Pub Date : 2023-07-01DOI: 10.1016/j.semnephrol.2023.151435
Martin Windpessl MD , Balazs Odler MD, PhD , Ingeborg M. Bajema MD, PhD , Duvuru Geetha MD , Marcus Säemann MD , Jiwon M. Lee MD , Augusto Vaglio MD , Andreas Kronbichler MD, PhD
Glomerular diseases are common causes of chronic kidney disease in childhood, adolescence, and adulthood. The epidemiology of glomerular diseases differs between different age groups, with minimal change disease being the leading cause of nephrotic syndrome in childhood, while membranous nephropathy and focal segmental glomerulosclerosis are more common in adulthood. IgA vasculitis is also more common in childhood. Moreover, there is a difference in disease severity with more children presenting with a relapsing form of nephrotic syndrome and a more acute presentation of antineutrophil cytoplasmic antibody–associated vasculitis and concomitant glomerulonephritis, as highlighted by the higher percentage of cellular crescents on kidney biopsy specimens in comparison with older patients. There is also a female preponderance in antineutrophil cytoplasmic antibody–associated vasculitis and more children present with tracheobroncholaryngeal disease. This article aims to summarize differences in the presentation of different glomerular diseases that are encountered commonly by pediatric and adult nephrologists and potential differences in the management.
{"title":"Glomerular Diseases Across Lifespan: Key Differences in Diagnostic and Therapeutic Approaches","authors":"Martin Windpessl MD , Balazs Odler MD, PhD , Ingeborg M. Bajema MD, PhD , Duvuru Geetha MD , Marcus Säemann MD , Jiwon M. Lee MD , Augusto Vaglio MD , Andreas Kronbichler MD, PhD","doi":"10.1016/j.semnephrol.2023.151435","DOIUrl":"10.1016/j.semnephrol.2023.151435","url":null,"abstract":"<div><div>Glomerular diseases are common causes of chronic kidney disease in childhood, adolescence, and adulthood. The epidemiology of glomerular diseases differs between different age groups, with minimal change disease being the leading cause of nephrotic syndrome in childhood, while membranous nephropathy and focal segmental glomerulosclerosis are more common in adulthood. IgA vasculitis is also more common in childhood. Moreover, there is a difference in disease severity with more children presenting with a relapsing form of nephrotic syndrome and a more acute presentation of antineutrophil cytoplasmic antibody–associated vasculitis and concomitant glomerulonephritis, as highlighted by the higher percentage of cellular crescents on kidney biopsy specimens in comparison with older patients. There is also a female preponderance in antineutrophil cytoplasmic antibody–associated vasculitis and more children present with tracheobroncholaryngeal disease. This article aims to summarize differences in the presentation of different glomerular diseases that are encountered commonly by pediatric and adult nephrologists and potential differences in the management.</div></div>","PeriodicalId":21756,"journal":{"name":"Seminars in nephrology","volume":"43 4","pages":"Article 151435"},"PeriodicalIF":2.8,"publicationDate":"2023-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"72015333","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-07-01DOI: 10.1016/j.semnephrol.2023.151437
Johannes Münch MD , Paul R. Goodyer MD , Carsten A. Wagner MD
The tubular system of the kidneys is a complex series of morphologic and functional units orchestrating the content of tubular fluid as it flows along the nephron and collecting ducts. Renal tubules maintain body water, regulate electrolytes and acid–base balance, reabsorb precious organic solutes, and eliminate specific metabolites, toxins, and drugs. In addition, decisive mechanisms to adjust blood pressure are governed by the renal tubules. Genetic as well as acquired disorders of these tubular functions may cause serious diseases that manifest both in childhood and adulthood. This article addresses a selection of tubulopathies and the underlying pathomechanisms, while highlighting the important differences in pediatric and adult nephrology care. These range from rare monogenic conditions such as nephrogenic diabetes insipidus, cystinosis, and Bartter syndrome that present in childhood, to the genetic and acquired tubular pathologies causing hypertension or nephrolithiasis that are more prevalent in adults. Both pediatric and adult nephrologists must be aware of these conditions and the age-dependent manifestations that warrant close interaction between the two subspecialties.
