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Onconephrology is a new subspecialty of nephrology that recognizes the important intersections of kidney disease with cancer. This intersection takes many forms and includes drug-induced nephrotoxicity, electrolyte disorders, paraneoplastic glomerulonephritis, and the interactions of chronic kidney disease with cancer. Data clearly demonstrate that, when patients with cancer develop acute or chronic kidney disease, outcomes are inferior, and the promise of curative therapeutic regimens is lessened. This highlights the imperative for collaborative care between oncologists and nephrologists in recognizing and treating kidney disease in patients with cancer. In response to this need, specific training programs in onconephrology as well as dedicated onconephrology clinics have appeared. This comprehensive review covers many of the critical topics in onconephrology, with a focus on acute kidney injury, chronic kidney disease, drug-induced nephrotoxicity, kidney disease in stem cell transplantation, and electrolyte disorders in patients with cancer.

Key Points The majority of patients with chronic kidney disease (CKD) incur neurological complications that might improve following renal transplantation Proteinuria, decreased glomerular filtration rate (GFR), and increased cystatin C are risk factors for cerebrovascular disease, which is in turn a risk factor for ongoing kidney dysfunction Stroke is a major complication of CKD in elderly patients undergoing dialysis; conventional ischaemic risk factors, as well as dialysis itself, can contribute to the development of stroke Patients undergoing dialysis often develop delirium after dialysis sessions, as well as chronic dementia, with prominent deficits in executive function and memory that are independent of age Systemic inflammation, oxidative stress, and dysregulation of sodium, potassium, and water channels in acute kidney injury can lead to brain injury, dysfunction, and oedema The kidney and the brain exhibit extensive organ crosstalk due to similarities in their vasculature and shared humoral and non-humoral pathways. In this Review, Claudio Ronco et al . evaluate the effects of chronic kidney disease, end-stage renal disease, and acute kidney injury on cognitive and cerebrovascular function. The authors also highlight the risk factors for cognitive impairment in patients undergoing dialysis. Patients with kidney disease often exhibit multiple organ dysfunction that is caused, in part, by marked connectivity between the kidney and other organs and tissues. Substantial crosstalk occurs between the kidney and the brain, as indicated by the frequent presentation of neurological disorders, such as cerebrovascular disease, cognitive impairment, and neuropathy during the natural history of chronic kidney disease. The underlying pathophysiology of such comorbid neurological disorders in kidney disease is governed by shared anatomic and vasoregulatory systems and humoral and non-humoral bidirectional pathways that affect both the kidney and the brain. During acute kidney injury, the brain and kidney might interact through the amplification of cytokine-induced damage, extravasation of leukocytes, oxidative stress, and dysregulation of sodium, potassium, and water channels. The advent of dialysis and renal transplantation programmes has led to a reduction in the rate of neurological complications associated with uraemia, but a new set of complications have arisen as a consequence of the effects of dialysis on the central nervous system over the short and long term. This Review discusses the clinical complications of acute and chronic renal failure from a neurologic perspective, and highlights current understanding of the underlying pathophysiologies.

Sepsis is the leading cause of acute kidney injury (AKI) in the intensive care unit (ICU). Septic AKI is a complex and multifactorial process that is incompletely understood. During sepsis, the disruption of the mucus membrane barrier, a shift in intestinal microbial flora, and microbial translocation may lead to systemic inflammation, which further alters host immune and metabolic homeostasis. This altered homeostasis may promote and potentiate the development of AKI. As part of this vicious cycle, when AKI develops, the clearance of inflammatory mediators and metabolic products is decreased. This will lead to further gut injury and breakdown in mucous membrane barriers. Thus, changes in the gut during sepsis can initiate and propagate septic AKI. This deleterious gut–kidney crosstalk may be a potential target for therapeutic maneuvers. This review analyses the underlying mechanisms in gut–kidney crosstalk in septic AKI.

Approximately 20% of patients with acute brain injury (ABI) also experience acute kidney injury (AKI), which worsens their outcomes. The metabolic and inflammatory changes associated with AKI likely contribute to prolonged brain injury and edema. As a result, recognizing its presence is important for effectively managing ABI and its sequelae. This review discusses the occurrence and effects of AKI in critically ill adults with neurological conditions, outlines potential mechanisms connecting AKI and ABI progression, and highlights AKI management principles. Tailored approaches include optimizing blood pressure, managing intracranial pressure, adjusting medication dosages, and assessing the type of administered fluids. Preventive measures include avoiding nephrotoxic drugs, improving hemodynamic and fluid balance, and addressing coexisting AKI syndromes. ABI patients undergoing renal replacement therapy (RRT) are more susceptible to neurological complications. RRT can negatively impact cerebral blood flow, intracranial pressure, and brain tissue oxygenation, with effects tied to specific RRT methods. Continuous RRT is favored for better hemodynamic stability and lower risk of dialysis disequilibrium syndrome. Potential RRT modifications for ABI patients include adjusted dialysate and blood flow rates, osmotherapy, and alternate anticoagulation methods. Future research should explore whether these strategies enhance outcomes and if using novel AKI biomarkers can mitigate AKI-related complications in ABI patients. Graphical abstract

