Diabetes is one of the most important comorbidities linked to the severity of all three known human pathogenic coronavirus infections, including severe acute respiratory syndrome coronavirus 2. Patients with diabetes have an increased risk of severe complications including Adult Respiratory Distress Syndrome and multi-organ failure. Depending on the global region, 20-50% of patients in the coronavirus disease 2019 (COVID-19) pandemic had diabetes. Given the importance of the link between COVID-19 and diabetes, we have formed an international panel of experts in the field of diabetes and endocrinology to provide some guidance and practical recommendations for the management of diabetes during the pandemic. We aim to briefly provide insight into potential mechanistic links between the novel coronavirus infection and diabetes, present practical management recommendations, and elaborate on the differential needs of several patient groups.

S20 Introduction S22 Summary of recommendation statements and practice points S30 Chapter 1: Comprehensive care in patients with diabetes and CKD S39 Chapter 2: Glycemic monitoring and targets in patients with diabetes and CKD S47 Chapter 3: Lifestyle interventions in patients with diabetes and CKD S58 Chapter 4: Antihyperglycemic therapies in patients with type 2 diabetes (T2D) and CKD S79 Chapter 5: Approaches to management of patients with diabetes and CKD S87 Methods for guideline development S96 Biographic and disclosure information S106 Acknowledgments S107 References The development and publication of this guideline were supported by KDIGO. The opinions or views expressed in this professional education supplement are those of the authors and do not necessarily reflect the opinions or recommendations of the International Society of Nephrology or Elsevier. Dosages, indications, and methods of use for products that are referred to in the supplement by the authors may reflect their clinical experience or may be derived from the professional literature or other clinical sources. Because of the differences between in vitro and in vivo systems and between laboratory animal models and clinical data in humans, in vitro and animal data may not necessarily correlate with clinical results.

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The last three decades have witnessed an epidemic rise in the number of people with diabetes, especially type 2 diabetes, and particularly in developing countries, where more than 80% of the people with diabetes live. The rise of type 2 diabetes in South Asia is estimated to be more than 150% between 2000 and 2035. Although aging, urbanization, and associated lifestyle changes are the major determinants for the rapid increase, an adverse intrauterine environment and the resulting epigenetic changes could also contribute in many developing countries. The International Diabetes Federation estimated that there were 382 million people with diabetes in 2013, a number surpassing its earlier predictions. More than 60% of the people with diabetes live in Asia, with almost one-half in China and India combined. The Western Pacific, the world’s most populous region, has more than 138.2 million people with diabetes, and the number may rise to 201.8 million by 2035. The scenario poses huge social and economic problems to most nations in the region and could impede national and, indeed, global development. More action is required to understand the drivers of the epidemic to provide a rationale for prevention strategies to address the rising global public health “tsunami.” Unless drastic steps are taken through national prevention programs to curb the escalating trends in all of the countries, the social, economic, and health care challenges are likely to be insurmountable.

OBJECTIVE— Recent genome-wide association studies have identified six novel genes for type 2 diabetes and obesity and confirmed TCF7L2 as the major type 2 diabetes gene to date in Europeans. However, the implications of these genes in Asians are unclear. RESEARCH DESIGN AND METHODS— We studied 13 associated single nucleotide polymorphisms from these genes in 3,041 patients with type 2 diabetes and 3,678 control subjects of Asian ancestry from Hong Kong and Korea. RESULTS— We confirmed the associations of TCF7L2 , SLC30A8 , HHEX , CDKAL1 , CDKN2A / CDKN2B , IGF2BP2 , and FTO with risk for type 2 diabetes, with odds ratios ranging from 1.13 to 1.35 (1.3 × 10 −12 < P unadjusted < 0.016). In addition, the A allele of rs8050136 at FTO was associated with increased BMI in the control subjects ( P unadjusted = 0.008). However, we did not observe significant association of any genetic variants with surrogate measures of insulin secretion or insulin sensitivity indexes in a subset of 2,662 control subjects. Compared with subjects carrying zero, one, or two risk alleles, each additional risk allele was associated with 17% increased risk, and there was an up to 3.3-fold increased risk for type 2 diabetes in those carrying eight or more risk alleles. Despite most of the effect sizes being similar between Asians and Europeans in the meta-analyses, the ethnic differences in risk allele frequencies in most of these genes lead to variable attributable risks in these two populations. CONCLUSIONS— Our findings support the important but differential contribution of these genetic variants to type 2 diabetes and obesity in Asians compared with Europeans.

OBJECTIVEThe objective of this study was to evaluate the effect of maternal hyperglycemia during pregnancy on cardiometabolic risk in offspring during early childhood.RESEARCH DESIGN AND METHODSA total of 970 mothers who had joined the Hyperglycemia and Adverse Pregnancy Outcome study were reevaluated, together with their child born during the study period, 7 years after delivery.RESULTSOffspring born to mothers diagnosed with gestational diabetes mellitus (GDM), as defined by the World Health Organization 2013 GDM criteria, had higher rates of abnormal glucose tolerance (4.7% vs. 1.7%; P = 0.04), higher rates of overweight or obesity, greater BMI, higher blood pressure (BP), lower oral disposition index, and a trend toward reduced β-cell function compared with those born to mothers without GDM. For each SD increase in maternal fasting, 1-h, and 2-h glucose levels on oral glucose tolerance tests (OGTTs) between 24 and 32 weeks of the index pregnancy, the risk of abnormal glucose tolerance in the offspring showed a corresponding increase (adjusted odds ratio [OR] 1.85–2.00). The associations were independent of BMI before pregnancy, childhood obesity, or being born large for gestational age. The area under the curve for glucose levels during the five-point OGTT increased to a similar extent in boys and girls with each SD increase in maternal 1-h and 2-h plasma glucose on OGTTs during pregnancy. All three maternal glucose levels were also associated with increased adjusted ORs for childhood overweight or obesity and adiposity among girls, but not boys.CONCLUSIONSMaternal hyperglycemia in pregnancy is independently associated with offsprings’ risk of abnormal glucose tolerance, obesity, and higher BP at 7 years of age. Its effect on childhood adiposity was apparent only in girls, not boys.

Bayer AG.

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