Decreasing microbiota-derived uremic toxins to improve CKD outcomes.

Chronic kidney disease (CKD) is set to become the fifth-leading global cause of death by 2040. This illustrates the many unknowns regarding its pathogenesis and therapy. A key unknown relates to the therapeutic impact of the interaction between CKD and the gut microbiome. The normal gut microbiome is essential for body homeostasis. There is evidence for multiple interactions between the microbiota and CKD-its causes, comorbidities and therapeutic interventions-that are only starting to be unraveled. Thus uremic retention products, such as urea itself, modify the gut microbiota biology and both dietary and drug prescriptions modify the composition and function of the microbiota. Conversely, the microbiota may influence the progression and manifestations of CKD through the production of biologically active compounds (e.g. short-chain fatty acids such as butyrate and crotonate) and precursors of uremic toxins. The present review addresses these issues and their relevance for novel therapeutic approaches ranging from dietary interventions to prebiotics, probiotics, synbiotics and postbiotics, to the prevention of the absorption of microbial metabolites and to increased clearance of uremic toxins of bacterial origin through optimized dialysis techniques or blockade of tubular cell transporters.

Sarcopenia as a potential cause of chronic hyponatremia in the elderly.

Hyponatremia is the most frequent electrolyte disorder found in clinical practice, particularly in hospitalized elderly patients, where it is associated with fractures, falls, hospital readmission, prolonged hospital stay and increased mortality. Pathophysiologically, hyponatremia can be induced by the reduction in sodium or potassium body content, and/or the increase in water body content. Sarcopenia is an ageing-associated progressive and generalized loss of musculoskeletal mass and strength which leads to low physical performance, particularly in the frail elderly. Since muscle mass is the main potassium body store, this condition usually represents a reduced body potassium content. In the present article it is hypothesized that sarcopenia, as a cause of low potassium body content, could induce or co-induce hyponatremia, particularly in elderly individuals suffering from frailty phenotype.

Novel acute kidney injury biomarkers: their characteristics, utility and concerns.

Acute kidney injury (AKI) consists of a rapid renal function decline which usually increases serum urea and creatinine levels. Since kidney injury begins by inducing biological and molecular changes which evolve to cellular damage, biomarkers could be used as tools for monitoring early AKI appearance, and predicting its recovery. Among the main AKI biomarkers the neutrophil gelatinase-associated lipocalin, cystatin C, kidney injury molecule-1, monocyte chemotactic peptide-1, N-acetyl-ß-D-glucosaminidase, interleukin-18, liver-type fatty acid-binding protein, netrin-1, cycle arrest markers, endogenous ouabain, selenium-binding protein 1, and BPIFA2 marker, have been described. Even though novel biomarkers seem to be more helpful to early detect AKI and/or predict the need for renal replacement, and mortality compared to serum creatinine, more comprehensive studies are still required to determine their clinical utility.