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Background/Objectives: Magnetic Resonance Imaging (MRI) is essential in diagnosing neurological conditions, offering detailed insights into brain pathology. Uremic encephalopathy (UE) is a severe neurological disorder resulting from renal failure, characterized by cognitive impairments and brain abnormalities due to the accumulation of uremic toxins (UTs). Despite extensive research on UTs, there is a significant gap in the detailed characterization of MRI findings in UE patients. This study aims to bridge this gap by conducting a comprehensive literature review of cerebral MRI findings in UE. We hypothesize that specific MRI patterns correlate with the severity and clinical manifestations of UE, thereby enhancing diagnostic accuracy and improving patient outcomes. Methods: A literature review was performed using PubMed, Cochrane Library, and Google Scholar. The search terms included "uremic encephalopathy MRI", "uremia and kidney failure MRI", and "toxic and metabolic or acquired encephalopathies MRI". The inclusion criteria were original articles on UE and MRI findings published in English. Results: Common MRI sequences include T1-weighted, T2-weighted, FLAIR, and DWI. Frequent MRI findings in UE are cytotoxic and vasogenic brain edema in regions such as the basal ganglia and periventricular white matter. Patterns like the "lentiform fork sign" and basal ganglia involvement are key indicators of UE. Conclusions: MRI plays a crucial role in diagnosing UE by identifying characteristic brain edema and specific patterns. A comprehensive diagnostic approach, incorporating clinical, laboratory, and imaging data, is essential for accurate diagnosis and management. The study calls for larger well-designed cohorts with long-term follow-up to improve the understanding and treatment of UE. [ABSTRACT FROM AUTHOR]

Background/Objectives: Magnetic Resonance Imaging (MRI) is essential in diagnosing neurological conditions, offering detailed insights into brain pathology. Uremic encephalopathy (UE) is a severe neurological disorder resulting from renal failure, characterized by cognitive impairments and brain abnormalities due to the accumulation of uremic toxins (UTs). Despite extensive research on UTs, there is a significant gap in the detailed characterization of MRI findings in UE patients. This study aims to bridge this gap by conducting a comprehensive literature review of cerebral MRI findings in UE. We hypothesize that specific MRI patterns correlate with the severity and clinical manifestations of UE, thereby enhancing diagnostic accuracy and improving patient outcomes. Methods: A literature review was performed using PubMed, Cochrane Library, and Google Scholar. The search terms included “uremic encephalopathy MRI”, “uremia and kidney failure MRI”, and “toxic and metabolic or acquired encephalopathies MRI”. The inclusion criteria were original articles on UE and MRI findings published in English. Results: Common MRI sequences include T1-weighted, T2-weighted, FLAIR, and DWI. Frequent MRI findings in UE are cytotoxic and vasogenic brain edema in regions such as the basal ganglia and periventricular white matter. Patterns like the “lentiform fork sign” and basal ganglia involvement are key indicators of UE. Conclusions: MRI plays a crucial role in diagnosing UE by identifying characteristic brain edema and specific patterns. A comprehensive diagnostic approach, incorporating clinical, laboratory, and imaging data, is essential for accurate diagnosis and management. The study calls for larger well-designed cohorts with long-term follow-up to improve the understanding and treatment of UE.

Key Clinical Message: A novel radiologic sign in patients with renal failure and uremic encephalopathy (UE) with metabolic acidosis has recently been identified as the lentiform fork sign. On magnetic resonance imaging (MRI), the "lentiform fork sign" has been described as bilateral symmetrical hyperintensities in the basal ganglia encircled by a hyperintese rim delineating the lentiform nucleus. Changes in uremic solute retention, aberrant blood–brain barrier transport, disordered vascular reactivity, altered electrolyte and acid–base balance, and altered hormone metabolism are the most likely causes of the condition. A 56‐year‐old male with end‐stage renal disease was brought to the emergency room for a progressive change in mental status and involuntary arm movements over the previous 5 days, which were accompanied by mild dyspnea. A brain MRI was performed, and it revealed hyperintensity on T2/FLAIR in the white matter surrounding the basal ganglia. the patient was treated with dialysis and improved greatly. Intensified hemodialysis and glycemic control are the cornerstones of treating diabetic uremic syndrome (DUS) with likely reversible clinical symptoms and remission of imaging abnormalities. [ABSTRACT FROM AUTHOR]

