Background: The connection between uric acid (UA) and renal impairment is well known due to the urate capacity to precipitate within the tubules or extra-renal system. Emerging studies allege a new hypothesis concerning UA and renal impairment involving a pro-inflammatory status, endothelial dysfunction, and excessive activation of renin–angiotensin–aldosterone system (RAAS). Additionally, hyperuricemia associated with oxidative stress is incriminated in DNA damage, oxidations, inflammatory cytokine production, and even cell apoptosis. There is also increasing evidence regarding the association of hyperuricemia with chronic kidney disease (CKD), cardiovascular disease, and metabolic syndrome or diabetes mellitus. Conclusions: Important aspects need to be clarified regarding hyperuricemia predisposition to oxidative stress and its effects in order to initiate the proper treatment to determine the optimal maintenance of UA level, improving patients’ long-term prognosis and their quality of life.

Acute kidney injury (AKI) is one of the main conditions responsible for chronic kidney disease (CKD), including end-stage renal disease (ESRD) as a long-term complication. Besides short-term complications, such as electrolyte and acid-base disorders, fluid overload, bleeding complications or immune dysfunctions, AKI can develop chronic injuries and subsequent CKD through renal fibrosis pathways. Kidney fibrosis is a pathological process defined by excessive extracellular matrix (ECM) deposition, evidenced in chronic kidney injuries with maladaptive architecture restoration. So far, cited maladaptive kidney processes responsible for AKI to CKD transition were epithelial, endothelial, pericyte, macrophage and fibroblast transition to myofibroblasts. These are responsible for smooth muscle actin (SMA) synthesis and abnormal renal architecture. Recently, AKI progress to CKD or ESRD gained a lot of interest, with impressive progression in discovering the mechanisms involved in renal fibrosis, including cellular and molecular pathways. Risk factors mentioned in AKI progression to CKD are frequency and severity of kidney injury, chronic diseases such as uncontrolled hypertension, diabetes mellitus, obesity and unmodifiable risk factors (i.e., genetics, older age or gender). To provide a better understanding of AKI transition to CKD, we have selected relevant and updated information regarding the risk factors responsible for AKIs unfavorable long-term evolution and mechanisms incriminated in the progression to a chronic state, along with possible therapeutic approaches in preventing or delaying CKD from AKI.

In the last decade, ultrasound elastography, an already widely used technique in the diagnosis of hepatic fibrosis, has raised the attention of nephrologists as a potential valuable noninvasive tool for the diagnosis of renal fibrosis. Due to renal deep location and anatomic complexity, the shear wave techniques are the most appropriate elastography methods for exploring native kidneys. Recent research offers promising results, but further larger studies are required for a better standardization of this method and also for establishing reference values of normal kidney elasticity. This article reviews the studies conducted for exploring the native kidney, highlighting the advantages and limitations of ultrasound elastography for assessing fibrosis development in chronic kidney diseases.

Severe burn injuries lead to acute kidney injury (AKI) development, increasing the mortality risk up to 28–100%. In addition, there is an increase in hospitalization days and complications appearance. Various factors are responsible for acute or late AKI debut, like hypovolemia, important inflammatory response, excessive load of denatured proteins, sepsis, and severe organic dysfunction. The main measure to improve the prognosis of these patients is rapidly recognizing this condition and reversing the underlying events. For this reason, different renal biomarkers have been studied over the years for early identification of burn-induced AKI, like neutrophil gelatinase-associated lipocalin (NGAL), cystatin C, kidney injury molecule-1 (KIM-1), tissue inhibitor of metalloproteinase-2 (TIMP-2), interleukin-18 (IL-18), and insulin-like growth factor-binding protein 7 (IGFBP7). The fundamental purpose of these studies is to find a way to recognize and prevent acute renal injury progression early in order to decrease the risk of mortality and chronic kidney disease (CKD) onset.

Burns, one of the main public health problems, lead to significant mortality and morbidity. Epidemiological studies regarding burn patients in Romania are scarce. The aim of this study is to identify the burn etiology, demographics, clinical characteristics, and outcomes in patients requiring treatment in a regional burn unit. Design. We performed a retrospective observational study of 2021. Patients. All patients admitted to our six-bed intensive care unit (ICU) were included. Interventions. The following data were collected for further analysis: demographics, burn pattern (etiology, size, depth, affected body region), type of ventilation, ABSI (Abbreviated Burn Severity Index) score, comorbidities, bioumoral parameters, and hospitalization days. Results. There were 93 burned patients included in our study that were divided into two groups: alive patients’ group (63.4%) and deceased patients’ group (36.6%). The mean age was 55.80 ± 17.16 (SD). There were 65.6% male patients, and 39.8% of the patients were admitted by transfer from another hospital. Further, 59 patients presented third-degree burns, from which 32.3% died. Burns affecting >37% of the total body surface area (TBSA) were noticed in 30 patients. The most vulnerable regions of the body were the trunk (p = 0.003), the legs (p = 0.004), the neck (p = 0.011), and the arms (p = 0.020). Inhalation injury was found in 60.2% of the patients. The risk of death in a patient with an ABSI score > 9 points was 72 times higher. Comorbidities were present in 44.1% of the patients. We observed a median LOS (length of stay) of 23 days and an ICU-LOS of 11 days. Logistic regression analysis showed that admission protein, creatinkinase, and leukocytes were independent risk factors for mortality. The general mortality rate was 36.6%. Conclusion. A thermal factor was responsible for the vast majority of burns, 94.6% of cases being accidents. Extensive and full-thickness burns, burns affecting the arms, inhalation injuries, the need for mechanical ventilation, and a high ABSI score represent important risk factors for mortality. Considering the results, it appears that prompt correction of protein, creatinkinase, and leukocytes levels may contribute to improvement in severe burn patients’ outcomes.