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Hyperkalemia (HK) is a life-threatening condition that often occurs in patients with chronic kidney disease (CKD). High serum potassium (sKsK) is responsible for a higher risk of end-stage renal disease, arrhythmias and mortality. This risk increases in patients that discontinue cardio-nephroprotective renin-angiotensin-aldosterone system inhibitor (RAASi) therapy after developing HK. Hence, the management of HK deserves the attention of the clinician in order to optimize the therapeutic strategies of chronic treatment of HK in the CKD patient. The adoption in clinical practice of the new hypokalaemic agents patiromer and sodium zirconium cyclosilicate (SZC) for the prevention and chronic treatment of HK could allow patients, suffering from heart failure and chronic renal failure, to continue to benefit from RAASi therapy. We have updated a narrative review of the clear variables, correct definition, epidemiology, pathogenesis, etiology and classifications for HK among non-dialysis CKD (ND CKD) patients. Furthermore, by describing the prognostic impact on mortality and on the progression of renal damage, we want to outline the strategies currently available for the control of potassium (K+) plasma levels., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2023 Costa, Patella, Provenzano, Ielapi, Faga, Zicarelli, Arturi, Coppolino, Bolignano, De Sarro, Bracale, De Nicola, Chiodini, Serra and Andreucci.)

Background and Aims: The observation of optical microcirculation gives us an extraordinary way to directly assess in vivo the responses of human circulation to stress stimuli. We run a pilot study to analyze optical coherence tomography angiography (OCT-A) metrics at determined time-points during a hemodialysis (HD) session to understand how these metrics gradually change and to evaluate possible correlations with patients' characteristics., Methods: After the eligibility screening, 15 patients (23 eyes) were included in the study. OCT-A parameters were collected at established time-points: Before treatment (t0), at first hour (t1), at second hour (t2), at third hour (t3), and finally at the end of HD treatment (t4). Patients were finally shared in hypotensive group if they occurred in a hypotensive episode during subsequent month methods or no hypotensive group. The instrument software automatically segmented OCT-A scans into four en-face slabs: The superficial capillary plexus (SCP), the deep capillary plexus (DCP), the outer retinal plexus and the choriocapillaris plexus. In this study we focus on SCP, DCP plexuses., Results: Overall, the majority of ophthalmic parameters remained unaffected and comparable at dialysis end; a significant reduction being observed at the end vs. starting of HD only for deep capillary plexus (DCP: Whole, fovea, and parafovea) and for central choroid thickness (CCT) ( p < 0.05). An overall trend during the session showed in general a decrease with a significance in particular for DCP (whole, fovea, and parafovea) and for CCT ( P = 0.006). In the hypotension group, Superficial capillary plexus (SCP: Fovea and parafovea) significantly increased comparing post vs. pre-dialysis values while CCT significantly decreased. Analyzing the trend during treatment only CCT maintained a significant trend ( p for trend = 0.002). In the no-hypotension group, neither pre- vs. post-analysis and trend analysis showed a statistical significance., Conclusion: Main achievement of our study was to measure, for the first time in literature, single parameters at different time-points of a HD session. As a result of this process we did not notice a brusque decreasing or increasing of OCT-A metrics but we can characterize the different effect of HD on the two distinct areas distinguishing ocular vessels: Retinal and choroidal circulation. As interesting sub-analysis, Hypotensive group showed for CCT a decreasing trend with a difference statistically significant respect to the group with no-hypotension maintaining a constant trend. In our opinion, these results suggest the role of autonomic system on vessel control in patients affected by uremia., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2022 Coppolino, Bolignano, Presta, Ferrari, Lionetti, Borselli, Randazzo, Andreucci, Bonelli, Errante, Campo, Mauro, Tripodi, Rejdak, Toro, Scorcia and Carnevali.)

