BackgroundThe United States is faced with an unprecedented epidemic of drug abuse. Every year thousands of Americans visit the emergency departments all over the country with illicit drug related complaints. These drugs have been known to be associated with a range of renal pathologies, from reversible acute kidney injuries to debilitating irreversible conditions like renal infarction. So far, no comprehensive study or systematic review has been published that includes the commonly used street drugs and designer drugs with potential nephrotoxic outcomes.MethodsWe conducted a systematic review of published case reports, case series, and cross sectional studies of nephrotoxicities related to drugs of abuse. Literature review was conducted using PubMed/Medline from January 1, 2005 -December 31, 2016 to search for publications related to drug abuse with a defined renal outcome. Publications which reported renal injury in relation to the use of illicit drugs were selected, specifically those cases with raised creatinine levels, clinically symptomatic patients, for instance those with oliguria and proven renal biopsies.ResultsA total of 4798 publications were reviewed during the search process and PRISMA flow chart and Moose protocol regarding systematic reviews were followed. 110 articles were shortlisted for the review. A total of 169 cases from case reports and case series, and 14 case studies were analyzed. Renal manifestations of specific illicit drug abuse were included in this review.ConclusionBased on the evidence presented, a wide range of renal manifestations were found to be associated with drug abuse. If the trend of increasing use of illicit drug use continues, it will put a significant percentage of the population at an elevated risk for poor renal outcomes. This study is limited by the nature of the literature reviewed being primarily case reports and case series.

Viral infections in the immunocompetent host can cause both acute and chronic kidney disease either as a direct damage to the infected kidney cells or as a consequence of systemic immune responses that impact kidney function. Since identifying these entities in the 1970s and 80s, major breakthroughs in the understanding of the viral mechanisms have occurred. Viruses have evolved mechanisms to hijack signaling pathways of infected cells to evade antiviral immune responses by the host. Over time, the clinical presentations and management of these diseases have evolved along with our in-depth understanding of the various pathophysiological mechanisms causing these conditions. Similarly, both at the cellular and systemic levels, the host has evolved mechanisms to counter viral subversion strategies for mutual survival. Since the start of the current COVID-19 pandemic, numerous cases of acute kidney injury have been reported in the literature with various possible pathophysiological mechanisms. In this review, we summarize lessons learned from prior viral pandemics related to viral mechanisms utilized in the pathogenesis of numerous renal manifestations to attempt to utilize this knowledge in predicting post-COVID-19 kidney disease.

Hyponatremia is the most common electrolyte disorder in clinical practice. Catastrophic complications can occur from severe acute hyponatremia and from inappropriate management of acute and chronic hyponatremia. It is essential to define the hypotonic state associated with hyponatremia in order to plan therapy. Understanding cerebral defense mechanisms to hyponatremia are key factors to its manifestations and classification and subsequently to its management. Hypotonic hyponatremia is differentiated on the basis of urine osmolality, urine electrolytes and volume status and its treatment is decided based on chronicity and the presence or absence of central nervous (CNS) symptoms. Proper knowledge of sodium and water homeostasis is essential in individualizing therapeutic plans and avoid iatrogenic complications while managing this disorder.

Objective The triad of obesity, a high‐protein diet from animal sources, and disturbed gut microbiota have been linked to poor clinical outcomes in patients with COVID‐19. In this report, the effect of oxidative stress resulting from the Na+/K+‐ATPase transporter signaling cascade is explored as a driver of this poor clinical outcome. Methods Protein–protein interactions with the SARS‐CoV‐2 proteome were identified from the interactome data for Na+/K+‐transporting ATPase subunit α‐1 (ATP1A1), epidermal growth factor receptor, and ERB‐B2 receptor tyrosine kinase 2, using the curated data from the BioGRID Database of Protein Interactions. Data for the gene expression pattern of inflammatory response were from the Gene Expression Omnibus database for cardiomyocytes post SARS‐CoV‐2 infection (number http://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE151879). Results The ATP1A1 subunit of the Na+/K+‐ATPase transporter is targeted by multiple SARS‐CoV‐2 proteins. Furthermore, receptor proteins associated with inflammatory response, including epidermal growth factor receptor and ERB‐B2 receptor tyrosine kinase 2 (which interact with ATP1A1), are also targeted by some SARS‐CoV‐2 proteins. This heightened interaction likely triggers a cytokine release that increases the severity of the viral infection in individuals with obesity. Conclusions The similarities between the effects of SARS‐CoV‐2 proteins and indoxyl sulphate on the Na+/K+‐ATPase transporter signaling cascade suggest the possibility of an augmentation of gene changes seen with COVID‐19 infection that can result in a hyperinduction of cytokine release in individuals with obesity.

looks quite similar to the one used by Kawasaki and associates representing fasting and early morning but in reality it is not. The process of reporting to a clinic then providing a spot urine sample in an unstandardized manner rather than providing the sample at the end of the urine collection in the same location can lead to significant differences in the results. It has been shown that urine flow rate and output of sodium and chloride are acutely reduced in the upright posture and such changes can last for hours. 9 In fact, a Kawasaki formula validation study of hypertensives addressed the position to be adopted prior to urine sampling and found that the recumbent position significantly overestimates salt intake and there was a significant statistical difference between sitting and sitting and standing postures. 10 This can be the result of alterations in glomerular filtration rate, renal blood flow, tubular function, and adrenocortical hormonal secretion secondary to change in posture.The lack of standardization of the sampling process in PURE can be expected to cause a major flaw in the results. Urine results were the only parameter measured by PURE investigators to come up with their conclusion; therefore, we do question the accuracy of this conclusion.PURE continues to be a well-done study as long as it sticks with its original design, which is survey based. Moreover, dietary sodium data as being part of the survey do not exist or at least are not reported. Such data, although they would be inferior to measured values, would be better than estimating sodium intake based on flawed and unstandardized methodology. There is a clear need to continue to find answers to the global question of dietary sodium and cardiovascular events.