Background: Rapidly progressive glomerulonephritis (RPGN) is clinically manifestations as a rapidly progressive renal failure and pathologically as crescentic and necrotizing lesions with infiltration of inflammatory cells in the glomeruli. Uremic encephalopathy (UE) usually develops in patients who are suffering from acute or chronic renal failure. Objective: The purpose of this article is to provide reference for clinical diagnosis and treatment of renal disease complicated with seizures. Patients Two cases of anti‐glomerular basement membrane type rapidly progressive glomerulonephritis complicated with seizures were reported. Materials & Methods: In case 1, a 40‐year‐old woman was hospitalized for the treatment of nausea, anorexia, and fever. On admission, she presented with elevated serum inflammatory indicators, moderate anemia, and advanced acute kidney injury requiring hemodialysis. Her anti‐glomerular basement membrane (GBM) antibody in serum and renal tissues was found to be extremely high. She was finally diagnosed with anti‐GBM disease. She was treated with a combination of corticosteroid pulse therapy, oral cyclophosphamide and prednisolone, and plasma exchange, while continued to require maintenance hemodialysis for end‐stage kidney disease. During treatment, she suddenly suffered blindness, seizure, and consciousness disturbance. She was diagnosed as posterior reversible leukoencephalopathy syndrome by magnetic resonance imaging (MRI). The posterior reversible leukoencephalopathy syndrome subsided quickly after control of her hypertension and reinforcement of immunosuppressive treatment. In case 2, the patient also developed epileptic symptoms on the basis of GBM disease, and was given treatment similar to that of Case 1, so that the epileptic symptoms were controlled. Result: Reversible posterior leukoencephalopathy syndrome, especially when accompanied by cerebral hemorrhage, may lead to irreversible and lethal neurological abnormalities, and nephrologists should, therefore, be aware of the potential risk of reversible posterior leukoencephalopathy syndrome in patients with anti‐GBM disease. We can discuss the current two cases in the light of the previous literature. [ABSTRACT FROM AUTHOR]

Abstract Background Rapidly progressive glomerulonephritis (RPGN) is clinically manifestations as a rapidly progressive renal failure and pathologically as crescentic and necrotizing lesions with infiltration of inflammatory cells in the glomeruli. Uremic encephalopathy (UE) usually develops in patients who are suffering from acute or chronic renal failure. Objective The purpose of this article is to provide reference for clinical diagnosis and treatment of renal disease complicated with seizures. Patients Two cases of anti‐glomerular basement membrane type rapidly progressive glomerulonephritis complicated with seizures were reported. Materials & Methods In case 1, a 40‐year‐old woman was hospitalized for the treatment of nausea, anorexia, and fever. On admission, she presented with elevated serum inflammatory indicators, moderate anemia, and advanced acute kidney injury requiring hemodialysis. Her anti‐glomerular basement membrane (GBM) antibody in serum and renal tissues was found to be extremely high. She was finally diagnosed with anti‐GBM disease. She was treated with a combination of corticosteroid pulse therapy, oral cyclophosphamide and prednisolone, and plasma exchange, while continued to require maintenance hemodialysis for end‐stage kidney disease. During treatment, she suddenly suffered blindness, seizure, and consciousness disturbance. She was diagnosed as posterior reversible leukoencephalopathy syndrome by magnetic resonance imaging (MRI). The posterior reversible leukoencephalopathy syndrome subsided quickly after control of her hypertension and reinforcement of immunosuppressive treatment. In case 2, the patient also developed epileptic symptoms on the basis of GBM disease, and was given treatment similar to that of Case 1, so that the epileptic symptoms were controlled. Result Reversible posterior leukoencephalopathy syndrome, especially when accompanied by cerebral hemorrhage, may lead to irreversible and lethal neurological abnormalities, and nephrologists should, therefore, be aware of the potential risk of reversible posterior leukoencephalopathy syndrome in patients with anti‐GBM disease. We can discuss the current two cases in the light of the previous literature.

Key Clinical Message A novel radiologic sign in patients with renal failure and uremic encephalopathy (UE) with metabolic acidosis has recently been identified as the lentiform fork sign. On magnetic resonance imaging (MRI), the “lentiform fork sign” has been described as bilateral symmetrical hyperintensities in the basal ganglia encircled by a hyperintese rim delineating the lentiform nucleus. Changes in uremic solute retention, aberrant blood–brain barrier transport, disordered vascular reactivity, altered electrolyte and acid–base balance, and altered hormone metabolism are the most likely causes of the condition. A 56‐year‐old male with end‐stage renal disease was brought to the emergency room for a progressive change in mental status and involuntary arm movements over the previous 5 days, which were accompanied by mild dyspnea. A brain MRI was performed, and it revealed hyperintensity on T2/FLAIR in the white matter surrounding the basal ganglia. the patient was treated with dialysis and improved greatly. Intensified hemodialysis and glycemic control are the cornerstones of treating diabetic uremic syndrome (DUS) with likely reversible clinical symptoms and remission of imaging abnormalities.