{"title":"Tubular Diseases and Stones Seen From Pediatric and Adult Nephrology Perspectives","authors":"Johannes Münch MD , Paul R. Goodyer MD , Carsten A. Wagner MD","doi":"10.1016/j.semnephrol.2023.151437","DOIUrl":"10.1016/j.semnephrol.2023.151437","url":null,"abstract":"<div><div>The tubular system of the kidneys is a complex series of morphologic and functional units orchestrating the content of tubular fluid as it flows along the nephron and collecting ducts. Renal tubules maintain body water, regulate electrolytes and acid–base balance, reabsorb precious organic solutes, and eliminate specific metabolites, toxins, and drugs. In addition, decisive mechanisms to adjust blood pressure are governed by the renal tubules. Genetic as well as acquired disorders of these tubular functions may cause serious diseases that manifest both in childhood and adulthood. This article addresses a selection of tubulopathies and the underlying pathomechanisms, while highlighting the important differences in pediatric and adult nephrology care. These range from rare monogenic conditions such as nephrogenic diabetes insipidus, cystinosis, and Bartter syndrome that present in childhood, to the genetic and acquired tubular pathologies causing hypertension or nephrolithiasis that are more prevalent in adults. Both pediatric and adult nephrologists must be aware of these conditions and the age-dependent manifestations that warrant close interaction between the two subspecialties.</div></div>","PeriodicalId":21756,"journal":{"name":"Seminars in nephrology","volume":"43 4","pages":"Article 151437"},"PeriodicalIF":2.8,"publicationDate":"2023-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"134649725","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-07-01DOI: 10.1016/j.semnephrol.2023.151433
Bärbel Lange-Sperandio MD , Hans-Joachim Anders MD , Maximilian Stehr MD , Robert L. Chevalier MD , Richard Klaus MD
Congenital anomalies of the kidney and urinary tract (CAKUT) are the leading cause of kidney failure in children and adolescents. CAKUT describes a wide spectrum of structural disorders with a prenatal origin. The etiology of CAKUT is multifactorial, including environmental, nongenetic, and genetic causes that impact kidney development as well as upper and lower urinary tract development. Adult nephrologists who treat patients with CAKUT may be challenged by the underlying diseases they are not familiar with and the accumulation of chronic kidney disease complications in childhood. This article discusses CAKUT etiology and presentation, the course during childhood and adolescence, as well as adult issues in CAKUT patients including CKD complications, urologic interventions, and genetic counseling. A smooth transition of CAKUT patients from pediatric to adult care can be challenging.
{"title":"Congenital Anomalies of the Kidney and Urinary Tract: A Continuum of Care","authors":"Bärbel Lange-Sperandio MD , Hans-Joachim Anders MD , Maximilian Stehr MD , Robert L. Chevalier MD , Richard Klaus MD","doi":"10.1016/j.semnephrol.2023.151433","DOIUrl":"10.1016/j.semnephrol.2023.151433","url":null,"abstract":"<div><div><span>Congenital anomalies of the kidney and </span>urinary tract<span><span><span> (CAKUT) are the leading cause of kidney failure in children and adolescents. CAKUT<span> describes a wide spectrum of structural disorders with a prenatal origin. The etiology of CAKUT is multifactorial, including environmental, nongenetic, and genetic causes that impact kidney development as well as upper and lower urinary tract development. Adult nephrologists who treat patients with CAKUT may be challenged by the underlying diseases they are not familiar with and the accumulation of </span></span>chronic kidney disease complications in childhood. This article discusses CAKUT etiology and presentation, the course during childhood and adolescence, as well as adult issues in CAKUT patients including CKD complications, urologic interventions, and genetic counseling. A smooth transition of CAKUT patients from </span>pediatric to adult care can be challenging.</span></div></div>","PeriodicalId":21756,"journal":{"name":"Seminars in nephrology","volume":"43 4","pages":"Article 151433"},"PeriodicalIF":2.8,"publicationDate":"2023-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"136127164","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-07-01DOI: 10.1016/j.semnephrol.2023.151434
Christian Hanna MD, MS , Ioan-Andrei Iliuta MD , Whitney Besse MD , Djalila Mekahli MD, PhD , Fouad T. Chebib MD
