Background: The etiology of acute metabolic acidosis (aMA) is heterogeneous, and the consequences are potentially life-threatening. The aim of this article was to summarize the causes and management of aMA from a clinician's perspective. Summary: We performed a systematic search on PubMed, applying the following search terms: "acute metabolic acidosis," "lactic acidosis," "metformin" AND "acidosis," "unbalanced solutions" AND "acidosis," "bicarbonate" AND "acidosis" AND "outcome," "acute metabolic acidosis" AND "management," and "acute metabolic acidosis" AND "renal replacement therapy (RRT)/dialysis." The literature search did not consider diabetic ketoacidosis at all. Lactic acidosis evolves from various conditions, either with or without systemic hypoxia. The incidence of metformin-associated aMA is actually quite low. Unbalanced electrolyte preparations can induce hyperchloremic aMA. The latter potentially worsens kidney-related outcome parameters. Nevertheless, prospective and controlled data are missing at the moment. Recently, bicarbonate has been shown to improve clinically relevant endpoints in the critically ill, even if higher pH values (> 7.3) are targeted. New therapeutics for aMA control are under development, since bicarbonate treatment can induce serious side effects. Key Messages: aMA is a frequent and potentially life-threatening complication of various conditions. Lactic acidosis might occur even in the absence of systemic hypoxia. The incidence of metformin-associated aMA is comparably low. Unbalanced electrolyte solutions induce hyperchloremic aMA, which most likely worsens the renal prognosis of critically ill patients. Bicarbonate, although potentially deleterious due to increased carbon dioxide production with subsequent intracellular acidosis, improves kidneyrelated endpoints in the critically ill.

Acute kidney injury (AKI) affects increasing numbers of in-hospital patients in Central Europe and the USA, the prognosis remains poor. Although substantial progress has been achieved in the identification of molecular/cellular processes that induce and perpetuate AKI, more integrated pathophysiological perspectives are missing. Metabolomics enables the identification of low-molecular-weight (< 1.5 kD) substances from biological specimens such as certain types of fluid or tissue. The aim of the article was to review the literature on metabolic profiling in experimental AKI and to answer the question if metabolomics allows the integration of distinct pathophysiological events such as tubulopathy and microvasculopathy in ischemic and toxic AKI. The following databases were searched for references: PubMed, Web of Science, Cochrane Library, Scopus. The period lasted from 1940 until 2022. The following terms were utilized: “acute kidney injury” OR “acute renal failure” OR “AKI” AND “metabolomics” OR “metabolic profiling” OR “omics” AND “ischemic” OR “toxic” OR “drug-induced” OR “sepsis” OR “LPS” OR “cisplatin” OR “cardiorenal” OR “CRS” AND “mouse” OR “mice” OR “murine” OR “rats” OR “rat”. Additional search terms were “cardiac surgery”, “cardiopulmonary bypass”, “pig”, “dog”, and “swine”. In total, 13 studies were identified. Five studies were related to ischemic, seven studies to toxic (lipopolysaccharide (LPS), cisplatin), and one study to heat shock-associated AKI. Only one study, related to cisplatin-induced AKI, was performed as a targeted analysis. The majority of the studies identified multiple metabolic deteriorations upon ischemia/the administration of LPS or cisplatin (e.g., amino acid, glucose, lipid metabolism). Particularly, abnormalities in the lipid homeostasis were shown under almost all experimental conditions. LPS-induced AKI most likely depends on the alterations in the tryptophan metabolism. Metabolomics studies provide a deeper understanding of pathophysiological links between distinct processes that are responsible for functional impairment/structural damage in ischemic or toxic or other types of AKI.

