Sharon Andreoli

Bio: Sharon Andreoli is an academic researcher from Indiana University. The author has contributed to research in topics: Kidney disease & Dialysis. The author has an hindex of 21, co-authored 94 publications receiving 3985 citations. Previous affiliations of Sharon Andreoli include Riley Hospital for Children.

Treatment and outcome of Shiga-toxin-associated hemolytic uremic syndrome (HUS).

Abstract: Hemolytic uremic syndrome (HUS) is the most common cause of acute renal failure in childhood and the reason for chronic renal replacement therapy. It leads to significant morbidity and mortality during the acute phase. In addition to acute morbidity and mortality, long-term renal and extrarenal complications can occur in a substantial number of children years after the acute episode of HUS. The most common infectious agents causing HUS are enterohemorrhagic Escherichia coli (EHEC)-producing Shiga toxin (and belonging to the serotype O157:H7) and several non-O157:H7 serotypes. D+ HUS is an acute disease characterized by prodromal diarrhea followed by acute renal failure. The classic clinical features of HUS include the triad of microangiopathic hemolytic anemia, thrombocytopenia, and acute renal failure. HUS mortality is reported to be between 3% and 5%, and death due to HUS is nearly always associated with severe extrarenal disease, including severe central nervous system (CNS) involvement. Approximately two thirds of children with HUS require dialysis therapy, and about one third have milder renal involvement without the need for dialysis therapy. General management of acute renal failure includes appropriate fluid and electrolyte management, antihypertensive therapy if necessary, and initiation of renal replacement therapy when appropriate. The prognosis of HUS depends on several contributing factors. In general “classic” HUS, induced by EHEC, has an overall better outcome. Totally different is the prognosis in patients with atypical and particularly recurrent HUS. However, patients with severe disease should be screened for genetic disorders of the complement system or other underlying diseases.

Hemolytic uremic syndrome: epidemiology, pathophysiology, and therapy.

Abstract: Shiga toxin (Stx)-producing Escherichia coli (STEC) were first linked to human disease in 1982 [1]. At that time an E. coli serotype (O157:H7) that had not previously been linked with human disease was found to be associated with outbreaks of hemorrhagic colitis [1]. Subsequent studies demonstrated that E. coli O157:H7 produced potent toxins that were genetically and physically very similar to Stx from Shigella dysenteriae type 1 [2]. The link between STEC infections and hemolytic uremic syndrome (HUS) was established in the 1980s in Canada by Karmali et al. [3] when they found that infection with various serotypes of STEC was strongly associated with the subsequent development of HUS. The most common E. coli serotype identified to cause hemorrhagic colitis and HUS in the United States was the single serotype – O157:H7. The reason this serotype is most commonly identified in STEC infections is that it is relatively easy to identify in clinical microbiology laboratories due to its inability to ferment sorbitol. Since the first description of O157:H7 as a human pathogen in 1983, it has become apparent that E. coli O157:H7 is but one of a much larger family of STEC whose primary virulence characteristic is the ability to produce Stxs [2, 3, 4]. STEC are clinically associated with both bloody and non-bloody diarrhea as well as systemic complications such as HUS [4]. It is now clear that there are at least 200 different types of STEC, of which approximately 60 have been associated with disease in humans [2, 4, 5]. Non-O157 STEC, especially E. coli O111, have been the cause of major outbreaks in both the United States and other parts of the world [6, 7]. However, apart from the occasional outbreak of nonO157 in the United States, the association of nonO157:H7 STEC with disease in this country is largely undetermined. Of note, the majority of laboratories do not routinely look for non-O157 STEC [8], suggesting that lack of diagnosis of non-O157:H7 disease is a failure of use of appropriate diagnostic techniques. Compatible with this hypothesis are at least two small studies in which non-O157:H7 STEC were routinely found in patients submitting stools for microbiological analysis in the United States. [9, 10]. Recent work from our laboratory in collaboration with multiple sites in the United States has attempted to determine the prevalence of both O157 and non-O157 STEC in selected sites in the United States. We have performed multi-site surveillance studies to determine the prevalence of O157 and non-O157 STEC in stool samples submitted to clinical microbiology laboratories for S.P. Andreoli is the editor of the Proceedings and H. Trachtman the associate editor. D.W.K. Acheson is the author of the section Microbiology and epidemiology of Shiga toxin-induced hemolytic uremic syndrome, R.L. Siegler is the author of the section Animal models of Stx-mediated HUS, T.G. Obrig is the author of the section Mechanisms of Stx-mediated cell injury, and H. Trachtman is author of the section New and future therapies for diarrhea-associated HUS.

