Diabetic kidney disease is a major cause of morbidity and mortality in both type 1 and 2 diabetes mellitus. It is strongly associated with cardiovascular disease, particularly heart failure, the incidence of which (SGLT-2) is about 15-fold greater with diabetic kidney disease. All-cause mortality in those with diabetic kidney disease is nearly 20–40 times higher than in those without it. Many people with diabetes, particularly type 2, and kidney impairment die from cardiovascular disease well before they progress to end-stage kidney disease. Nevertheless, diabetic kidney disease is the most common single cause of end-stage kidney disease worldwide. Suboptimal glycaemic control and higher blood pressure are particularly important risk factors for developing diabetic kidney disease. Over a lifetime, diabetic kidney disease (any stage) occurs in approximately 30–35% of people with types 1 and 2 diabetes. The disease can usually be detected many years before the development of advanced kidney failure, by identifying raised urinary albumin excretion. Early detection allows time for a multifactorial approach with intensive treatment of glycaemic control, including use of sodium-glucose co-transporter 2 inhibitors, blood pressure reduction (renin–angiotensin system inhibitors as first-line treatment), diet and lifestyle modifications, and lipid-lowering therapy to reduce the associated morbidity and mortality.

We report a case of severe hypercalcaemia secondary to rhabdomyolysis in a woman with COVID-19 (SARS CoV-2) infection. The patient presented with myalgia and anuria with an acute kidney injury requiring haemodialysis. Creatine kinase peaked at 760 000 IU/L. A biphasic calcaemic response was observed with initial severe hypocalcaemia followed by severe, symptomatic hypercalcaemia, persistent despite haemodialysis. Control of the calcium levels was achieved by continuous haemofiltration.

Diabetic nephropathy is a major underlying cause of morbidity and mortality in both type 1 and type 2 diabetes mellitus. It is strongly associated with cardiovascular disease, particularly heart failure, the incidence of which is about 15-fold greater in patients with diabetic nephropathy. All-cause mortality in patients with diabetic nephropathy is nearly 20–40 times higher than in patients without nephropathy. Many patients with diabetes, in particular type 2 diabetes, and renal impairment die from cardiovascular disease well before they progress to end-stage renal disease. Nevertheless, diabetic nephropathy is the most common single cause of end-stage renal disease worldwide. Suboptimal glycaemic control and a higher blood pressure are particularly important risk factors for the development of diabetic nephropathy. Over a lifetime, diabetic nephropathy occurs in approximately 30–35% of patients with type 1 and type 2 diabetes. The disease can usually be detected many years before the development of advanced renal failure through the detection of raised urinary albumin excretion. Early detection allows time for the intensive treatment of glycaemic control, blood pressure and other cardiovascular risk factors, such as lipids, to reduce the morbidity and mortality.

Diabetic nephropathy is a major underlying cause of morbidity and mortality in both type 1 and type 2 diabetes mellitus, giving rise principally to cardiovascular disease, in particular heart failure, the incidence of which is about 15-fold greater in patients with diabetic kidney disease. The all-cause mortality in patients with diabetic nephropathy is nearly 20–40 times higher than in patients without nephropathy. Many patients with diabetes, in particular type 2 diabetes, and renal impairment die from cardiovascular disease well before they progress to end-stage renal disease. Nevertheless, diabetic nephropathy is the most common cause of end-stage renal disease worldwide. Suboptimal glycaemic control and a higher blood pressure are particularly important risk factors for the development of diabetic nephropathy. Over a lifetime, diabetic nephropathy occurs in approximately 30–35% of patients with type 1 and type 2 diabetes. The disease can be detected in most cases many years before the development of advanced renal failure through the detection of raised urinary albumin excretion – microalbuminuria. Early detection allows time for the intensive treatment of glycaemic control, blood pressure and other cardiovascular risk factors, such as lipids, in order to reduce the morbidity and mortality.

Aim To examine the prediction of gestational diabetes in obese women using routine clinical measures and measurement of biomarkers related to insulin resistance in the early second trimester.Methods A total of 117 obese pregnant women participating in a pilot trial of a complex intervention of dietary advice and physical activity were studied. Blood samples were obtained at recruitment (15(+0)-17(+6) weeks' gestation) and demographic, clinical history and anthropometric measures recorded. The biomarkers analysed were plasma lipids (HDL cholesterol, LDL cholesterol, triglycerides), high-sensitivity C-reactive protein, alanine transaminase, aspartate transaminase, ferritin, fructosamine, insulin, adiponectin, tissue plasminogen activator, interleukin-6, visfatin and leptin. Univariate and logistic regression analyses were performed to determine independent predictors and area under the receiver-operating curve was calculated for the model.Results Of the 106 participants included in the analysis, 29 (27.4%) developed gestational diabetes. Participants with gestational diabetes were older (P = 0.002), more often of parity >= 2, had higher systolic (P = 0.02) and diastolic blood pressure (P = 0.02) and were more likely to be black (P = 0.009). Amongst the blood biomarkers measured, plasma adiponectin alone remained independently associated with gestational diabetes in adjusted models (P = 0.002). The area under the receiver-operating curve for clinical factors alone (0.760) increased significantly (area under the curve 0.834, chi-square statistic (1) = 4.00, P = 0.046) with the addition of adiponectin.Conclusions A combination of routinely measured clinical factors and adiponectin measured in the early second trimester in obese women may provide a useful approach to the prediction of gestational diabetes. Validation in a large prospective study is required to determine the usefulness of this algorithm in clinical practice. (Clinical Trial Registry No: ISRCTN89971375)