Cystic kidney diseases, when broadly defined, have a wide differential diagnosis extending from recessive diseases with a prenatal or pediatric diagnosis, to the most common autosomal-dominant polycystic kidney disease primarily affecting adults, and several other genetic or acquired etiologies that can manifest with kidney cysts. The most likely diagnoses to consider when assessing a patient with cystic kidney disease differ depending on family history, age stratum, radiologic characteristics, and extrarenal features. Accurate identification of the underlying condition is crucial to estimate the prognosis and initiate the appropriate management, identification of extrarenal manifestations, and counseling on recurrence risk in future pregnancies. There are significant differences in the clinical approach to investigating and managing kidney cysts in children compared with adults. Next-generation sequencing has revolutionized the diagnosis of inherited disorders of the kidney, despite limitations in access and challenges in interpreting the data. Disease-modifying treatments are lacking in the majority of kidney cystic diseases. For adults with rapid progressive autosomal-dominant polycystic kidney disease, tolvaptan (V2-receptor antagonist) has been approved to slow the rate of decline in kidney function. In this article, we examine the differences in the differential diagnosis and clinical management of cystic kidney disease in children versus adults, and we highlight the progress in molecular diagnostics and therapeutics, as well as some of the gaps meriting further attention.
{"title":"Cystic Kidney Diseases in Children and Adults: Differences and Gaps in Clinical Management","authors":"Christian Hanna MD, MS , Ioan-Andrei Iliuta MD , Whitney Besse MD , Djalila Mekahli MD, PhD , Fouad T. Chebib MD","doi":"10.1016/j.semnephrol.2023.151434","DOIUrl":"10.1016/j.semnephrol.2023.151434","url":null,"abstract":"<div><div>Cystic kidney diseases, when broadly defined, have a wide differential diagnosis extending from recessive diseases with a prenatal or pediatric<span><span><span> diagnosis, to the most common autosomal-dominant polycystic kidney disease primarily affecting adults, and several other genetic or acquired etiologies that can manifest with kidney cysts. The most likely diagnoses to consider when assessing a patient with cystic kidney disease differ depending on family history, age stratum, radiologic characteristics, and extrarenal features. Accurate identification of the underlying condition is crucial to estimate the prognosis and initiate the appropriate management, identification of extrarenal manifestations, and counseling on recurrence risk in future pregnancies. There are significant differences in the </span>clinical approach<span> to investigating and managing kidney cysts in children compared with adults. Next-generation sequencing has revolutionized the diagnosis of inherited disorders of the kidney, despite limitations in access and challenges in interpreting the data. Disease-modifying treatments are lacking in the majority of kidney cystic diseases. For adults with rapid progressive autosomal-dominant polycystic kidney disease, tolvaptan (V2-receptor antagonist) has been approved to slow the rate of decline in kidney function. In this article, we examine the differences in the differential diagnosis and clinical management of cystic kidney disease in children versus adults, and we highlight the progress in </span></span>molecular diagnostics and therapeutics, as well as some of the gaps meriting further attention.</span></div></div>","PeriodicalId":21756,"journal":{"name":"Seminars in nephrology","volume":"43 4","pages":"Article 151434"},"PeriodicalIF":2.8,"publicationDate":"2023-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138299946","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-07-01DOI: 10.1016/j.semnephrol.2023.151439
Rolando Claure-Del Granado MD , Javier A. Neyra MD , Rajit K. Basu MD, MS
Acute kidney injury (AKI) occurs frequently in hospitalized patients, regardless of age or prior medical history. Increasing awareness of the epidemiologic problem of AKI has directly led to increased study of global recognition, diagnostic tools, both reactive and proactive management, and analysis of long-term sequelae. Many gaps remain, however, and in this article we highlight opportunities to add significantly to the increasing bodies of evidence surrounding AKI. Practical considerations related to initiation, prescription, anticoagulation, and monitoring are discussed. In addition, the importance of AKI follow-up evaluation, particularly for those surviving the receipt of renal replacement therapy, is highlighted as a push for global equity in the realm of critical care nephrology is broached. Addressing these gaps presents an opportunity to impact patient care directly and improve patient outcomes.