Background: Over the last decades, acute kidney injury (AKI) has been identified as a potentially fatal diagnosis which substantially increases in-hospital mortality in the short term and morbidity/mortality in the long term. However, reliable biomarkers for predicting AKI-associated outcomes are still missing. In this study, we assessed whether serum sodium, measured at different time points during the in-hospital treatment period, provided prognostic information in AKI.Methods: This was a retrospective, observational cohort study. AKI subjects were identified via the in-hospital AKI alert system. Serum sodium and potassium levels were documented at five pre-defined time points: hospital admission, AKI onset, minimum estimated glomerular filtration rate, minimum and maximum of the respective electrolyte during the treatment period. In-hospital death, the need for kidney replacement therapy (KRT) and recovery of kidney function were defined as endpoints.Results: Patients who suffered in-hospital death (n = 37, 23.1%) showed significantly higher serum sodium levels at diagnosis of AKI (survivors: 145.7 ± 2.13 vs. non-survivors: 138.8 ± 0.636 mmol/L, P = 0.003). A logistic regression model was significant for serum sodium levels in patients with in-hospital death (X 2 , P = 0.003; odds ratio = 1.08 (1.022 -1.141); R 2 = 0.082; d = 0.089). This suggests an increase of the relative risk for in-hospital death by 8% with every unit of serum sodium increase. Patients with a sodium above the upper normal range at AKI diagnosis were also more likely to suffer in-hospital death (P = 0.001). Conclusion:In summary, we present evidence that serum sodium, measured at time of AKI diagnosis, potentially serves as a predictor for in-hospital death in patients with AKI.

Cardiorenal syndromes (CRS) have increasingly been recognized as distinct disorders that affect the heart and kidneys simultaneously, either with acute or chronic onset. The different types share common pathophysiological characteristics. The concept “cardiorenal” shall emphasize the inter- or even multidisciplinary approach to respective patients. Anticongestive therapy becomes mandatory in many subjects that suffer from CRS. In recent years, the role of dialysis treatment in a broader sense has been investigated in CRS in more detail. We performed a search for studies related to the topic in the following databases: MEDLINE, PROSPERO, and Web of Science. The following keywords were used for reference identification: “CRS”, “cardiorenal syndrome”, “dialysis”, “hemodialysis”, “hemofiltration”, “renal replacement therapy”, “kidney replacement therapy”, “peritoneal dialysis”, and “aquapheresis”. Finally, a total number of 22 studies, partly performed as retrospective cohort studies, and partly designed as prospective investigations, were included. The selected studies evaluated different modes of peritoneal dialysis (PD) or of non-PD procedures including intermittent hemodialysis, continuous procedures, and so-called aquapheresis. Inclusion and outcome parameters were almost not comparable between selected trials. Some studies revealed dialysis as effective, with reasonable tolerability. Particularly so-called “pure” ultrafiltration (e.g., aquapheresis) was associated with higher rates of adverse events. Future studies should be designed in a more homogenous manner, particularly concerning the inclusion criteria, the respective dialysis procedure applied, and endpoints in the short- and long-term.

Acute kidney injury (AKI) affects up to 30% of all hospitalized patients in Central Europe and the USA. New biomarker molecules have been identified in recent years; most studies performed so far however aimed to identify markers for diagnostic purposes. Serum electrolytes such as sodium and potassium are quantified in more or less all hospitalized patients. Aim of the article is to review the literature on the AKI predictive role of four distinct serum electrolytes in evolving/progressing AKI. The following databases were searched for references: PubMed, Web of Science, Cochrane Library, and Scopus. The period lasted from 2010 until 2022. The following terms were utilized: "AKI" AND "sodium" OR "potassium" OR "calcium" OR "phosphate" AND "risk" OR "dialysis" OR "recovery of kidney function" OR "renal recovery" OR "kidney recovery" OR "outcome". Finally, 17 references were selected. The included studies were mostly retrospective in nature. Particularly, hyponatremia has been shown to be associated with an overall poor clinical outcome. The association between dysnatremia and AKI is anything but consistent. Hyperkalemia and potassium variability are most likely AKI predictive. Serum calcium and AKI risk are associated in a Ushaped manner. Higher phosphate levels potentially predict AKI in non-coronavirus disease 2019 (COVID-19) patients. The literature suggests that admission electrolytes can offer valuable information about AKI onset during follow-up. Limited data are however available on follow-up characteristics such as the need for dialysis or the chance of renal recovery. These aspects are of particular interest from the nephrologist's perspective.