BACKGROUND: Paediatric acute kidney injury (AKI) is associated with significant adverse outcomes such as increased mortality, progression to chronic kidney disease and longer length of stay in hospital. Postoperative AKI is a common and recognized complication after surgery in adults. In the paediatric population, AKI postoperatively to cardiac surgery has been extensively studied. However, the incidence of postoperative AKI after non-cardiac surgery is less clear. Therefore, we aim to assess the available literature on this topic.
METHODS: We will conduct a systematic review of observational and randomized controlled trials assessing the incidence of paediatric postoperative AKI after non-cardiac surgery. Pairs of reviewers will independently screen the literature and extract data and assess risk of bias from eligible studies. The databases Pubmed, Cochrane and Web of Sciences will be searched. We will conduct the review in accordance with the Preferred Reporting Items for Systematic Review and Meta-Analysis (PRISMA) guidelines and the Grading of Recommendation, Assessment, Development and Evaluation (GRADE) approach. If sufficient homogeneity within the included trials we will conduct meta-analyses.
CONCLUSIONS: This systematic review aims to investigate the incidence of postoperative AKI in the paediatric non-cardiac surgery population. The results of this review will provide a foundation for future research in the field of paediatric postoperative AKI.

Clostridial myonecrosis, commonly known as gas gangrene (GG), is a rapidly progressing and potentially fatal bacterial infection that primarily affects muscle and soft tissue. In the United States, the incidence of GG is roughly 1000 cases per year, while, in developing countries, the incidence is higher. This condition is most often caused by Clostridium perfringens, a Gram-positive, spore-forming anaerobic bacterium widely distributed in the environment, although other Clostridium species have also been reported to cause GG. The CP genome contains over 200 transport-related genes, including ABC transporters, which facilitate the uptake of sugars, amino acids, nucleotides, and ions from the host environment. There are two main subtypes of GG: traumatic GG, resulting from injuries that introduce Clostridium spores into deep tissue, where anaerobic conditions allow for bacterial growth and toxin production, and spontaneous GG, which is rarer and often occurs in immunocompromised patients. Clostridium species produce various toxins (e.g., alpha, theta, beta) that induce specific downstream signaling changes in cellular pathways, causing apoptosis or severe, fatal immunological conditions. For example, the Clostridium perfringens alpha toxin (CPA) targets the host cell\'s plasma membrane, hydrolyzing sphingomyelin and phosphatidylcholine, which triggers necrosis and apoptosis. The clinical manifestations of clostridial myonecrosis vary. Some patients experience the sudden onset of severe pain, swelling, and muscle tenderness, with the infection progressing rapidly to widespread tissue necrosis, systemic toxicity, and, if untreated, death. Other patients present with discharge, pain, and features of cellulitis. The diagnosis of GG primarily involves clinical evaluation, imaging studies such as X-rays, computer tomography (CT) scans, and culture. The treatment of GG involves surgical exploration, broad-spectrum antibiotics, antitoxin, and hyperbaric oxygen therapy, which is considered an adjunctive treatment to inhibit anaerobic bacterial growth and enhance the antibiotic efficacy. Early recognition and prompt, comprehensive treatment are critical to improving the outcomes for patients affected by this severe and life-threatening condition.

Metformin is a widely prescribed medication for the management of type 2 diabetes. It is known to have a high safety index; however, it can cause serious adverse effects such as lactic acidosis, particularly in patients with chronic kidney disease. Elderly patients are at higher risk of developing metformin-associated lactic acidosis (MALA) due to aging kidneys. We present an 82-year-old male with a past medical history of diabetes, stage 2 chronic kidney disease, atrial fibrillation on apixaban, stroke, and chronic stage 4 sacral decubitus ulcer who was sent to the emergency department (ED) for altered mental status. He was admitted to the intensive care unit for the management of septic shock, pulseless electrical activity (PEA) cardiac arrest, and acute hypoxemic respiratory failure requiring intubation. Laboratory tests showed lactic acidosis and anion gap metabolic acidosis in the absence of an infectious source. The patient had chronic kidney disease with acute renal failure on metformin. He was diagnosed with MALA. This case highlights the potential risks associated with metformin use in older adults with chronic kidney disease and acute kidney injury from infections, dehydration, and decreasing oral intake due to acute illness, aging, or dementia. There are expected physiological changes in the aging kidney, including cellular dysfunction and nephrosclerosis, that can cause unexpected kidney injury in older adults, causing their estimated glomerular filtration rate (eGFR) to drop acutely. Age-related changes in renal function and decreased clearance of drugs place elderly patients at higher risk of developing MALA. Guidelines for reducing or deprescribing metformin can be considered in older adults. This could prevent morbidity, mortality, and adverse outcomes in frail older adults with diabetes.