{"title":"Acute Kidney Injury: Gaps and Opportunities for Knowledge and Growth","authors":"Rolando Claure-Del Granado MD , Javier A. Neyra MD , Rajit K. Basu MD, MS","doi":"10.1016/j.semnephrol.2023.151439","DOIUrl":"10.1016/j.semnephrol.2023.151439","url":null,"abstract":"<div><div><span><span>Acute kidney injury<span> (AKI) occurs frequently in hospitalized patients, regardless of age or prior medical history. Increasing awareness of the epidemiologic problem of AKI has directly led to increased study of global recognition, diagnostic tools, both reactive and proactive management, and analysis of long-term </span></span>sequelae<span><span>. Many gaps remain, however, and in this article we highlight opportunities to add significantly to the increasing bodies of evidence surrounding AKI. Practical considerations related to initiation, prescription, anticoagulation, and monitoring are discussed. In addition, the importance of AKI follow-up evaluation, particularly for those surviving the receipt of </span>renal replacement therapy, is highlighted as a push for global equity in the realm of critical care </span></span>nephrology is broached. Addressing these gaps presents an opportunity to impact patient care directly and improve patient outcomes.</div></div>","PeriodicalId":21756,"journal":{"name":"Seminars in nephrology","volume":"43 4","pages":"Article 151439"},"PeriodicalIF":2.8,"publicationDate":"2023-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"134649724","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-07-01DOI: 10.1016/j.semnephrol.2023.151441
Robert H. Mak MD, PhD , Arpana Iyengar MD, PhD , Angela Yee-Moon Wang MD, PhD
Common goals of nutritional therapy across the spectrum of pediatric and adult chronic kidney disease (CKD) include maintaining normal body mass and composition and reducing associated morbidity and mortality. Adult nephrologists caring for children and adolescents may be challenged by the existing complexities in identifying and interpreting the nutritional status and growth in children. Pediatric nephrologists may face situations that call for a sound knowledge of assessing nutritional status and providing nutrition therapy for adolescents and young adults. One important additional nutrition goal in children is to achieve normal growth and development. Children are growing and therefore need more calories and nutrients than just maintaining their body weight and composition. Lack of weight and height gain actually is considered failure to thrive in children. Some fundamental differences in approaches to nutritional therapy in CKD are necessitated based on the etiology of CKD. A large proportion of adults with CKD are diabetics, so the approach would be a low-carbohydrate diet. Children with CKD, especially young ones, often are anorexic, so calorie supplements that could include quite a lot of carbohydrates often are prescribed. More adults with CKD have hypertension and atherosclerotic comorbidities, which result in recommendations for low-salt and low-fat diets. Children with CKD often have salt and electrolyte wasting disease states and would require normal- or even high-salt diets, and fats often are included in supplements to bolster calorie intake. Low-protein diets often are recommended in adults with predialysis CKD to slow disease progression. Children are growing and have a higher protein daily requirement. Low-protein diets have not been found to be efficacious in children with CKD, in achieving normal growth, or in slowing disease progression. Adult nephrologists caring for children and adolescents may be challenged by the existing complexities in identifying and interpreting nutritional status and growth in children. Pediatric nephrologists may face situations that call for a sound knowledge of assessing nutritional status and providing nutrition therapy for adolescents and young adults. This article discusses the differences in the assessment of nutritional status between children and adults, as well as provides a comprehensive approach to nutritional management for CKD across the age spectrum.