Teaching point: Lentiform fork sign is a rare finding on MRI of the brain, found in patients with metabolic acidosis, in a critically ill patient with low consciousness and renal failure, this sign can correspond to uremic encephalopathy.

Lentiform fork sign is a rare neuroradiological abnormality with bilateral basal ganglion changes. It is seen in a variety of conditions characterized by metabolic acidosis, mostly seen with uremia of diabetic end-stage renal disease. Metabolic acidosis associated with uremia of acute pancreatitis has never been reported to be associated with this sign. Features of uremic encephalopathy are reversible with hemodialysis. The onset of worsening neurological symptoms along with a lack of improvement in encephalopathy despite hemodialysis must prompt the physician to do Magnetic Resonance Imaging (MRI) Brain in search of this sign. The scope of acute pancreatitis in its causation also needs to be investigated further. We report a case of acute kidney injury in a patient with acute pancreatitis who presented with metabolic acidosis and uremic encephalopathy. After initial improvement with hemodialysis, he gradually and sequentially went on to develop quadriplegia, generalized rigidity and distal upper limb tremor and later on full recovery along with lentiform fork sign on his MRI brain.

Chronic kidney disease (CKD) results in various central nervous systems (CNS) disorders including cognitive dysfunction, depression, anxiety, movement disorders, seizures and encephalopathy. Uremic retention products, oxidative stress, inflammation and impaired blood-brain barrier have been implicated as the major mediators of CKD-induced CNS disorders. However, mechanisms of CKD-induced cerebral tissue oxidative stress, inflammation and impaired blood brain barrier have not been fully elucidated and were explored. Male Sprague Dawley rats underwent sham operation or 5/6 nephrectomy and were observed for 10 weeks. Arterial pressure, body weight, and renal function were monitored. Under general anesthesia the animals' cerebral cortex was harvested. Nuclear translocations of NF-κB and Nrf2 and their key target gene products, neuronal, endothelial and inducible NO synthase (NOS) isoforms, markers of oxidative, nitrosative and myeloperoxidase reactions, fibrosis mediators and key protein constituents of capillary endothelial junctional complex were determined by Western blot analysis. The CKD rats exhibited reduced body weight, hypertension, elevated serum urea and creatinine concentrations. Compared to control group cerebral cortex of the CKD group showed activation (increased nuclear translocation) of NF-κB, elevation of pro-oxidant and pro-inflammatory molecules, diminished nuclear translocation of Nrf2 and expression of cytoprotective antioxidant molecules and depletion of the key protein constituents of endothelial junctional complex. In conclusion CKD results in the cerebral tissue activation of inflammatory and oxidative pathways, inhibition of antioxidant and cytoprotective system and erosion of cerebral capillary junctional complex, events that contribute to CNS dysfunction and impaired blood brain barrier.

The aim of this study was to investigate the magnetic resonance imaging (MRI) findings for the diagnose uremic encephalopathy and describe the usefulness of MRI findings in the ultimate diagnosis of uremic encephalopathy (UE). A total of 20 patients with uremic encephalopathy admitted to the hospital were evaluated in this prospective study. The clinical manifestations, laboratory and MRI imaging findings, demographic information, and clinical outcome were analyzed for each patient. We observed that the 20 prospectively reviewed patients with UE had no involvement of the basal ganglia or the lentiform fork sign (LFS). However, two-thirds of the patients had white matter involvement, and 80% of the subjects had cerebral or cortical atrophy. The arterial blood gas (ABG) analysis revealed that 50% of the patients suffered from metabolic acidosis (n=10). The results of the present study demonstrated that although the observation of Lentiform Fork Sign and Basal Ganglia involvement in MRI of UE patients is a specific finding the absence of which does not rule out UE. Thus, simultaneous examination of clinical manifestation and laboratory test analyses, along with imaging findings, should also be taken into account. [ABSTRACT FROM AUTHOR]

The aim of this study was to investigate the magnetic resonance imaging (MRI) findings for the diagnose uremic encephalopathy and describe the usefulness of MRI findings in the ultimate diagnosis of uremic encephalopathy (UE). A total of 20 patients with uremic encephalopathy admitted to the hospital were evaluated in this prospective study. The clinical manifestations, laboratory and MRI imaging findings, demographic information, and clinical outcome were analyzed for each patient. We observed that the 20 prospectively reviewed patients with UE had no involvement of the basal ganglia or the lentiform fork sign (LFS). However, two-thirds of the patients had white matter involvement, and 80% of the subjects had cerebral or cortical atrophy. The arterial blood gas (ABG) analysis revealed that 50% of the patients suffered from metabolic acidosis (n=10). The results of the present study demonstrated that although the observation of Lentiform Fork Sign and Basal Ganglia involvement in MRI of UE patients is a specific finding the absence of which does not rule out UE. Thus, simultaneous examination of clinical manifestation and laboratory test analyses, along with imaging findings, should also be taken into account.