UNASSIGNED: AF is a global health concern, with systemic complications including renal dysfunction. This systematic review and meta-analysis compares the effects of rivaroxaban, a Factor Xa inhibitor, and vitamin K antagonists (VKAs) on renal outcomes in AF patients.
UNASSIGNED: The study protocol is registered in PROSPERO (ID: CRD42023462756). We systematically searched the PubMed, Embase and Cochrane Library databases from 1 January 2017 to 30 June 2023 for real-world studies comparing the effects of rivaroxaban and VKAs on renal outcomes in AF patients, including acute kidney injury, a .30% decrease in estimated glomerular filtration rate, doubling of serum creatinine and worsening renal function. Subgroup analyses targeted diabetes, pre-existing kidney disease, the elderly (age .65 years) and Asian populations. The risk of bias was assessed used the Robins-I tool. HRs and 95% CIs were synthesised through a random-effects model. Two sensitivity analyses were performed, using a fixed-effects model and excluding conference abstracts.
UNASSIGNED: We identified 1,666 records. After screening, 14 studies comparing rivaroxaban and VKAs were included. Rivaroxaban exhibited superiority over VKAs in preventing: acute kidney injury (HR 0.68; 95% CI [0.61.0.77]; p<0.00001); a .30% decrease in estimated glomerular filtration rate (HR 0.71; 95% CI [0.60.0.84]; p<0.0001); doubling of serum creatinine (HR 0.50; 95% CI [0.36.0.70]; p<0.0001); and worsening renal function (HR 0.56; 95% CI [0.45.0.69]; p<0.00001). Subgroup and sensitivity analyses consistently confirmed rivaroxaban\'s favourable effects on renal outcomes in diabetes, pre-existing kidney disease, the elderly and Asian populations.
UNASSIGNED: Our findings support the preference of rivaroxaban over VKAs for renal outcomes in AF. The findings endorse rivaroxaban as the preferred anticoagulant to mitigate renal complications, offering clinicians valuable insights for tailored strategies.

DRESS (Drug Rash with Eosinophilia and Systemic Symptoms) syndrome is a rare, life-threatening, hypersensitivity reaction. The prolonged course and non-specific symptoms of the condition make diagnosis challenging. We present a case of DRESS syndrome that was misdiagnosed as urticaria. Investigations revealed deranged liver and kidney functions and abnormal blood count. The presented case emphasizes the need to have a high suspicion for DRESS syndrome in patients who present with jaundice, generalized rash, acute renal failure, and acute liver failure.

Kidney-liver crosstalk plays a crucial role in normal and certain pathological conditions. In pathologic states, both renal-induced liver damage and liver-induced kidney diseases may happen through these kidney-liver interactions. This bidirectional crosstalk takes place through the systemic conditions that mutually influence both the liver and kidneys. Ischemia and reperfusion, cytokine release and pro-inflammatory signaling pathways, metabolic acidosis, oxidative stress, and altered enzyme activity and metabolic pathways establish the base of this interaction between the kidneys and liver. In these concomitant kidney-liver diseases, the survival rates strongly correlate with early intervention and treatment of organ dysfunction. Proper care of a nephrologist and hepatologist and the identification of pathological conditions using biomarkers at early stages are necessary to prevent the complications induced by this complex and potentially vicious cycle. Therefore, understanding the characteristics of this crosstalk is essential for better management. In this review, we discussed the available literature concerning the detrimental effects of kidney failure on liver functions and liver-induced kidney diseases.

