[A rare cause of acute heart failure? : Aorto-right atrial fistula!] / Eine seltene Ursache für akute Herzinsuffizienz? : Aorta-rechtsatriale Fistel!

BACKGROUND: Acute heart failure with symptoms such as dyspnea and edema has various causes. In rare cases cardiac fistulas can cause acute heart failure. Herein we present a case of subacute heart failure due to an acquired fistula between the aorta and right atrium. CASE REPORT: A 48-year-old male was referred to the emergency room with increasing dyspnea on exercise and pitting edema of the lower extremities starting approximately 4 weeks previously. Echocardiographic workup showed an aorta-to-right atrium fistula. The patient was referred to a cardiothoracic surgery center for closure of the fistula.

Increased Serum Sodium at Acute Kidney Injury Onset Predicts In-Hospital Death.

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 (X2, P = 0.003; odds ratio = 1.08 (1.022 - 1.141); R2 = 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.

Stratification of Acute Kidney Injury Risk, Disease Severity, and Outcomes by Electrolyte Disturbances.

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 U-shaped 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.

Kidney Replacement Therapy in Cardiorenal Syndromes.

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.

Kidney-Related Outcome in Cardiorenal Syndrome Type 3.

METHODS: A single-center, retrospective and observational trial. All subjects with positive AKI alert, treated at the University Hospital Brandenburg between January and December 2019, were evaluated. Definition of CRS type 3 was according to predefined criteria. The three endpoint categories were in-hospital death, dialysis, and recovery of kidney function. RESULTS: . A total number of 1,334 AKI alerts were screened. Finally, 95 subjects received the diagnosis CRS type 3. The survival rates were 47.1% (females) and 43.6% (males). 46.8% of affected females and 33.3% of the males required dialysis therapy. Complete recovery at the time of discharge occurred in 35.8%, and no recovery at all was found in 54.7%. CONCLUSIONS: . All three predefined study endpoints, the mortality, the prevalence of dialysis, and the percentage of subjects without recovery of kidney function, were notably high. Therefore, AKI patients with imminent or established cardiac complications require the highest attention of nephrologists in charge.

Experimental Cardiorenal Syndrome Type 3: What Is Known so Far?

BACKGROUND: The concept of cardiorenal syndrome (CRS) has been established more than 10 years ago. Five distinct types of CRS have been defined. In CRS type 3, acute kidney injury (AKI) induces cardiac complications such as ventricular decompensation due to arrhythmias, myocardial ischemia, or fluid retention with or without arterial hypertension. The risk of cardiovascular events in AKI has been known for many years, even long before the introduction of the CRS concept. However, epidemiological and clinical studies published in recent years increasingly emphasized CRS type 3 (and the remaining four types also) as separate entity which requires particular therapeutic attention in an interdisciplinary manner. However, only a limited number of experimental studies specifically addressed CRS type 3 so far. Our review aims to summarize experimental studies on the pathological mechanisms in CRS type 3. METHODS: The following search criteria were employed in order to identify articles published on the topic: "cardiorenal syndrome 3" OR "cardiorenal syndrome type 3" OR "CRS type 3" OR "CRS 3" AND "experimental" OR "mouse" OR "mice" OR "rats" OR "animals"; additional criteria were "myocardium" AND "ischemia" AND "kidney" OR "renal". By applying the search criteria mentioned earlier, 10 references were finally selected. RESULTS: By applying the search strategy, 10 experimental studies were finally selected. All included cardiac outcome analysis in AKI animals. The data clearly provide evidence for cardiac complications that evolve independently from excretory kidney dysfunction. Pathological processes that emerge in the heart of animals subjected to renal ischemia involve inflammation, a dysbalance of redox components, pro-apoptotic processes, and mitochondrial dysfunction. CONCLUSION: The findings may explain why AKI increases the risk of acute cardiac complications even if dialysis treatment has been initiated.

Knockout of aminopeptidase A in mice causes functional alterations and morphological glomerular basement membrane changes in the kidneys.

Aminopeptidase A is one of the most potent enzymes within the renin-angiotensin system in terms of angiotensin II degradation. Here, we examined whether there is a kidney phenotype and any compensatory changes in other renin angiotensin system enzymes involved in the metabolism of angiotensin II associated with aminopeptidase A deficiency. Kidneys harvested from aminopeptidase A knockout mice were examined by light and electron microscopy, immunohistochemistry and immunofluorescence. Kidney angiotensin II levels and the ability of renin angiotensin system enzymes in the glomerulus to degrade angiotensin II ex vivo, their activities, protein and mRNA levels in kidney lysates were evaluated. Knockout mice had increased blood pressure and mild glomerular mesangial expansion without significant albuminuria. By electron microscopy, knockout mice exhibited a mild increase of the mesangial matrix, moderate thickening of the glomerular basement membrane but a striking appearance of knob-like structures. These knobs were seen in both male and female mice and persisted after the treatment of hypertension. In isolated glomeruli from knockout mice, the level of angiotensin II was more than three-fold higher as compared to wild type control mice. In kidney lysates from knockout mice angiotensin converting enzyme activity, protein and mRNA levels were markedly decreased possibly as a compensatory mechanism to reduce angiotensin II formation. Thus, our findings support a role for aminopeptidase A in the maintenance of glomerular structure and intra-kidney homeostasis of angiotensin peptides.