Introduction: To find the real etiology of the twiling state could represent a challenge. Acute kidney injury is characterized by an abrupt increase of serum creatinine and urea levels along with a glomerular filtration below 15ml/min which can lead within hours or days to cognitive dysfunction. Case Report: We present a case of a 53 years old women, arrived at the emergency room with the following vital signs: obnubilation state, with tachypnea ( respiratory rate 25-30/min), respiratory effort, intercostal retraction, oxigen saturation pO2 90%, heart rate 99b/min, high blood pressure 188/90 mmHg and Glasgow Coma Scale (GCS) 9 points. Blood gas analysis revealed sever metabolic acidosis with hiperkalemia: Ph = 6,9, pCO2 = 18.9 mmHg, K+ = 7.21 mmol/L, HCO3 = 4.08 mmol/L. Blood tests showed microcytic hypochromic anemia, elevated levels of trombocytes (724.00 x 103/µL), leucocites (31.12 x 103/µL), acute phase reactants: C-reactive protein (CRP) = 90mg/dl and procalcitonin (PCT) = 232 mg/dl and extremely elevated serum creatinine level (19mg/dl) and urea 232mg/dl with a rate of kidney filtration < 3ml/min. At the nephrology examination was performed abdominal ultrasound which demonstrated : an abnormal mass developed in the bladder 81/54 mm with marked bilateral hydronephrosis stage 4 caused by post-renal obstruction, renal parenchymal index for the right kidney was 1.36 cm and for the left kidney was 0.8cm. Considering the worsening status of the patient the best therapeutic approach was to perform an emergent percutaneous nephrostomy for the left kidney. In the following 36h the patient presented a diuresis of 3.6 L/24h, with a favorable evolution of metabolic acidosis (pH = 6.9 - 7.25 - 7.36 - 7.4) and renal function, observed from progressively decreased values of creatinine and urea. The neurological status improved, the patient became hemodynamically stabel and was transferred to the urology department for further examinations. Discussions : The etiology of AKI is extremly wide, but we can classify it in 3 categories: pre-renal, renal and post-renal. One of the most serious complication is high serum urea levels which can cause uremic encephalopathy (UE). It is essential to make the differential diagnosis with the pathological conditions which can mimic UE such as cerebrovascular accidents, osmotic demyelination and infections. Conclusions: Considering the significant impact of AKI, a prompt recognition with early intervention is essential to prevent the sever complications of the brain, the kidneys and body physiology. [ABSTRACT FROM AUTHOR]

Background Uremic encephalopathy is defined as cerebral dysfunction due to toxin accumulation in patients with chronic kidney disease (CKD). This condition is characterized by subtle to florid symptoms, and its clinical course is always progressive when untreated but partially reversible with renal replacement therapy. While no test exists to measure subclinical uremic encephalopathy, two tests have been validated to measure minimal hepatic encephalopathy: the critical flicker frequency (CFF) test and the psychometric hepatic encephalopathy score (PHES). Objective To use CFF and PHES to measure the prevalence of cerebral dysfunction in individuals with CKD. Methods This cross-sectional study included a total of 69 patients with stage-5 CKD. Cutoff points for minimal encephalopathy were established using existing clinical guidelines: ≤39 Hz for CFF and

Objective: To describe the clinical profile and outcome of emergencies in children with chronic kidney disease (CKD). Methods: This retrospective analysis studied children with CKD presenting with acute emergencies. The clinical profile, renal and patient outcomes were compared between incidentally diagnosed - iCKD, previously diagnosed not on dialysis - pCKD and those on maintenance dialysis - dCKD groups. Results: 82 children (67 boys, median age - 8 years) with 99 visits were included. Uremic encephalopathy was the most common emergency in iCKD (64.7%) and pCKD (38.4 %), and access-related infections (32.1%) in dCKD group. Children with iCKD had higher Pediatric Risk of Mortality score (P<0.001), emergent initiation of dialysis (P=0.03) and discontinuation of treatment (P<0.001) when compared to the pCKD group. Conclusion: Uremic encephalopathy and access-related infections were the most common emergencies in children with CKD. Incidentally diagnosed CKD had a worse clinical profile and outcome. [ABSTRACT FROM AUTHOR]

Abstract Background Lentiform fork sign is a neuroradiological abnormality which is encountered in the clinical practice associated with uremic encephalopathy, dialysis disequilibrium syndrome and metabolic acidosis. Case presentation We describe here a case of this neuro-radiological abnormality which was encountered in a patient with uraemia and high anion gap metabolic acidosis who presented with generalised convulsion and later had some tremor in her hands. In our patient, there were few predisposing factors which might have possibly resulted in this abnormality chronic kidney disease, diabetes mellitus, and metabolic acidosis. Conclusion The Lentiform fork sign is a rare occurrence which can be related to a long list of toxic and metabolic causes but in conjunction with metabolic acidosis in chronic kidney disease patients, it can narrow down this list of alternate diagnosis.