The theory of fetal programming of adult diseases was first proposed by David J.P. Barker in the eighties of the previous century, to explain the higher susceptibility of some people toward the development of ischemic heart disease. According to his hypothesis, poor maternal living conditions during gestation represent an important risk factor for the onset of atherosclerotic heart disease later in life. The analysis of the early phases of fetal development is a fundamental tool for the risk stratification of children and adults, allowing the identification of susceptible or resistant subjects to multiple diseases later in life. Here, we provide a narrative summary of the most relevant evidence supporting the Barker hypothesis in multiple fields of medicine, including neuropsychiatric disorders, such as Parkinson disease and Alzheimer disease, kidney failure, atherosclerosis, coronary heart disease, stroke, diabetes, cancer onset and progression, metabolic syndrome, and infectious diseases including COVID-19. Given the consensus on the role of body weight at birth as a practical indicator of the fetal nutritional status during gestation, every subject with a low birth weight should be considered an \"at risk\" subject for the development of multiple diseases later in life. The hypothesis of the \"physiological regenerative medicine,\" able to improve fetal organs\' development in the perinatal period is discussed, in the light of recent experimental data indicating Thymosin Beta-4 as a powerful growth promoter when administered to pregnant mothers before birth.

Overhydration (OH) is a prevalent medical problem that occurs in patients with kidney failure, but a specific marker has still not been found. Patients requiring kidney replacement therapy suffer from a water imbalance, which is correlated with mortality rates in this population. Currently, clinicians employ techniques such as bioimpedance spectroscopy (BIS) and ultrasound (USG) markers of overhydration or markers of heart and kidney function, namely NT-pro-BNP, GFR, or creatinine levels. New serum markers, including but not limited to Ca-125, galectin-3 (Gal-3), adrenomedullin (AMD), and urocortin-2 (UCN-2), are presently under research and have displayed promising results. Ca-125, which is a protein mainly used in ovarian cancer diagnoses, holds great potential to become an OH marker. It is currently being investigated by cardiologists as it corresponds to the volume status in heart failure (HF) and ventricular hypertrophy, which are also associated with OH. The need to ascertain a more precise marker of overhydration is urgent mainly because physical examinations are exceptionally inaccurate. The signs and symptoms of overhydration, such as edema or a gradual increase in body mass, are not always present, notably in patients with chronic kidney disease. Metabolic disruptions and cachexia can give a false picture of the hydration status. This review paper summarizes the existing knowledge on the assessment of a patient\'s hydration status, focusing specifically on kidney diseases and the role of Ca-125.

Commonly associated with autoimmune and renal disorders, calcinosis cutis is a disorder of systemic calcium deposition in soft tissues. The pathophysiology of such deposition varies based on subtype, therefore treatment options vary not only in terms of severity of disease but also with subtype. This case report describes a 52-year-old female with systemic sclerosis and an extensive past medical history who initially presented with complaints of worsening left lower leg pain, a negative workup for deep vein thrombosis, and an extensive palpable mass in the posterior thigh with erythema, drainage, and purulence. With multiple treatment options exhausted from her autoimmune disorders, she ultimately required surgical resection for her refractory infected calcinosis cutis. Identification of calcinosis cutis subtype in conjunction with appropriate history and physical is crucial to determining indications for treatment.

OBJECTIVE: We present the case of a 67-year-old woman with severely reduced renal clearance suffering from ceftazidime-induced encephalopathy. Subsequently, we search the literature to review and describe the neurotoxicity of ceftazidime.
METHODS: A search string was developed to search PubMed for relevant cases from which relevant information was extracted. Using the collected data a ROC analysis was performed in R to determine a neurotoxicity threshold.
RESULTS: Our patient suffered from progressive loss of consciousness and myoclonic seizures, with improvements noted a few days after discontinuation of treatment. The dose was not appropriately reduced to take into account her reduced renal function. The highest ceftazidime concentration recorded was 234.9 mg/mL. Using the Naranjo score we found a probable relationship between our patient\'s encephalopathy and ceftazidime administration. In the literature we found a total of 32 similar cases, most of which also had some form of renal impairment. Using our collected data and ceftazidime concentrations provided in the literature, a ROC analysis provided a neurotoxicity threshold of 78 mg/L for ceftazidime neurotoxicity.
CONCLUSIONS: Ceftazidime-related neurotoxicity is a known issue, especially in patients with severe renal impairment. Yet no concrete toxicity threshold has been reported so far. We propose the first toxicity threshold for ceftazidime of 78 mg/L. Future prospective studies are needed to validate and optimize the neurotoxicity threshold as upper limit for ceftazidime therapeutic drug monitoring.