The beneficial impact of dietary fiber on the prevention and management of several chronic conditions associated with aging, including diabetes, neurodegenerative, cardiovascular diseases, and cancer, is well-known. High fiber intake has been associated with reduced inflammatory mediators counteracting the low-grade chronic inflammation typical of older age. In addition, dietary fiber improves postprandial glucose response and insulin resistance. In contrast, during acute diseases, its effects on insulin resistance and modulation of immune response are unclear. The aim of this narrative is to summarize the evidence for the potential impact of dietary fiber on inflammation and insulin resistance in older adults, with a particular focus on those acutely ill. Available evidence suggests that dietary fiber has the potential to counteract acute inflammation and to improve metabolic health. In addition, modulation of gut microbiota composition may contribute to improved immune function, particularly in the setting of aging-associated dysbiosis. This phenomenon has relevant implications in those acutely ill, in whom dysbiosis can be exacerbated. Our review leads to the conclusion that dietary interventions based on fiber manipulation could exploit its beneficial effects on inflammation and insulin resistance, if conducted from a precision nutrition perspective. This could also be true for the acutely ill patient, even though strong evidence is lacking.

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Background: Coronavirus Disease-19 (COVID-19) has an important impact on the kidney, however, the involvement of the last part of the nephron has not been previously documented. Methods: We present the case of a 71 years old man with respiratory failure in Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) pneumonia who, after about 20 days of hospitalization, presented the typical symptoms of diabetes insipidus. The water deprivation test led to the diagnosis of nephrogenic diabetes insipidus. The analysis of the underlying cause was complex because of the patient’s pharmacological and medical history. In particular, potential alternative causes for nephrogenic diabetes insipidus including urinary tract infection and previous lithium therapy had to be ruled out. Results: The sequence of pathognomonic events typical of diabetes insipidus associated with anamnestic, clinical and laboratory evidences strongly supported the diagnosis of nephrogenic diabetes insipidus due to SARS-CoV-2, rather than to other etiologies. Conclusions: The collecting duct could represent a target for SARS-CoV-2 infection, directly or indirectly as a result of lesions of upstream portions of the nephron which would cascade into the distal segment. Other molecules, besides angiotensin 2 converting enzyme, might be involved in facilitating the viral aggression. The complexity of the geriatric patient shows the importance of a comprehensive approach which integrates a careful monitoring of clinical signs and symptoms,  laboratory and instrumental tests. This is especially important in the context of SARS-CoV-2 infection and in the management of its unexpected complications.