Hyperkalemia is common in patients treated with renin-angiotensin-aldosterone system inhibitors (RAASis), and it represents the main cause of the large gap reported between guideline recommendations and real-world practice in chronic kidney disease (CKD). We conducted a CKD-population-based restrospective study to determine the prevalence of patients with CKD treated with RAASis, incidence of hyperkalemia in patients with CKD treated with RAASis, and proportion of patients with RAASi medication change after experiencing incident hyperkalemia. Among 809 patients with CKD analyzed, 556 (68.7%) were treated with RAASis, and RAASi prescription was greater in stages 2-4 of CKD. Hyperkalemia occurred in 9.2% of RAASi-treated patients, and the adjusted rate of hyperkalemia among patients with stage 4-5 CKD was 3-fold higher compared with patients with eGFR > 60 ml/min/1.73 m 2 . RAASi treatment was discontinued in 55.3% of the patients after hyperkalemia event (74.2% discontinued therapy, 3.2% received a reduced dose, and 22.6% reduced the number of RAASi drugs). This study shows that the incidence of hyperkalemia is frequently observed in patients with CKD patients with RAASis, and that rates increase with deteriorating levels of kidney function from stages 1 to 3. RAASi medication change following an episode of hyperkalemia occurred in almost half of the patients after experiencing hyperkalemia., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2022 Riccio, Capuano, Buonanno, Andreucci, Provenzano, Amicone, Rizzo and Pisani.)

Diabetic nephropathy is the most common cause of end-stage renal disease worldwide. Control of blood glucose and blood pressure (BP) reduces the risk of developing this complication, but once diabetic nephropathy is established, it is then only possible to slow its progression. Sodium-glucose cotransporter-2 inhibitors (SGLT2is) are a novel class of oral hypoglycemic agents that increase urinary glucose excretion by suppressing glucose reabsorption at the renal proximal tubule. SGLT2is lower glycated hemoglobin (HbA1c) without increasing the risk of hypoglycemia, induce weight loss and improve various metabolic parameters including BP, lipid profile, albuminuria and uric acid. Several clinical trials have shown that SGLT2is (empagliflozin, dapagliflozin canagliflozin, and ertugliflozin) improve cardiovascular and renal outcomes and mortality in patients with type 2 diabetes. Effects of SGLT2is on the kidney can be explained by multiple pathways. SGLT2is may improve renal oxygenation and intra-renal inflammation thereby slowing the progression of kidney function decline. Additionally, SGLT2is are associated with a reduction in glomerular hyperfiltration, an effect which is mediated by the increase in natriuresis, the re-activation of tubule-glomerular feedback and independent of glycemic control. In this review, we will focus on renal results of major cardiovascular and renal outcome trials and we will describe direct and indirect mechanisms through which SGLT2is confer renal protection., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2021 Provenzano, Pelle, Zaffina, Tassone, Pujia, Ricchio, Serra, Sciacqua, Michael, Andreucci and Arturi.)

Objective: The resistance index (RI) and the blood flow volume (Q a ) are the most used Doppler ultrasound (DUS) parameters to identify the presence of stenosis in arteriovenous fistula (AVF). However, the reliability of these indexes is now matter of concern, particularly in predicting subsequent thrombosis. In this study, we aimed at testing the diagnostic capacity of the Q a /RI ratio (Q x ) for the early identification of AVF stenosis and for thrombosis risk stratification. Methods: From a multicentre source population of 336 HD patients, we identified 119 patients presenting at least one "alarm sign" for clinical suspicious of stenosis. Patients were therefore categorized by DUS as stenotic ( n = 60) or not-stenotic ( n = 59) and prospectively followed. Q a , RI, and Q X , together with various clinical and laboratory parameters, were recorded. Results: Q a and Q x were significantly higher while RI was significantly lower in non-stenotic vs. stenotic patients ( p < 0.001 for each comparison). At ROC analyses, Q x had the best discriminatory power in identifying the presence of stenosis as compared to Q a and RI (AUCs 0.976 vs. 0.953 and 0.804; p = 0.037 and p < 0.0001, respectively). During follow-up, we registered 30 thrombotic events with an incidence rate of 12.65 (95% CI 8.54-18.06) per 100 patients/year. In Cox-regression proportional hazard models, Q x showed a better capacity to predict thrombosis occurrence as compared to Q a (difference between c-indexes: 0.012; 95% CI 0.004-0.01). Conclusions: In chronic haemodialysis patients, Q x might represent a more reliable and valid indicator for the early identification of stenotic AVFs and for predicting the risk of following thrombosis., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2021 Colombo, Provenzano, Rivoli, Donato, Capria, Leonardi, Chiarella, Andreucci, Fuiano, Bolignano and Coppolino.)