{"title":"Nutrition Management for Chronic Kidney Disease: Differences and Special Needs for Children and Adults","authors":"Robert H. Mak MD, PhD , Arpana Iyengar MD, PhD , Angela Yee-Moon Wang MD, PhD","doi":"10.1016/j.semnephrol.2023.151441","DOIUrl":"10.1016/j.semnephrol.2023.151441","url":null,"abstract":"<div><div>Common goals of nutritional therapy across the spectrum of pediatric and adult chronic kidney disease (CKD) include maintaining normal body mass and composition and reducing associated morbidity and mortality. Adult nephrologists caring for children and adolescents may be challenged by the existing complexities in identifying and interpreting the nutritional status and growth in children. Pediatric nephrologists may face situations that call for a sound knowledge of assessing nutritional status and providing nutrition therapy for adolescents and young adults. One important additional nutrition goal in children is to achieve normal growth and development. Children are growing and therefore need more calories and nutrients than just maintaining their body weight and composition. Lack of weight and height gain actually is considered failure to thrive in children. Some fundamental differences in approaches to nutritional therapy in CKD are necessitated based on the etiology of CKD. A large proportion of adults with CKD are diabetics, so the approach would be a low-carbohydrate diet. Children with CKD, especially young ones, often are anorexic, so calorie supplements that could include quite a lot of carbohydrates often are prescribed. More adults with CKD have hypertension and atherosclerotic comorbidities, which result in recommendations for low-salt and low-fat diets. Children with CKD often have salt and electrolyte wasting disease states and would require normal- or even high-salt diets, and fats often are included in supplements to bolster calorie intake. Low-protein diets often are recommended in adults with predialysis CKD to slow disease progression. Children are growing and have a higher protein daily requirement. Low-protein diets have not been found to be efficacious in children with CKD, in achieving normal growth, or in slowing disease progression. Adult nephrologists caring for children and adolescents may be challenged by the existing complexities in identifying and interpreting nutritional status and growth in children. Pediatric nephrologists may face situations that call for a sound knowledge of assessing nutritional status and providing nutrition therapy for adolescents and young adults. This article discusses the differences in the assessment of nutritional status between children and adults, as well as provides a comprehensive approach to nutritional management for CKD across the age spectrum.</div></div>","PeriodicalId":21756,"journal":{"name":"Seminars in nephrology","volume":"43 4","pages":"Article 151441"},"PeriodicalIF":2.8,"publicationDate":"2023-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138047843","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Progression of chronic kidney disease in type 2 diabetes has been understood conventionally as a consequence of intraglomerular hemodynamic changes and aberrant metabolic pathways. However, an increasing body of experimental evidence has highlighted the role of inflammatory response in the progression of diabetic kidney disease. Macrophage polarization in response to specific microenvironmental stimuli affects the pathology of diabetic kidneys. The diabetic milieu also up-regulates inflammatory cytokines, chemokines, and adhesion molecules, and promotes inflammatory signal transduction pathways, including inflammasomes. Therefore, from a reverse translational perspective, modulation of the inflammatory response may be the driving force of the renoprotective effects of renin-angiotensin system inhibitors, sodium-glucose cotransporter-2 inhibitors, and mineralocorticoid receptor antagonists, all of which have been shown to slow disease progression. Currently, many agents that target the inflammation in the kidneys directly are evaluated in clinical trials. This article discusses recent clinical and experimental milestones in drug development for diabetic kidney disease with a perspective on inflammation in the kidneys. Such insights may enable a targeted approach to discovering novel drugs against chronic kidney disease in type 2 diabetes.