A 53-year-old man developed progressive sensory disturbance and weakness in the legs, sphincter disturbance, back pain, systemic symptoms, and pancytopenia. Electrophysiological tests indicated a widespread lumbosacral polyradiculopathy. Spinal magnetic resonance imaging and routine cerebrospinal fluid analysis showed minor nonspecific abnormalities. Bone marrow and liver biopsies showed hemophagocytosis; and polymerase chain reaction of cerebrospinal fluid, bone marrow, and serum suggested active infection with human herpesvirus-6. Autopsy revealed that his neurological symptoms resulted from intravascular lymphomatosis (angiotropic large cell lymphoma), a rare variant of lymphoma with predilection for the nervous system.

BJOG: An International Journal of Obstetrics & GynaecologyVolume 104, Issue 12 p. 1413-1415 Thromboembolic disease as a presentation of-gynaecological malignancy Simon A. Butler-Manuel, Corresponding Author Simon A. Butler-Manuel Research Fellow Division of Gynaecological Oncology, Department of Obstetrics and Gynaecology, St Georges Hospital, London.Correspondence: Mr S. A. Butler-Manuel, Division of Gynaecological-Oncology, Department of Obstetrics and Gynaecology,-St George's Hospital, Blackshaw Road, London SWl 7 ORE, UK.Search for more papers by this authorDeborah A. Gould, Deborah A. Gould Research Fellow Division of Gynaecological Oncology, Department of Obstetrics and Gynaecology, St Georges Hospital, London.Search for more papers by this authorStephen M. Thomas, Stephen M. Thomas Senior Registrar Department of Radiology, St Georges Hospital, London.Search for more papers by this authorPaul G. Carter, Paul G. Carter Senior Registrar Division of Gynaecological Oncology, Department of Obstetrics and Gynaecology, St Georges Hospital, London.Search for more papers by this authorDesmond P. J. Barton, Desmond P. J. Barton Consultant Division of Gynaecological Oncology, Department of Obstetrics and Gynaecology, St Georges Hospital, London.Search for more papers by this author Simon A. Butler-Manuel, Corresponding Author Simon A. Butler-Manuel Research Fellow Division of Gynaecological Oncology, Department of Obstetrics and Gynaecology, St Georges Hospital, London.Correspondence: Mr S. A. Butler-Manuel, Division of Gynaecological-Oncology, Department of Obstetrics and Gynaecology,-St George's Hospital, Blackshaw Road, London SWl 7 ORE, UK.Search for more papers by this authorDeborah A. Gould, Deborah A. Gould Research Fellow Division of Gynaecological Oncology, Department of Obstetrics and Gynaecology, St Georges Hospital, London.Search for more papers by this authorStephen M. Thomas, Stephen M. Thomas Senior Registrar Department of Radiology, St Georges Hospital, London.Search for more papers by this authorPaul G. Carter, Paul G. Carter Senior Registrar Division of Gynaecological Oncology, Department of Obstetrics and Gynaecology, St Georges Hospital, London.Search for more papers by this authorDesmond P. J. Barton, Desmond P. J. Barton Consultant Division of Gynaecological Oncology, Department of Obstetrics and Gynaecology, St Georges Hospital, London.Search for more papers by this author First published: 19 August 2005 https://doi.org/10.1111/j.1471-0528.1997.tb11014.xCitations: 5Read the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat Citing Literature Volume104, Issue12December 1997Pages 1413-1415 RelatedInformation

Australian and New Zealand Journal of MedicineVolume 23, Issue 2 p. 216-217 Hypoplastic crisis with persistent arthralgia and prolonged parvovirus B19 viraemia detected by polymerase chain reaction M. G. CATTON, M. G. CATTON Registrar, Department of Virology and Immunology, Auckland Public Hospital, Auckland, New Zealand.Search for more papers by this authorS. M. THOMAS, S. M. THOMAS Scientific Officer, Department of Virology and Immunology, Auckland Public Hospital, Auckland, New Zealand.Search for more papers by this authorH. A. BLACKLOCK, H. A. BLACKLOCK Consultant Haematologist, Department of Haematology, Middlemore Hospital, Auckland, New Zealand.Search for more papers by this authorM. C. CROXSON, M. C. CROXSON Virologist in Charge, Department of Virology and Immunology, Auckland Public Hospital, Auckland, New Zealand.Search for more papers by this author M. G. CATTON, M. G. CATTON Registrar, Department of Virology and Immunology, Auckland Public Hospital, Auckland, New Zealand.Search for more papers by this authorS. M. THOMAS, S. M. THOMAS Scientific Officer, Department of Virology and Immunology, Auckland Public Hospital, Auckland, New Zealand.Search for more papers by this authorH. A. BLACKLOCK, H. A. BLACKLOCK Consultant Haematologist, Department of Haematology, Middlemore Hospital, Auckland, New Zealand.Search for more papers by this authorM. C. CROXSON, M. C. CROXSON Virologist in Charge, Department of Virology and Immunology, Auckland Public Hospital, Auckland, New Zealand.Search for more papers by this author First published: April 1993 https://doi.org/10.1111/j.1445-5994.1993.tb01820.xAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinkedInRedditWechat No abstract is available for this article. Volume23, Issue2April 1993Pages 216-217 RelatedInformation