Recent studies have highlighted the close relationship between the kidney and the gastrointestinal (GI) tract—frequently referred to as the kidney–gut axis—in patients with chronic kidney disease (CKD). In this regard, two important pathophysiological concepts have evolved: (i) production and accumulation of toxic end-products derived from increased bacterial fermentation of protein and other nitrogen-containing substances in the GI tract, (ii) translocation of endotoxins and live bacteria from gut lumen into the bloodstream, due to damage of the intestinal epithelial barrier and quantitative/qualitative alterations of the intestinal microbiota associated with the uraemic milieu. In both cases, these gut-centred alterations may have relevant systemic consequences in CKD patients, since they are able to trigger chronic inflammation, increase cardiovascular risk and worsen uraemic toxicity. The present review is thus focused on the kidney–gut axis in CKD, with special attention to the alterations of the intestinal barrier and the local microbiota (i.e. the collection of microorganisms living in a symbiotic coexistence with their host in the intestinal lumen) and their relationships to inflammation and uraemic toxicity in CKD. Moreover, we will summarize the most important clinical data suggesting the potential for nutritional modulation of gut-related inflammation and intestinal production of noxious by-products contributing to uraemic toxicity in CKD patients.

Sepsis is a serious medical condition that can lead to multi-organ failure and shock, and it is associated with increased mortality. Acute kidney injury (AKI) is a frequent complication of sepsis in critically ill patients, and often requires renal replacement therapy. The pathophysiology of AKI in sepsis has not yet been fully defined. In the past, classic theories were mainly focused on systemic hemodynamic derangements, underscoring the key role of whole kidney hypoperfusion due to reduced renal blood flow. However, a growing body of experimental and clinical evidence now shows that, at least in the early phase of sepsis-associated AKI, renal blood flow is normal, or even increased. This could suggest a dissociation between renal blood flow and kidney function. In addition, the scant data available from kidney biopsies in human studies do not support diffuse acute tubular necrosis as the predominant lesion. Instead, increasing importance is now attributed to kidney damage resulting from a complex interaction between immunologic mechanisms, inflammatory cascade activation, and deranged coagulation pathways, leading to microvascular dysfunction, endothelial damage, leukocyte/platelet activation with the formation of micro-thrombi, epithelial tubular cell injury and dysfunction. Moreover, the same processes, through maladaptive responses leading to fibrosis acting from the very beginning, may set the stage for progression to chronic kidney disease in survivors from sepsis-associated AKI episodes. The aim of this narrative review is to summarize and discuss the latest evidence on the pathophysiological mechanisms involved in septic AKI, based on the most recent data from the literature.

Context: Primary aldosteronism (PA) is the most frequent form of secondary hypertension, accounting for up to 5–10% of all hypertensive patients, and the diagnosis of PA can present an important challenge for the clinician. After a positive screening test, the diagnosis is confirmed by a suppression test, often an iv saline load test (SLT) or a fludrocortisone suppression test (FST). The FST is considered by many to be the most reliable but is more complex and expensive. Objective and Design: Our objective was to compare the specificity of SLT with FST for the diagnosis of PA. Patients and Setting: The study included 100 hypertensive patients referred to hypertension units with suspected PA after the screening test. Intervention: All patients underwent FST and SLT. Main Outcome Measures: We assessed plasma aldosterone concentrations (PAC) before and after FST and SLT. Results: After iv SLT, 10.4% of the PA patients were negative and 16.1% of patients with essential hypertension were positive after SLT; that is, a correct diagnosis with SLT was obtained in 88% of patients compared with FST. PAC after SLT and PAC after FST were highly correlated (P < 0.0001). Receiver operator characteristic curve analysis demonstrated that the best cutoff for PAC after SLT was 5 ng/dl. Patients with aldosterone-producing adenoma displayed a smaller reduction of PAC compared with patients with bilateral adrenal hyperplasia; a PAC after SLT greater than 6 ng/dl identified all patients eventually diagnosed as having aldosterone-producing adenoma. Conclusions: This study demonstrates that the iv SLT is a reasonably good alternative to the more expensive and complex FST for the diagnosis of PA after a positive screening test.