therapy and multimorbidity impact negatively on quality of life (QoL). Further, they invite polypharmacy which puts the patient at higher risk of drug-related problems like drug interactions, adverse drug reactions and addition of potentially improper medications, etc. In older adults with cancer, the incidence of potentially inappropriate medications (PIMs) was between 41% and 52%. Over the decades, multiple strategies have been developed to assess the appropriateness of therapy. One such approach is deprescribing. OncPal and oncoSTRIP (Systematic Tool to Reduce Inappropriate Prescribing) are the cancer specific guidelines whereas BEERs criteria, Screening Tool to Alert to Right Treatment/Screening Tool of Older Person's Prescriptions criteria (START/STOPP criteria), medication appropriateness index (MAI) are the cancer nonspecific tools to identify PIM among cancer patients. Here, we provided an integrative approach and algorithm for deprescribing in oncology setting which includes patient and caregiver goals, life expectancy (LE), review of medications, determining medication appropriateness, assessment of time to benefit (TTB), symptomatic and asymptomatic care, identifying medications to cease, implementation of the plan, monitoring and reviewing.

Deprescribing in oncology setting is a novel and effective patient-centric approach to counteract the use of PIM, which helps to mitigate polypharmacy, drug-drug interactions, and adverse effects.

In patients with renal impairment, we studied apatinib and its major metabolites (M1-1, M1-2, M1-6, and M9-2) for pharmacokinetics.

Subjects with different renal functions were given a single oral dose of apatinib mesylate tablets of 250 mg. Pharmacokinetic samples were collected at 1 hour before dosing,0.25, 0.5, 1, 2, 3, 4, 6, 8, 24, 48, 72, and 96 h after dosing. The pharmacokinetic parameters of apatinib and its major metabolites were calculated by noncompartmental analysis.

Comparing PK parameters of the mild or moderate renal impairment group with the healthy group: the geometric mean ratios of maximum observed drug concentration (Cmax), the area under the plasma drug concentration-time curve from time 0 to the final quantifiable time (AUC0-t), and the area under the plasma concentration-time curve from time 0 extrapolated to infinity (AUC0-inf) were all about one. No significant effect of mild and moderate renal impairment on apatinib pharmacokinetics was observed. Mild and moderate renal impairment was also not observed to have a significant effect on the pharmacokinetics of metabolites M1-1, M1-2, and M1-6. However, mild and moderate renal impairment had a certain increase in exposure to the metabolite M9-2. Considering that M9-2 has no inhibitory effect on protein tyrosine kinase, it has no clinical significance. In addition, the proportion of cumulative excretion of apatinib and its major metabolites was small and almost negligible in all three groups of subjects.

Patients with mild and moderate renal impairment do not need to adjust the dose of apatinib when using low dose (250 mg) apatinib.

BACKGROUND. Patients with cancer undergo frequent CT examinations with iodinated contrast media and may be uniquely predisposed to contrast-associated acute kidney injury (CA-AKI). OBJECTIVE. The purpose of this study was to develop and validate a model for predicting the risk of CA-AKI after contrast-enhanced CT in patients with cancer. METHODS. This retrospective study included 25,184 adult patients (12,153 men, 13,031 women; mean age, 62.3 ± 13.7 [SD] years) with cancer who underwent 46,593 contrast-enhanced CT examinations between January 1, 2016, and June 20, 2020, at one of three academic medical centers. Information was recorded regarding demographics, malignancy type, medication use, baseline laboratory values, and comorbid conditions. CA-AKI was defined as a 0.3-mg/dL or greater increase in serum creatinine level from baseline within 48 hours after CT or a 1.5-fold or greater increase in the peak measurement within 14 days after CT. Multivariable models accounting for correlated data were used to identify risk factors for CA-AKI. A risk score for predicting CA-AKI was generated in a development set (n = 30,926) and tested in a validation set (n = 15,667). RESULTS. CA-AKI occurred after 5.8% (2682/46,593) of CT examinations. The final multivariable model for predicting CA-AKI included hematologic malignancy, diuretic use, angiotensin-converting enzyme inhibitor or angiotensin receptor blocker use, chronic kidney disease (CKD) stage 3a, CKD stage 3b, CKD stage 4 or 5, serum albumin level less than 3.0 g/dL, platelet count less than 150 × 103/μL, 1+ or greater proteinuria on baseline urinalysis, diabetes mellitus, heart failure, and contrast medium volume 100 mL or greater. A risk score (range, 0-53 points) was generated with these variables. The most points (13) were for CKD stage 4 or 5 and for albumin level less than 3 g/dL. The frequency of CA-AKI progressively increased in higher risk categories. For example, in the validation set, CA-AKI occurred after 2.2% of CT examinations in the lowest risk category (score ≤ 4) and after 32.7% of CT examinations in the highest risk category (score ≥ 30). The Hosmer-Lemeshow test result indicated that the risk score was a good fit (p = .40). CONCLUSION. A risk model in which readily available clinical data are used to predict the likelihood of CA-AKI after contrast-enhanced CT in patients with cancer was developed and validated. CLINICAL IMPACT. The model may help facilitate appropriate implementation of preventive measures in the care of patients at high risk of CA-AKI.