{"title":"Role of Inflammation in Progression of Chronic Kidney Disease in Type 2 Diabetes Mellitus: Clinical Implications","authors":"Yasuhiro Oda MD, Hiroshi Nishi MD, PhD, Masaomi Nangaku MD, PhD","doi":"10.1016/j.semnephrol.2023.151431","DOIUrl":"10.1016/j.semnephrol.2023.151431","url":null,"abstract":"<div><p><span><span>Progression of chronic kidney disease<span> in type 2 diabetes has been understood conventionally as a consequence of intraglomerular hemodynamic changes and aberrant metabolic pathways. However, an increasing body of experimental evidence has highlighted the role of inflammatory response in the progression of </span></span>diabetic kidney disease<span><span><span><span>. Macrophage polarization in response to specific microenvironmental stimuli affects the pathology of diabetic kidneys. The diabetic milieu also up-regulates </span>inflammatory cytokines, </span>chemokines, and </span>adhesion molecules<span>, and promotes inflammatory signal transduction pathways<span><span>, including inflammasomes. Therefore, from a reverse translational perspective, modulation of the inflammatory response may be the driving force of the renoprotective effects of renin-angiotensin system inhibitors, sodium-glucose cotransporter-2 inhibitors, and </span>mineralocorticoid receptor antagonists<span>, all of which have been shown to slow disease progression. Currently, many agents that target the inflammation in the kidneys directly are evaluated in </span></span></span></span></span>clinical trials<span>. This article discusses recent clinical and experimental milestones in drug development for diabetic kidney disease with a perspective on inflammation in the kidneys. Such insights may enable a targeted approach to discovering novel drugs against chronic kidney disease in type 2 diabetes.</span></p></div>","PeriodicalId":21756,"journal":{"name":"Seminars in nephrology","volume":"43 3","pages":"Article 151431"},"PeriodicalIF":3.3,"publicationDate":"2023-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"49692289","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-05-01DOI: 10.1016/j.semnephrol.2023.151428
Keith C. Norris MD, PhD , Sandra F. Williams DMD, MB , Robert Nee MD
Diabetic kidney disease (DKD) remains a major health care issue and is beset with significant racial and ethnic disparities in regard to its incidence, progression, and complication rate. An individual's health is influenced strongly by an array of societal-level factors commonly called the social determinants of health. Among these, DKD is influenced highly by structured resources and opportunities, as well as an individual's socioeconomic status, health insurance status, access to care, education, health literacy, nutrition, green space exposure, level of trust in the medical community, and more. Health equity is considered a state in which everyone has a fair and just opportunity to attain his or her highest level of health. Conversely, health inequities are a consequence of a structured discriminatory system of inequitable allocation of social determinants of health. When this discriminatory system is race-based it is referred to as structural racism, which eventually leads to racial and ethnic health disparities. The further downstream sequela of structural racism, consciously or unconsciously, impacts health systems, providers, and patients, and can lead to disparities in DKD development, progression, and complications. In this article, we explore potential interventions at the societal, health system, and provider levels that can help flatten the playing field and reduce racial and ethnic disparities in DKD.
{"title":"Flattening the Playing Field for Treatment of Diabetic Kidney Disease","authors":"Keith C. Norris MD, PhD , Sandra F. Williams DMD, MB , Robert Nee MD","doi":"10.1016/j.semnephrol.2023.151428","DOIUrl":"10.1016/j.semnephrol.2023.151428","url":null,"abstract":"<div><p>Diabetic kidney disease (DKD) remains a major health care issue and is beset with significant racial and ethnic disparities in regard to its incidence, progression, and complication rate. An individual's health is influenced strongly by an array of societal-level factors commonly called the <em>social determinants of health</em>. Among these, DKD is influenced highly by structured resources and opportunities, as well as an individual's socioeconomic status, health insurance status, access to care, education, health literacy, nutrition, green space exposure, level of trust in the medical community, and more. Health equity is considered a state in which everyone has a fair and just opportunity to attain his or her highest level of health. Conversely, health inequities are a consequence of a structured discriminatory system of inequitable allocation of social determinants of health. When this discriminatory system is race-based it is referred to as <em>structural racism</em>, which eventually leads to racial and ethnic health disparities. The further downstream sequela of structural racism, consciously or unconsciously, impacts health systems, providers, and patients, and can lead to disparities in DKD development, progression, and complications. In this article, we explore potential interventions at the societal, health system, and provider levels that can help flatten the playing field and reduce racial and ethnic disparities in DKD.</p></div>","PeriodicalId":21756,"journal":{"name":"Seminars in nephrology","volume":"43 3","pages":"Article 151428"},"PeriodicalIF":3.3,"publicationDate":"2023-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0270929523001389/pdfft?md5=8da2a2adae7b67bb92525d4b6dcbd70a&pid=1-s2.0-S0270929523001389-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"49692287","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-05-01DOI: 10.1016/j.semnephrol.2023.151426