The article reports that Uremic encephalopathy in patients with kidney failure features manifests with neurologic symptoms. Topics include Brain magnetic resonance imaging (MRI) is a useful tool for diagnosis of uremic encephalopathy; and findings are categorized into three types of image data with Cortical and subcortical white matter disorders for posterior reversible leukoencephalopathy.

Uremic encephalopathy is defined as cerebral dysfunction due to toxin accumulation in patients with chronic kidney disease (CKD). This condition is characterized by subtle to florid symptoms, and its clinical course is always progressive when untreated but partially reversible with renal replacement therapy. While no test exists to measure subclinical uremic encephalopathy, two tests have been validated to measure minimal hepatic encephalopathy: the critical flicker frequency (CFF) test and the psychometric hepatic encephalopathy score (PHES). To use CFF and PHES to measure the prevalence of cerebral dysfunction in individuals with CKD. This cross-sectional study included a total of 69 patients with stage-5 CKD. Cutoff points for minimal encephalopathy were established using existing clinical guidelines: ≤39 Hz for CFF and < −4 for PHES. All participants were also screened for cognitive function and depression. Eighteen cases (26.1%) of cerebral dysfunction linked to uremic encephalopathy were detected with CFF, while twelve (17.4%) were detected by PHES; only six cases (8.7%) were diagnosed by both methods. Half of the cases (50%) had diabetes, and 61% were on hemodialysis. Cognitive function scores did not differ significantly between those receiving dialysis, hemodialysis, or no renal replacement therapy. It is essential to identify cerebral dysfunction when uremic encephalopathy is in early subclinical stages to reduce preventable events as traffic and work accidents. [ABSTRACT FROM AUTHOR]

Abstract Background Uremic encephalopathy (UE), a toxic metabolic encephalopathy, is an uncommon complication resulting from endogenous uremic toxins in patients with severe renal failure. UE syndrome can range from mild inattention to coma. The imaging findings of UE include cortical or subcortical involvement, basal ganglia involvement and white matter involvement. The basal ganglia type is uncommon, although previous cases have reported that Asian patients with diabetes mellitus (DM) are usually affected. Case presentation A 32 year-old woman with a history of non-diabetic hemodialysis for 3 years suffered from severe involuntary movement, and brain magnetic resonance imaging showed symmetrical T2-weighted imaging (T2WI) and T2/fluid-attenuated inversion recovery (T2FLAIR) hyperintense nonhemorrhagic lesions in the bilateral basal ganglia. She was diagnosed with UE as syndrome of bilateral basal ganglia lesions, due to a combined effect of uremic toxins and hyperthyroidism. After treatment with high frequency and high flux dialysis, hyperbaric oxygen therapy and declining parathyroid hormone, the patient achieved complete remission with normal body movement and was discharged. Conclusion UE with basal ganglia involvement is uncommon, although generally seen in Asian patients with DM. Our case reported a hemodialysis patient that had non-diabetic UE with typical bilateral basal ganglia lesions, presenting with involuntary movement.

The high mortality rates associated with acute kidney injury are mainly due to extra-renal complications that occur following distant-organ involvement. Damage to these organs, which is commonly referred to as multiple organ dysfunction syndrome, has more severe and persistent effects. The brain and its sub-structures, such as the hippocampus, are vulnerable organs that can be adversely affected. Acute kidney injury may be associated with numerous brain and hippocampal complications, as it may alter the permeability of the blood-brain barrier. Although the pathogenesis of acute uremic encephalopathy is poorly understood, some of the underlying mechanisms that may contribute to hippocampal involvement include the release of multiple inflammatory mediators that coincide with hippocampus inflammation and cytotoxicity, neurotransmitter derangement, transcriptional dysregulation, and changes in the expression of apoptotic genes. Impairment of brain function, especially of a structure that has vital activity in learning and memory and is very sensitive to renal ischemic injury, can ultimately lead to cognitive and functional complications in patients with acute kidney injury. The objective of this review was to assess these complications in the brain following acute kidney injury, with a focus on the hippocampus as a critical region for learning and memory.