A New Equation to Estimate Glomerular Filtration Rate

Abstract: The Modification of Diet in Renal Disease (MDRD) Study equation underestimates glomerular filtration rate (GFR) in patients with mild kidney disease. Levey and associates therefore developed and va...

Vitamin D Deficiency

Abstract: Once foods in the United States were fortified with vitamin D, rickets appeared to have been conquered, and many considered major health problems from vitamin D deficiency resolved. But vitamin D deficiency is common. This review considers the role of vitamin D in skeletal and nonskeletal health and suggests strategies for the prevention and treatment of vitamin D deficiency.

Standards of Medical Care in Diabetes

Abstract: XI. STRATEGIES FOR IMPROVING DIABETES CARE D iabetes is a chronic illness that requires continuing medical care and patient self-management education to prevent acute complications and to reduce the risk of long-term complications. Diabetes care is complex and requires that many issues, beyond glycemic control, be addressed. A large body of evidence exists that supports a range of interventions to improve diabetes outcomes. These standards of care are intended to provide clinicians, patients, researchers, payors, and other interested individuals with the components of diabetes care, treatment goals, and tools to evaluate the quality of care. While individual preferences, comorbidities, and other patient factors may require modification of goals, targets that are desirable for most patients with diabetes are provided. These standards are not intended to preclude more extensive evaluation and management of the patient by other specialists as needed. For more detailed information, refer to Bode (Ed.): Medical Management of Type 1 Diabetes (1), Burant (Ed): Medical Management of Type 2 Diabetes (2), and Klingensmith (Ed): Intensive Diabetes Management (3). The recommendations included are diagnostic and therapeutic actions that are known or believed to favorably affect health outcomes of patients with diabetes. A grading system (Table 1), developed by the American Diabetes Association (ADA) and modeled after existing methods, was utilized to clarify and codify the evidence that forms the basis for the recommendations. The level of evidence that supports each recommendation is listed after each recommendation using the letters A, B, C, or E.

Pathogenic Escherichia coli

Abstract: Few microorganisms are as versatile as Escherichia coli. An important member of the normal intestinal microflora of humans and other mammals, E. coli has also been widely exploited as a cloning host in recombinant DNA technology. But E. coli is more than just a laboratory workhorse or harmless intestinal inhabitant; it can also be a highly versatile, and frequently deadly, pathogen. Several different E. coli strains cause diverse intestinal and extraintestinal diseases by means of virulence factors that affect a wide range of cellular processes.

Mineral Metabolism, Mortality, and Morbidity in Maintenance Hemodialysis

Abstract: Mortality rates in ESRD are unacceptably high. Disorders of mineral metabolism (hyperphosphatemia, hypercalcemia, and secondary hyperparathyroidism) are potentially modifiable. For determining associations among disorders of mineral metabolism, mortality, and morbidity in hemodialysis patients, data on 40,538 hemodialysis patients with at least one determination of serum phosphorus and calcium during the last 3 mo of 1997 were analyzed. Unadjusted, case mix-adjusted, and multivariable-adjusted relative risks of death were calculated for categories of serum phosphorus, calcium, calcium x phosphorus product, and intact parathyroid hormone (PTH) using proportional hazards regression. Also determined was whether disorders of mineral metabolism were associated with all-cause, cardiovascular, infection-related, fracture-related, and vascular access-related hospitalization. After adjustment for case mix and laboratory variables, serum phosphorus concentrations >5.0 mg/dl were associated with an increased relative risk of death (1.07, 1.25, 1.43, 1.67, and 2.02 for serum phosphorus 5.0 to 6.0, 6.0 to 7.0, 7.0 to 8.0, 8.0 to 9.0, and >/=9.0 mg/dl). Higher adjusted serum calcium concentrations were also associated with an increased risk of death, even when examined within narrow ranges of serum phosphorus. Moderate to severe hyperparathyroidism (PTH concentrations >/=600 pg/ml) was associated with an increase in the relative risk of death, whereas more modest increases in PTH were not. When examined collectively, the population attributable risk percentage for disorders of mineral metabolism was 17.5%, owing largely to the high prevalence of hyperphosphatemia. Hyperphosphatemia and hyperparathyroidism were significantly associated with all-cause, cardiovascular, and fracture-related hospitalization. Disorders of mineral metabolism are independently associated with mortality and morbidity associated with cardiovascular disease and fracture in hemodialysis patients.