Friedrich C. Luft MD
The good old days were not good, at least in terms of treating patients with type 2 diabetes. In the 1960s, the development of a radioimmunoassay for insulin permitted determination of the distinguishing features of type 1 and type 2 diabetes. The latter was treated with sulfonylureas and then phenformin, although the mechanisms of action at the time were unknown. The University Group Diabetes Program was a randomized controlled trial experienced by my medical generation, and the results were dramatic, both medically and legally. Next came the thiazolidinediones. All compounds were associated with weight gain and any end point benefits were uncertain. Nevertheless, basic science explained how glucose is sensed and even found a home for sulfonylureas in some patients. Next came the boom in renin-angiotensin-aldosterone system blockade, sacred ground for many, albeit the benefits were less than astounding. Other wonder drugs came and went. Over the decades, great strides were made in defining the pathology of diabetic renal disease, which is appropriate because the condition has become a primary cause of end-stage renal failure. Nonetheless, recent advances have turned around a depressing situation and are reasons for optimism. We now have compounds that actually could help patients with type 2 diabetes. One hundred years after insulin's introduction, it is high time.
{"title":"Sixty Years of Confronting Diabetes and Kidney Disease","authors":"Friedrich C. Luft MD","doi":"10.1016/j.semnephrol.2023.151426","DOIUrl":"10.1016/j.semnephrol.2023.151426","url":null,"abstract":"<div><p>The good old days were not good, at least in terms of treating patients with type 2 diabetes. In the 1960s, the development of a radioimmunoassay for insulin permitted determination of the distinguishing features of type 1 and type 2 diabetes. The latter was treated with sulfonylureas and then phenformin, although the mechanisms of action at the time were unknown. The University Group Diabetes Program was a randomized controlled trial experienced by my medical generation, and the results were dramatic, both medically and legally. Next came the thiazolidinediones. All compounds were associated with weight gain and any end point benefits were uncertain. Nevertheless, basic science explained how glucose is sensed and even found a home for sulfonylureas in some patients. Next came the boom in renin-angiotensin-aldosterone system blockade, sacred ground for many, albeit the benefits were less than astounding. Other wonder drugs came and went. Over the decades, great strides were made in defining the pathology of diabetic renal disease, which is appropriate because the condition has become a primary cause of end-stage renal failure. Nonetheless, recent advances have turned around a depressing situation and are reasons for optimism. We now have compounds that actually could help patients with type 2 diabetes. One hundred years after insulin's introduction, it is high time.</p></div>","PeriodicalId":21756,"journal":{"name":"Seminars in nephrology","volume":"43 3","pages":"Article 151426"},"PeriodicalIF":3.3,"publicationDate":"2023-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"49682107","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-05-01DOI: 10.1016/j.semnephrol.2023.151427
Joshua J. Neumiller PharmD , Radica Z. Alicic MD , Katherine R. Tuttle MD
Chronic kidney disease (CKD) represents a particularly challenging diabetes complication. Diabetes now is responsible for half of all cases of CKD, thus making diabetes the most common cause of kidney failure worldwide. In patients with diabetes, CKD frequently coexists with heart failure and atherosclerotic cardiovascular disease, which together are associated with marked increases in the risk of cardiovascular and all-cause mortality. Fortunately, new therapeutic agents from several classes now are available with proven benefits for kidney and heart protection when used in patients with type 2 diabetes and CKD. Agents from the sodium-glucose cotransporter-2 inhibitor, glucagon-like peptide-1–receptor agonist, and nonsteroidal mineralocorticoid-receptor antagonist classes now are considered standard of care to improve kidney, heart, and overall survival outcomes in patients with type 2 diabetes. Efforts to educate health care providers on the benefits of these therapies are critically needed to help increase their utilization and improve clinical outcomes. Care decisions should be driven by a holistic view of patient priorities and goals with consideration of a multimodal therapeutic approach to maximize heart and kidney benefits.
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