Teaching point: Lentiform fork sign is a rare finding on MRI of the brain, found in patients with metabolic acidosis, in a critically ill patient with low consciousness and renal failure, this sign can correspond to uremic encephalopathy., Competing Interests: The authors have no competing interests to declare., (Copyright: © 2024 The Author(s).)

This study investigates some clinical characteristics of maintenance hemodialysis patients with new‐onset epilepsy. Thirty‐five patients with new‐onset epilepsy who underwent maintenance hemodialysis were selected for study. Sixty patients undergoing routine hemodialysis were selected as the control group. We evaluated and compared the general characteristics, clinical features, and prognosis of patients in both groups. Investigation of the etiology of the 35 cases of new‐onset epilepsy identified 17 cases of metabolic encephalopathy, six cases of viral encephalitis, five cases of cerebral infarction, five cases of cerebral hemorrhage, and two cases of purulent meningitis. Among the 35 patients, 19 experienced improvement in their condition and 16 patients died. The overall mortality rate was 45.71%. There were statistically significant differences between the epilepsy group and control group in gender, incidence of fever, application of antibiotic treatment, levels of serum albumin, and the clinical course of hypertension (P < 0.05). Maintenance hemodialysis patients who experience new‐onset epilepsy are often critically ill with rapid progression of disease and a high mortality rate. Female dialysis patients complicated with infections, antibiotics use and hypoalbuminemia are more likely to develop epilepsy. [ABSTRACT FROM AUTHOR]

Abstract Background Uremic Encephalopathy (UE) is a neurological complication associated with acute or chronic renal failure. Imaging findings of UE may present involvement of the basal ganglia, cortical or subcortical regions, and white matter. We report a rare case of UE caused by neurogenic bladder with isolated brainstem involvement revealed by magnetic resonance imaging (MRI). Immediate therapy resulted in full recovery of neurological signs and changes on MRI. Case presentation A 14-year-old Han Chinese woman with a history of chronic renal failure caused by neurogenic bladder. On admission, she was unconscious and her pupils presented different sizes, while her vital signs were normal. MRI showed high signal in the dorsal pontine base and in the mid brain on fluid-attenuated inversion-recovery (FLAIR) imaging and on T2-weighted imaging while the signal was normal on diffusion-weighted images (DWI). Blood analysis revealed renal failure and acidosis. After urinary retention treatment and acidosis correction, the patient soon recovered. Follow-up MRI 2 months after the discharge revealed complete resolution of UE in the brainstem. Conclusion We reported a rare case of a patient with UE that had unusual imaging manifestations for whom timely diagnosis and treatment assured recovery.

The accumulation of uremic solutes in kidney failure may impair mental function. The present study profiled the accumulation of uremic solutes in the cerebrospinal fluid (CSF) in acute renal failure. CSF and plasma ultrafiltrate were obtained from rats at 48 h after sham operation (control; n + 10) or bilateral nephrectomy (n + 10) and analyzed using an established metabolomic platform. Two hundred forty-eight solutes were identified as uremic based on their accumulation in the plasma ultrafiltrate of nephrectomized compared with control rats. CSF levels of 124 of these solutes were sufficient to allow calculation of CSF-to-plasma ultrafiltrate concentration ratios. Levels of many of the uremic solutes were normally lower in the CSF than in the plasma ultrafiltrate, indicating exclusion of these solutes from the brain. CSF levels of the great majority of the uremic solutes increased in renal failure. The increase in the CSF was, however, relatively less than in the plasma ultrafiltrate for most solutes. In particular, for the 31 uremic solutes with CSFto-plasma ultrafiltrate ratios of 0.25 in control rats, the average CSF-to-plasma ultrafiltrate ratio decreased from 0.13 = 0.07 in control rats to 0.09 = 0.06 in nephrectomized rats, revealing sustained ability to exclude these solutes from the brain. In summary, levels of many uremic solutes are normally kept lower in the CSF than in the plasma ultrafiltrate by the action of the blood-brain and blood-CSF barriers. These barriers remain functional but cannot prevent accumulation of uremic solutes in the CSF when the kidneys fail. [ABSTRACT FROM AUTHOR]

