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.

Recent years have brought shear wave elastography to the attention of nephrologists as a non-invasive method for detecting kidney fibrosis and, therefore, as a potential tool for reducing the need for kidney biopsy. Few studies are performed on native kidney. We aimed to compare cortical stiffness, assessed by measuring Young's modulus (YM, kPa) with SuperSonic Imaging technology, in patients with various degrees of chronic kidney disease (CKD) compared with healthy individuals. Cortical stiffness was measured by two operators, in different sessions, in 32 patients with CKD stages 3-5 and 20 healthy individuals. Comparison between mean YM values in CKD and those in controls and also between the different stages of CKD was our primary objective. The influence of other possible confounders on YM readings was also investigated and analyzed. Mean YM was significantly greater in CKD patients than in controls. Estimated YM was not able to differentiate the stages of CKD, except stage 5. Intra-subject variability was greater in CKD than in controls. Body mass index was the most important confounder in multiple analyses, in both the CKD and control groups. Our results highlight a positive correlation between increased cortical stiffness and presence of CKD. Further studies are needed to validate this method for implementation in daily clinical practice.

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.

Native arteriovenous fistula (AVF) is the most appropriate type of vascular access for chronic dialysis. Its patency rates depend on vascular wall characteristics. Ketoacid analogues of essential amino acids (KA/EAA) are prescribed in end-stage renal disease (ESRD) pre-dialysis patients to lower toxic metabolic products generation and improve nutritional status. We hypothesized that very-low protein diet (VLPD) supplemented with KA/EAA may influence arterial wall stiffness and affect AVF maturation rates and duration in pre-dialysis ESRD patients. In a prospective, cohort, 3 years study we enrolled 67 consecutive non-diabetic early referral ESRD patients that underwent AVF creation in our hospital. Patients were divided in two groups based on their regimen 12 months prior to surgery: a VLPD supplemented with KA/EAA study group versus a low protein diet non-KA/EAA-supplemented control group. For each patient we performed serum analysis for the parameters of bone mineral disease, inflammation and nutritional status, one pulse wave velocity (PWV) measurement and one Doppler ultrasound (US) determination prior the surgery, followed by consequent Doppler US assessments at 4, 6, 8 and 12 weeks after it. Rates and duration of mature AVF achievement were noted. We used logistic regression to analyze the association between AVF maturation and KA/EAA administration, by comparing rates and durations between groups, unadjusted and adjusted for systolic blood pressure, C-reactive protein, PWV, phosphorus values. All parameters in the logistic model were transformed in binary variables. A p-value < α = 0.05 was considered significant; data were processed using SPSS 16 software and Excel. In the study group (n = 28, aged 57 ± 12.35, 13 females) we registered better serum phosphate (p = 0.022) and C-reactive protein control (p = 0.021), lower PWV (p = 0.007) and a higher percent of AVF creation success (33.3 % versus 17.8 %, p < 0.05). AVF maturation duration was lower in study group (5.91 versus 7.15 weeks, p < 0.001). VLPD supplemented with KA/EAA appear to improve the native AVF primary outcome, decreasing the initial vascular stiffness, possible by preserving vascular wall quality in CKD patients through a better serum phosphate levels control and the limitation of inflammatory response.