Background: Epidemics of chronic kidney disease of uncertain etiology (CKDu) are occurring on the Pacific coast of Central America, in Sri Lankan and Indian agricultural communities, and in other hotspots around the world. CKDu primarily affects male agricultural workers, and traditional risk factors such as diabetes and hypertension are not involved in the pathogenesis. Although a causal factor has not yet been identified, culprits include repeated volume depletion-induced kidney injury, as well as exposure to agrichemicals, heavy metals and nephrotoxins contained in drugs, beverages, and traditional medications. Multiple risk factors may interact in a synergistic fashion thus resulting in chronic kidney damage. The absence of undefined protective factors may amplify the risk. Summary: This review focuses on the current understanding of CKDu by analyzing epidemiology, potential risk factors, and clinical and pathological features as well as geographical peculiarities of each disease. We also focus our attention on the etiology of these conditions in which multiple factors may synergistically contribute to the development and progression of the disease. The last part of the manuscript is dedicated to the research agenda and practical recommendations. Key Messages: Since renal replacement therapy is not extensively available in areas where CKDu is widespread, prevention by avoiding all known potential risk factors is crucial. Innovative healthcare solutions and social policies in endemic areas along with collaborative clinical research projects are needed to better identify factors involved in disease promotion and progression.

The incidence of acute kidney injury, which is common in patients with cancer, depends on the type and stage of cancer, the treatment regimen, and coexisting conditions. This review provides an overview of acute kidney injury in patients with cancer. Acute kidney injury is common in patients with cancer 1 , 2 ; the incidence and severity vary, depending on the type and stage of cancer, the treatment regimen, and coexisting conditions. 3 In a 7-year Danish study of 37,267 incident cases of cancer, the 1-year risk of acute kidney injury, as defined by the risk, injury, failure, loss of kidney function, and end-stage kidney disease (RIFLE) classification (Table 1), was 17.5%. 4 The 5-year risk for the individual risk, injury, and failure categories was 27.0%, 14.6%, and 7.6%, respectively. Furthermore, 5.1% of patients in whom acute kidney injury developed required long-term dialysis within . . .

Aims High‐flow arteriovenous fistula (AVF) for haemodialysis leads to profound haemodynamic changes and sometimes to heart failure (HF). Cardiac output (CO) is divided between the AVF and body tissues. The term effective CO (COef) represents the difference between CO and AVF flow volume (Qa) and better characterizes the altered haemodynamics that may result in organ hypoxia. We investigated the effects of Qa reduction on systemic haemodynamics and on brain oxygenation. Methods and results This is a single‐centre interventional study. Twenty‐six patients on chronic haemodialysis with high Qa (>1500 mL/min) were indicated for surgical Qa reduction for HF symptoms and/or signs of structural heart disease on echocardiography. The included patients underwent three sets of examinations: at 4 months and then 2 days prior and 6 weeks post‐surgical procedure. Clinical status, echocardiographical haemodynamic assessment, Qa, and brain oximetry were recorded. All parameters remained stable from selection to inclusion. After the procedure, Qa decreased from 3.0 ± 1.4 to 1.3 ± 0.5 L/min, P < 0.00001, CO from 7.8 ± 1.9 to 6.6 ± 1.5 L/min, P = 0.0002, but COef increased from 4.6 ± 1.4 to 5.3 ± 1.4 L/min, P = 0.036. Brain tissue oxygen saturation increased from 56 ± 11% to 60 ± 9%, P = 0.001. Conclusions Qa reduction led to increased COef. This was explained by a decreased proportion of CO running through the AVF in patients with Qa > 2.0 L/min. These observations were mirrored by higher brain oxygenation and might explain HF symptoms and improved haemodynamics even in asymptomatic high Qa patients.

The care of patients with acute kidney injury (AKI) has been limited due to the lack of effective therapeutics that can either prevent AKI during high-risk situations or treat AKI once established. A revolution in the scientific understanding of the pathogenesis of AKI has led to the identification of potential therapeutic targets. These targets include pathways involved in inflammation, cellular repair and fibrosis, cellular metabolism and mitochondrial function, oxidative stress, apoptosis, and hemodynamics and oxygen delivery. Many compounds are entering early-phase clinical trials. In addition, efforts to better describe sub-categories of AKI (through endo-phenotyping) hold promise to target therapies more effectively based upon pathways that are operative in the pathogenesis. These advances bring optimism that the care of patients with AKI will be transformed with the hope of better outcomes.

Hypomagnesemia is a frequent and often underrecognized electrolyte disturbance with important clinical consequences, especially in hospitalized and critically ill patients. This multifactorial condition arises from impaired intestinal absorption, renal magnesium wasting, and the effects of various medications. Magnesium, the second most abundant intracellular cation, is crucial in enzymatic and physiological processes; its deficiency is associated with neuromuscular, cardiovascular, and metabolic complications. This narrative review focuses on the mechanisms and clinical consequences of drug-induced hypomagnesemia, highlighting the major drug classes involved such as diuretics, antibiotics, antineoplastic agents, and immunosuppressants. Management strategies include magnesium supplementation and adjunctive therapies like amiloride and SGLT2 inhibitors to reduce renal magnesium losses. Recognizing and addressing drug-induced hypomagnesemia is essential to improve patient outcomes and prevent long-term complications.