Introduction: Uremic syndrome of chronic kidney disease (CKD) is a term used to describe clinical, metabolic, and hormonal abnormalities associated with progressive kidney failure. It is a rapidly growing public health problem worldwide. Nervous system complications occur in every patient with uremic syndrome of CKD. Areas covered: This review summarized central and peripheral nervous system complications of uremic syndrome of CKD and their pathogenic mechanisms. They include cognitive deterioration, encephalopathy, seizures, asterixis, myoclonus, restless leg syndrome, central pontine myelinolysis, stroke, extrapyramidal movement disorders, neuropathies, and myopathy. Their pathogenic mechanisms are complex and multiple. They include (1) accumulation of uremic toxins resulting in neurotoxicity, blood-brain barrier injury, neuroinflammation, oxidative stress, apoptosis, brain neurotransmitters imbalance, ischemic/microvascular changes, and brain metabolism dysfunction (e.g. dopamine deficiency), (2) metabolic derangement (as acidosis, hypocalcemia, hyperphosphatemia, hypomagnesemia, and hyperkalemia); (3) secondary hyperparathyroidism, (4) erythropoietin and iron deficiency anemia, (5) thiamin, vitamin D, and other nutritional deficiencies, (6) hyperhomocysteinemia, and (7) coagulation problems. Expert commentary: Nervous system complications of uremia contribute to the patients' morbidity and mortality. Optimizing renal replacement therapy, correction of associated metabolic and medical conditions, and improved understanding of possible pathogenic mechanisms of these complications is a major target for their prevention and treatment. [ABSTRACT FROM AUTHOR]

The high mortality rates associated with acute kidney injury are mainly due to extra-renal complications that occur following distant-organ involvement. Damage to these organs, which is commonly referred to as multiple organ dysfunction syndrome, has more severe and persistent effects. The brain and its sub-structures, such as the hippocampus, are vulnerable organs that can be adversely affected. Acute kidney injury may be associated with numerous brain and hippocampal complications, as it may alter the permeability of the blood-brain barrier. Although the pathogenesis of acute uremic encephalopathy is poorly understood, some of the underlying mechanisms that may contribute to hippocampal involvement include the release of multiple inflammatory mediators that coincide with hippocampus inflammation and cytotoxicity, neurotransmitter derangement, transcriptional dysregulation, and changes in the expression of apoptotic genes. Impairment of brain function, especially of a structure that has vital activity in learning and memory and is very sensitive to renal ischemic injury, can ultimately lead to cognitive and functional complications in patients with acute kidney injury. The objective of this review was to assess these complications in the brain following acute kidney injury, with a focus on the hippocampus as a critical region for learning and memory. [ABSTRACT FROM AUTHOR]

Neurological complications are common in patients with acute or chronic renal failure, especially when there is marked reduction in the glomerular filtration rate (GFR). One such clinical syndrome, uremic encephalopathy (UE), occurs due to widespread dysfunction of central nervous system (CNS). It manifests with myriad clinical features and usually is suggested by bedside elicitation of asterixis (flapping tremor). Symptomatic involvement of the basal ganglia manifesting as choreoathetosis and clinical and radiological resolution with hemodialysis has been reported in the medical literature, but only rarely. The present report details such a case. [ABSTRACT FROM AUTHOR]

Uremic encephalopathy is a severe complication of renal failure. The underlying pathogenesis is unknown although several mechanisms have been suggested. Renal failure causes oxidative stress leading to cardiovascular complications. It has been suggested as the potential mediator of uremic encephalopathy as well, but it is largely unknown whether brain tissue itself undergoes oxidative damage in uremia. The aim of our experiment was to analyze oxidative stress markers in different brain regions in an animal model of acute kidney injury (AKI). AKI was induced by ischemia-reperfusion injury in male Wistar rats. Urine was collected in metabolic cages after 24 h. Samples of plasma and several brain regions were collected after 48 h. Markers of lipid peroxidation, protein oxidation and total antioxidant capacity were assessed. Renal failure was confirmed by high plasma creatinine, urea and urinary albumin to creatinine ratio. Our data confirmed increased systemic oxidative stress in the AKI group with plasma concentrations of markers of oxidative damage being twice as high compared to the sham-operated control group. No effect was seen in the urine. In the hippocampus, lipid and protein oxidation was higher, while antioxidant capacity was lower in the rats with AKI. Lipid oxidation markers in the frontal cortex were higher by 33%. No differences to controls were found in the cerebellum and hypothalamus. In conclusion, our results indicate that AKI leads to oxidative stress in the brain, especially in the hippocampus and in the frontal cortex. This kidney-brain crosstalk mediated by increased oxidative stress might explain some of the symptoms of uremic encephalopathy. The causes and consequences of oxidative damage observed in the brain during AKI remain to be elucidated. [ABSTRACT FROM AUTHOR]

