Introduction: The gut microbiota has coevolved with humans for a mutually beneficial coexistence and plays an important role in health and disease. A dysbiotic gut microbiome may contribute to progression to chronic kidney disease (CKD) and CKD-related complications such as cardiovascular disease. Microbiota modulation through the administration of prebiotics may represent an important therapeutic target. Aim: We sought to evaluate the effects of a low-protein diet (LPD) (0.6 g/kg/day) with or without the intake of the prebiotic inulin (19 g/day) on microbiota and clinical parameters in CKD patients. Materials and Methods: We performed a longitudinal, prospective, controlled, and interventional study on 16 patients: 9 patients treated with LPD (0.6 g/kg/day) and inulin (19 g/day) and 7 patients (control group) treated only with LPD (0.6 g/kg/day). Clinical evaluations were performed and fecal samples were collected for a subsequent evaluation of the intestinal microbiota in all patients. These tests were carried out before the initiation of LPD, with or without inulin, at baseline (T0) and at 6 months (T2). The microbiota of 16 healthy control (HC) subjects was also analyzed in order to identify potential dysbiosis between patients and healthy subjects. Results: Gut microbiota of CKD patients was different from that of healthy controls. The LPD was able to significantly increase the frequencies of Akkermansiaceae and Bacteroidaceae and decrease the frequencies of Christensenellaceae, Clostridiaceae, Lactobacillaceae, and Pasteurellaceae. Only Bifidobacteriaceae were increased when the LPD was accompanied by oral inulin intake. We showed a significant reduction of serum uric acid (SUA) and C-reactive protein (CRP) in patients treated with LPD and inulin (p = 0.018 and p = 0.003, respectively), an improvement in SF-36 (physical role functioning and general health perceptions; p = 0.03 and p = 0.01, respectively), and a significant increase of serum bicarbonate both in patients treated with LPD (p = 0.026) or with LPD and inulin (p = 0.01). Moreover, in patients treated with LPD and inulin, we observed a significant reduction in circulating tumor necrosis factor alpha (TNF-α) (p = 0.041) and plasma nicotinamide adenine dinucleotide phosphate (NADPH) oxidase (NOX2) (p = 0.027) levels. We did not find a significant difference in the circulating levels of Interleukin (IL)-1β (p = 0.529) and IL-6 (p = 0.828) in the two groups. Conclusions: LPD, associated or not with inulin, modified gut microbiota and modulated inflammatory and metabolic parameters in patients with CKD. Our results suggest that interventions attempting to modulate the gut microbiome may represent novel strategies to improve clinical outcomes in CKD patients and may provide useful therapeutic effects.

Background Chronic kidney disease (CKD) is a highly prevalent condition. Urologic disorders are known causes of CKD, but often remain undiagnosed and underestimated also for their insidious onset and slow progression. We aimed to evaluate the prevalence of urological unrecognized diseases in CKD patients by uroflowmetry. Methods We enrolled consecutive stable CKD outpatients. The patients carried out two questionnaires, the International Prostate Symptom Score and Incontinence Questionnaire-Short Form, and they also underwent uroflowmetry, evaluating max flow rate ( Q max ), voiding time and voided volume values. Results A total of 83 patients (43 males, mean age of 59.8 ± 13.3 years) were enrolled. Our study showed 28 males and 10 females with a significant reduction of Q max (P < 0.001) while 21 females reported a significant increase of Q max (P < 0.001) with a prevalence of 49.5% of functional urological disease. Moreover, we showed a significant association between Q max and creatinine (P = 0.013), estimated glomerular filtration rate (P = 0.029) and voiding volume (P = 0.05). We have not shown significant associations with age (P = 0.215), body mass index (P = 0.793), systolic blood pressure (P = 0.642) or diastolic blood pressure (P = 0.305). Moreover, Pearson’s chi-squared test showed a significant association between Q max altered with CKD (χ 2 = 1.885, P = 0.170) and recurrent infection (χ 2 = 8.886, P = 0.012), while we have not shown an association with proteinuria (χ 2 = 0.484, P = 0.785), diabetes (χ 2 = 0.334, P = 0.563) or hypertension (χ 2 = 1.885, P = 0.170). Conclusions We showed an elevated prevalence of urological diseases in nephropathic patients; therefore, we suggest to include uroflowmetry in CKD patient assessment, considering the non-invasiveness, repeatability and low cost of examination. Uroflowmetry could be used to identify previously unrecognized urological diseases, which may prevent the onset of CKD or progression to end-stage renal disease and reduce the costs of management.

Drug-resistant arterial hypertension (RH) is a major risk factor for cardiovascular disease. However, it is often due to underlying causes, the identification of which poses significant clinical challenges because interfering drugs are used by definition in RH patients. In this setting, primary aldosteronism (PA) is a frequent cause of RH and its prevalence in RH patients is likely higher than 20%. The pathophysiological link between PA and the development and maintenance of RH involves target organ damage and the cellular and extracellular effects of aldosterone excess that promote pro-inflammatory and pro-fibrotic changes in the kidney and vasculature. The feasibility of adrenal vein sampling in RH patients, who have PA, and the clinical benefit achieved by adrenalectomy further emphasize the need of implementing the systematic screening for this common form of secondary hypertension in the management of a high-risk population as RH patients. We herein review the current knowledge of the factors that contribute to the RH phenotype with a focus on PA, and discuss the issues regarding the screening for PA in the setting of RH, and the therapeutical approaches (surgical and medical) aimed at resolving RH caused by PA.

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IntroductionVascular access recirculation during hemodialysis is associated with reduced effectiveness and worse survival outcomes. To evaluate recirculation, an increase in pCO2 in the blood of the arterial line during hemodialysis (threshold of 4.5 mmHg) was proposed. The blood returning from the dialyzer in the venous line has significantly higher pCO2, so in the presence of recirculation, pCO2 in the arterial blood line may increase (ΔpCO2) during hemodialysis sessions. The aim of our study was to evaluate ΔpCO2 as a diagnostic tool for vascular access recirculation in chronic hemodialysis patients.MethodsWe evaluated vascular access recirculation with ΔpCO2 and compared it with the results of a urea recirculation test, which is the gold standard. ΔpCO2 was obtained from the difference in pCO2 in the arterial line at baseline (pCO2T1) and after 5 min of hemodialysis (pCO2T2). ∆pCO2 = pCO2T2–pCO2T1.FindingsIn 70 hemodialysis patients (mean age: 70.52 ± 13.97 years; hemodialysis vintage of 41.36 ± 34.54, KT/V 1.4 ± 0.3), ∆pCO2 was 4 ± 4 mmHg, and urea recirculation was 7% ± 9%. Vascular access recirculation was identified using both methods in 17 of 70 patients, who showed a ∆pCO2 of 10 ± 5 mmHg and urea recirculation of 20% ± 9%; time in months of hemodialysis was the only difference between vascular access recirculation and non‐vascular access recirculation patients (22 ± 19 vs. 46 ± 36, p: 0.05). In the non‐vascular access recirculation group, the average ΔpCO2 was 1.9 ± 2 (p: 0.001), and the urea recirculation % was 2.8 ± 3 (p: 0.001). The ΔpCO2 correlated with the urea recirculation % (R: 0.728; p < 0.001).DiscussionΔpCO2 in the arterial blood line during hemodialysis is an effective and reliable diagnostic tool for identifying recirculation of the vascular access but not its magnitude. The ΔpCO2 test application is simple and economical and does not require special equipment.