Objective: Available biomarkers for monitoring primary glomerulonephritides (GNs), often lack the ability to assess longitudinal changes and have great variability with poor sensitivity. Accruing evidence has demonstrated that Neutrophil Gelatinase-Associated Lipocalin (NGAL), holds promising capacities in predicting renal function worsening in various renal diseases. We aimed at analyzing urinary NGAL (uNGAL) levels in a cohort of individuals with biopsy-proven GNs in order to evaluate its ability to reflect the entity of renal damage and to predict disease evolution overtime., Methods: We enrolled 61 consecutive GNs patients still naïve to pathogenic therapy. uNGAL levels were measured at baseline and patients prospectively followed until the manifestation of a combined outcome of doubling of baseline serum creatinine and/or end-stage kidney disease requiring permanent dialysis support., Results: Median uNGAL levels were 107[35-312] ng/mL. At univariate and multivariate analyses an inverse correlation was found between eGFR and uNGAL levels ( p = 0.001). Progressor subjects showed exceedingly increased baseline uNGAL values as compared with non-progressors ( p < 0.001). Twenty-one patients (34%) reached the composite renal endpoint. Subjects with uNGAL values above the optimal, ROC-derived, cut-off of 107 ng/mL experienced a more rapid progression to the renal endpoint ( p < 0.001; HR: 5.47; 95% CI 2.31-12.95) with a mean follow-up time to progression of 73.4 vs 83.5 months., Conclusion: In patients affected by primary glomerulonephritides, uNGAL may represent a real-time indicator of renal damage and an independent predictor of renal disease progression. Further studies on larger populations are warranted to confirm these findings., (Copyright © 2020 Coppolino, Comi, Bolignano, Patella, Comi, Provenzano, Rivoli, Andreucci and Fuiano.)

Chronic kidney disease (CKD), defined by an estimated glomerular filtration rate <60 ml/min/1.73 m 2 and/or an increase in urine protein excretion (i.e., albuminuria), is an important public health problem. Prevalence and incidence of CKD have risen by 87 and 89%, worldwide, over the last three decades. The onset of either albuminuria and eGFR reduction has found to predict higher cardiovascular (CV) risk, being this association strong, independent from traditional CV risk factors and reproducible across different setting of patients. Indeed, this relationship is present not only in high risk cohorts of CKD patients under regular nephrology care and in those with hypertension or type 2 diabetes, but also in general, otherwise healthy population. As underlying mechanisms of damage, it has hypothesized and partially proved that eGFR reduction and albuminuria can directly promote endothelial dysfunction, accelerate atherosclerosis and the deleterious effects of hypertension. Moreover, the predictive accuracy of risk prediction models was consistently improved when eGFR and albuminuria have been added to the traditional CV risk factors (i.e., Framingham risk score). These important findings led to consider CKD as an equivalent CV risk. Although it is hard to accept this definition in absence of additional reports from scientific Literature, a great effort has been done to reduce the CV risk in CKD patients. A large number of clinical trials have tested the effect of drugs on CV risk reduction. The targets used in these trials were different, including blood pressure, lipids, albuminuria, inflammation, and glucose. All these trials have determined an overall better control of CV risk, performed by clinicians. However, a non-negligible residual risk is still present and has been attributed to: (1) missed response to study treatment in a consistent portion of patients, (2) role of many CV risk factors in CKD patients not yet completely investigated. These combined observations provide a strong argument that kidney measures should be regularly included in individual prediction models for improving CV risk stratification. Further studies are needed to identify high risk patients and novel therapeutic targets to improve CV protection in CKD patients., (Copyright © 2019 Provenzano, Coppolino, De Nicola, Serra, Garofalo, Andreucci and Bolignano.)