Background and objectives: Uremic encephalopathy is the most important complication of renal failure and urgent dialysis treatment is required. Parathormone (PTH) contributes to the etiopathogenesis of uremic encephalopathy. PTH is a hormone that acts in the calcium balance in the organism. The aim of our study was to investigate the effect of serum adjusted and ionized calcium on the development of uremic encephalopathy in patients with acute renal injury (acute kidney injury network (AKIN) stage 3). Materials and Methods: Our study was supported by Canakkale Onsekiz Mart University Scientific Research Projects Unit (ID:1278). Three groups were formed for the study. The first group was acute renal failure AKIN stage 3 (N: 23), the second group was AKIN stage 3, and the patients who had emergency hemodialysis (N: 17) and the third group (N: 9) had AKIN stage 3 hemodialysis due to uremic encephalopathy. In these patient groups, 25-hydroxy vitamin D, PTH, calcium, albumin, urea, creatinine, and blood-gas-ionized calcium were observed in their serum during the first application. Calcium, albumin, urea, creatinine, and ionized calcium in blood gas were also examined in serum at 24th and 72th hours. Data were analyzed using SPSS version 19.0. Kruskal–Wallis test and Mann–Whitney U test were applied for the variables that did not comply with normal distribution. p < 0.005 was accepted statistically. Results: A statistically significant difference was found between the measurement creatinine values at the 24th and 72th hours of admission in AKIN stage 3 patients who applied to the emergency department (p = 0.008). A statistically significant difference was found in the measured calcium values (p = 0.013). A statistically significant difference was found in the measured ionized calcium values (p = 0.035). Conclusions: In our study, the effect of ionized calcium level on uremic encephalopathy in serum creatinine, calcium, and blood gas in patients presenting with acute renal injury, AKIN stage 3, was significant, but studies with new and large groups are needed.

An 81-year-old woman was hospitalized with progressive consciousness disturbance. Blood tests showed acidemia with severe renal dysfunction, and a cerebral spinal fluid (CSF) test showed pleocytosis with myelin basic protein (MBP) elevation. Brain magnetic resonance imaging showed unilaterally dominant subcortical white matter lesions with lentiform fork sign on T2-weighted imaging. After initiating hemodialysis, her consciousness disturbance and white matter lesions improved, suggesting uremic encephalopathy (UE). Unilaterally dominant leukoencephalopathy and high pleocytosis with MBP elevation in CSF are less common than previously identified characteristics of UE. When unilateral leukoencephalopathy occurs in patients with renal failure, UE should be considered.

Thrombotic thrombocytopenic purpura (TTP) is a rare variant of thrombotic microangiopathy. We report a case of TTP in a Nigerian chronic kidney disease (CKD) patient who was previously on clopidogrel. The features of TTP resolved soon after clopidogrel was withdrawn. Clopidogrel is a cardio-protective anti-platelet drug used in CKD patients at risk of dyspepsia. However, its potential to cause TTP should be recognized and considered in acute kidney injury (AKI) patients previously on clopidogrel., (© 2023 Ndulue CN et al.)

Objectives: To noninvasively assess global cerebral blood flow (CBF), oxygen extraction fraction (OEF) and cerebral metabolic rate of oxygen (CMRO2) in young adults with end-stage renal disease (ESRD).Methods: Thirty-six patients and 38 healthy volunteers were included and took part in MR examinations, blood and neuropsychological tests. CBF and OEF were measured by phase-contrast and T2-relaxation-under-spin-tagging MRI techniques, respectively. CMRO2 was computed from CBF, OEF and hematocrit according to Fick's principle. Correlations were performed between MR measurements, blood biochemistry measurements and neuropsychological test scores.Results: Compared with controls, ESRD patients had elevated CBF (72.9 ± 12.5 vs. 63.8 ± 8.5 ml min(-1) 100 g(-1), P < 0.001), elevated OEF (47.2 ± 10.2 vs. 35.8 ± 5.4 %, P < 0.001), but unaffected CMRO2 (199.5 ± 36.4 vs. 193.8 ± 28.6 μmol O2 min(-1) 100 g(-1), P = 0.879). Hematocrit negatively correlated with CBF (r = -0.640, P < 0.001) and OEF (r = -0.701, P < 0.001), but not with CMRO2. Altered neuropsychological test scores of ESRD patients were associated with OEF and CBF, but not with CMRO2. There were weak relationships between eGFR and hematocrit (r = 0.308, P = 0.068) or CBF (r = 0.318, P = 0.059).Conclusion: Our findings suggested that anaemic young adults with ESRD may afford higher CBF and OEF to maintain a normal CMRO2. Despite this compensatory process, however, cognitive function was still impaired and its severity was correlated with their CBF and OEF abnormality.Key Points: • Anaemic young adults with ESRD may afford higher CBF and OEF. • Anaemic young adults with ESRD maintain a normal CMRO 2 . • Cognitive function was still impaired in young ESRD adults. • The severity of cognitive dysfunction correlated with CBF and OEF changes. [ABSTRACT FROM AUTHOR]

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