The dilemma of sodium intake in preeclampsia: beneficial or detrimental?

Preeclampsia (PE) is a disorder involving de novo development of hypertension plus end organ damage after 20 weeks of gestation. PE is considered to be a heterogeneous disease. There are 2 main types of PE: early-onset (<34 weeks of gestation), which is considered to be a placental disorder and is associated with vasoconstriction, low cardiac output, and placental hypoperfusion and organ damage due to decreased microcirculation to maternal organs; and late-onset PE, which is primarily a disorder of pregnant women with obesity, diabetes, and/or cardiovascular abnormalities. In late-onset PE, there is avid sodium reabsorption by the maternal kidneys, causing hypervolemia and increased cardiac output, along with vasodilatation causing venous congestion of organs. Although PE has been a well-known disease for a long time, it is interesting to note that there is no specific sodium (salt) intake recommendation for these patients. This may be due to the fact that studies since as far back as the 1900s have shown conflicting results, and the reasons for the inconsistent findings have not been fully explained; furthermore, the type of PE in these studies was not specifically defined. Some studies suggest that sodium restriction may be detrimental in early-onset PE, but may be feasible in late-onset PE. To explore this paradox, the current review explains the hemodynamic factors involved in these 2 types of PE, summarizes the findings of the current studies, and highlights the knowledge gaps and the research needed to determine whether increase or restriction of salt or sodium intake is beneficial in different types of PE.

Vitamin Supplement Use in Patients With CKD: Worth the Pill Burden?

All vitamins play essential roles in various aspects of body function and systems. Patients with chronic kidney disease (CKD), including those receiving dialysis, may be at increased risk of developing vitamin deficiencies due to anorexia, poor dietary intake, protein energy wasting, restricted diet, dialysis loss, or inadequate sun exposure for vitamin D. However, clinical manifestations of most vitamin deficiencies are usually subtle or undetected in this population. Testing for circulating levels is not undertaken for most vitamins except folate, B12, and 25-hydroxyvitamin D because assays may not be available or may be costly to perform and do not always correlate with body stores. The last systematic review through 2016 was performed for the Kidney Disease Outcome Quality Initiative (KDOQI) 2020 Nutrition Guideline update, so this article summarizes the more recent evidence. We review the use of vitamins supplementation in the CKD population. To date there have been no randomized trials to support the benefits of any vitamin supplementation for kidney, cardiovascular, or patient-centered outcomes. The decision to supplement water-soluble vitamins should be individualized, taking account the patient's dietary intake, nutritional status, risk of vitamins deficiency/insufficiency, CKD stage, comorbid status, and dialysis loss. Nutritional vitamin D deficiency should be corrected, but the supplementation dose and formulation need to be personalized, taking into consideration the degree of 25-hydroxyvitamin D deficiency, parathyroid hormone levels, CKD stage, and local formulation. Routine supplementation of vitamins A and E is not supported due to potential toxicity. Although more trial data are required to elucidate the roles of vitamin supplementation, all patients with CKD should undergo periodic assessment of dietary intake and aim to receive various vitamins through natural food sources and a healthy eating pattern that includes vitamin-dense foods.

Sodium Management in Kidney Disease: Old Stories, New Tricks.

Excessive dietary sodium intake is associated with an increased risk of hypertension, especially in the setting of chronic kidney disease (CKD). Although implementation of a low-sodium diet in patients with CKD generally is recommended, data supporting the efficacy of this practice is mostly opinion-based. Few controlled studies have investigated the specific association of dietary sodium intake and cardiovascular events and mortality in CKD. Furthermore, in epidemiologic studies, the association of sodium intake with CKD progression, cardiovascular risk, and mortality is not homogeneous, and both low- and high-sodium intake has been associated with adverse health outcomes in different studies. In general, the adverse effects of high dietary sodium intake are more apparent in the setting of advanced CKD. However, there is no established definitive target level of dietary sodium intake in different CKD stages based on glomerular filtration rate and albuminuria/proteinuria. This review discusses the current challenges regarding the rationale of sodium restriction, target levels and assessment of sodium intake, and interventions for sodium restrictions in CKD in relation to clinical outcomes.

Fibroblast Growth Factor 23 and Muscle Wasting: A Metabolic Point of View.

Protein energy wasting (PEW), mostly characterized by decreased body stores of protein and energy sources, particularly in the skeletal muscle compartment, is highly prevalent in patients with moderate to advanced chronic kidney disease (CKD). Fibroblast growth factor 23 (FGF23) is an endocrine hormone secreted from bone and has systemic actions on skeletal muscle. In CKD, FGF23 is elevated and its coreceptor α-klotho is suppressed. Multiple lines of evidence suggest that FGF23 is interconnected with various mechanisms of skeletal muscle wasting in CKD, including systemic and local inflammation, exaggerated oxidative stress, insulin resistance (IR), and abnormalities in adipocytokine metabolism. Investigation of metabolic actions of FGF23 on muscle tissue could provide new insights into metabolic and nutritional abnormalities observed in patients with CKD.

Sweet dreams: therapeutic insights, targeting imaging and physiologic evidence linking sleep, melatonin and diabetic nephropathy.

Melatonin is the main biochronologic molecular mediator of circadian rhythm and sleep. It is also a powerful antioxidant and has roles in other physiologic pathways. Melatonin deficiency is associated with metabolic derangements including glucose and cholesterol dysregulation, hypertension, disordered sleep and even cancer, likely due to altered immunity. Diabetic nephropathy (DN) is a key microvascular complication of both type 1 and 2 diabetes. DN is the end result of a complex combination of metabolic, haemodynamic, oxidative and inflammatory factors. Interestingly, these same factors have been linked to melatonin deficiency. This report will collate in a clinician-oriented fashion the mechanistic link between melatonin deficiency and factors contributing to DN.

Pathological features of COVID-19 infection from biopsy and autopsy series.

Novel coronavirus disease 2019 (COVID-19) which is caused by severe acute respiratory syndrome corona virus 2 (SARS-CoV-2) was first identified in December 2019 in Chinese town Wuhan and considered as a pandemic by World Health Organization. The disease has variety of symptoms including fever, shortness of breath, cough, fatigue, loss of smell and taste and diarrhea. While the majority of cases have mild symptoms, some progress to viral pneumonia, multi-organ failure, or cytokine storm and mortality is mostly caused by hypoxemic respiratory failure. Until now, more than 3.5 million people worldwide were infected and more than 240.000 mortality has been occurred. Thus, there is now evidence the disease may affect variety of organs according to accumulating biopsy and autopsy studies. Such pathological studies have potential role on the understanding of clinical outcomes and in the development of novel targeted therapeutic approaches. Given these aforementioned data, in the current manuscript we have summarized the pathological features of COVID-19 derived from biopsy and autopsy series.

COVID-19 and acute kidney injury.

The Coronavirus disease 2019 (COVID-19) pandemic caused by severe acute respiratory syndrome-coronavirus-2 (SARS-CoV-2) started in December 2019 and has affected millions of lives worldwide, while many aspects of the illness are still unknown. Current data show that many hospitalized COVID-19 patients suffer from kidney damage, in the form of proteinuria, hematuria or acute kidney injury (AKI). AKI is especially prevalent among severe and critically ill COVID-19 patients and is a predictor of mortality. The pathophysiology of AKI in COVID-19 is unclear. Early reports of histopathologic examination from autopsied kidney tissue show SARS-CoV-2 viral particles in renal tubular cells and podocytes, suggesting direct viral infection, as well as findings of acute tubular necrosis, while rhabdomyolysis-associated AKI and glomerulopathies may also occur. As of today, only remdesivir has been authorized to treat COVID-19. Ongoing research investigates potential of anti-viral and anti-inflammatory agents along with safety and efficacy of commonly prescribed drugs such as renin-angiotensin-aldosterone system blockers. This review discusses the prevalence of AKI and its association with outcome, while highlighting possible mechanisms of AKI and suggesting organ protective measures to prevent the development of kidney damage.

Air pollution and kidney disease: review of current evidence.

Along with amazing technological advances, the industrial revolution of the mid-19th century introduced new sources of pollution. By the mid-20th century, the effects of these changes were beginning to be felt around the world. Among these changes, health problems due to environmental air pollution are increasingly recognized. At the beginning, respiratory and cardiovascular diseases were emphasized. However, accumulated data indicate that every organ system in the body may be involved, and the kidney is no exception. Although research on air pollution and kidney damage is recent, there is now scientific evidence that air pollution harms the kidney. In this holistic review, we have summarized the epidemiology, disease states and mechanisms of air pollution and kidney damage.

HbA1c is related with uremic pruritus in diabetic and nondiabetic hemodialysis patients.

OBJECTIVE: Uremic pruritus (UP) remains a frequent problem in hemodialysis (HD) patients and is related to mortality. Poor glycemic control, as evaluated by hemoglobin A1c (HbA1c), is also associated with morbidity and mortality in HD patients. In this study, we investigated the relationship between UP and HbA1c in HD patients. METHODS: Sociodemographic, clinical, and laboratory variables, depressive symptoms, and health-related quality of life were assessed. Severity of UP was evaluated by visual analogue scale (VAS). The scale consisted of a 10 cm horizontal line marked from 0 (denoting no itch) to 10 (denoting worst possible imaginable itch). RESULTS: Totally, 75 patients (male/female, 41/34; diabetic/nondiabetic, 29/46; age, 51.9 ± 13.5 years) were included. The VAS pruritus score was higher in diabetic patients compared with nondiabetic patients (4.7 ± 2.8 vs. 3.0 ± 1.0, p : 0.015). In diabetics, VAS pruritus score was independently related with calcium-phosphorus product (ß : +0.637, p < 0.0001), intact parathyroid hormone (ß : +0.343, p : 0.017), HbA1c (ß : +0.310, p : 0.027), and Beck depression score (ß : +0.474, p : 0.002). In nondiabetics, VAS pruritus score was independently related with calcium-phosphorus product (ß : +0.486, p : 0.004), intact parathyroid hormone (ß : +0.302, p : 0.041), and HbA1c (ß : +0.341, p : 0.033). In the whole patient group, VAS pruritus score was independently related with calcium-phosphorus product (ß : +0.372, p : 0.001), intact parathyroid hormone (ß : +0.241, p : 0.008), HbA1c (ß : +0.227, p : 0.031), and Beck depression score (ß : +0.298, p : 0.003). CONCLUSIONS: In both diabetic and nondiabetic patients, HbA1c is closely related with pruritus in HD patients.