Advances in chronic kidney disease最新文献

Normallly the kidneys handle the daily acid load arising from net endogenous acid production from the metabolism of ingested animal protein (acid) and vegetables (base). With chronic kidney disease, reduced acid excretion by the kidneys is primarily due to reduced ammonium excretion such that when acid excertion falls below acid porduction, acid accumulation occurs. With even mild reductions in glomerular filtration rate (60 to 90 ml/min), net acid excretion may fall below net acid production resulting in acid retention which may be initially sequestered in interstitial compartments in the kidneys, bones, and muscles resulting in no fall in measured systemic bicarbonate levels (eubicarbonatemic metabolic acidosis). With greater reductions in kidney function, the greater quantities of acid retained spillover systemically resulting in low pH (overt metabolic acidosis). The evaluation of acid-base balance in patients with CKD is complicated by the heterogeneity of clinical acid-base disorders and by the eubicarbonatemic nature of the early phase of acid retention. If supported by more extensive studies, blood gas analyses to confirm the acid-base disorder and newer ways for assessing the presence of acidosis such as urinary citrate measurements may become routine tools to evaluate and treat acid-base disorders in individuals with CKD.

Recent trends in the diagnosis, treatment, and classification of collagen IV-associated kidney disease are likely to result in increasing numbers of people in adult nephrology practices who have a confirmed diagnosis of Alport syndrome. These trends include the increasing use of genetic testing in the diagnostic evaluation of people with hematuria, focal segmental glomerulosclerosis, and chronic kidney disease of unknown etiology; early treatment with inhibitors of the renin-angiotensin-aldosterone system to delay kidney failure; and application of an expanded definition of Alport syndrome based on genotype rather than phenotype. This commentary discusses these trends and their implications for the adult nephrologist.

Common causes of pediatric ESRD are distinct from those seen in the adult population. In the pediatric population, the most common are congenital anomalies of the kidney and urinary tract (CAKUT), affecting approximately 30% of children with CKD. These structural anomalies often require coordinated care with the pediatric urology team to address voiding issues, bladder involvement, and the potential need for surgical intervention. For pediatric nephrologists and urologists, common CAKUT that are encountered include antenatal hydronephrosis, obstructive uropathies (eg, posterior urethral valves), and vesicoureteral reflux. As more pediatric patients with CAKUT, CKD, and ESRD transition to adult care, it is important for receiving adult nephrologists to understand the clinical presentation, natural history, and prognosis for these diagnoses. This review outlines the diagnosis and potential interventions for these conditions, including strategies to address bladder dysfunction that is often seen in children with CAKUT. A discussion of these management decisions (including surgical intervention) for CAKUT, which are quite common to pediatric nephrology and urology practices, may provide unique learning opportunities for adult nephrologists who lack familiarity with these pediatric conditions.

Adolescent obesity and CKD are both significant public health issues independently. When seen as comorbid conditions, they can cause deleterious health outcomes that put them on the fast track to necessitate dialysis or transplantation. This paper analyzes the effects of various biomarkers and comorbidities seen in the intersection of obesity and CKD in the adolescent population. We illustrate the estimated prevalence of these biomarkers and comorbidities through a review of the literature, available treatment, and obesity-related glomerulopathies. We found significant prevalence of the biomarkers, microalbuminuria (9.42% ± 9.31% and interquartile range [IQR] of 9.5%), hypertension (23.60% ± 22.5% and IQR of 9.5%), low high-density lipoprotein (14.34% ± 5.46% and IQR of 5%), hyperfiltration (3.12% ± 5.16% and IQR of 4%), and lower estimated glomerular filtration rate 4.59 ± 2.75 and IQR of 3%. Identification of prevalent biomarkers and their manifestations can serve to inform clinicians what to look for in daily setting and help elucidate the magnitude of this growing issue. Additionally, pertinent treatment options from pharmacotherapy to bariatric surgery are outlined to provide care providers with the full spectrum of treatment options for obesity in adolescent populations.

Chronic kidney disease is common and causes significant morbidity including shortened lifespans and decrease in quality of life for patients. The major cause of mortality in chronic kidney disease is cardiovascular disease. Cardiovascular disease within the chronic kidney disease population is closely tied with disordered calcium and phosphorus metabolism and driven in part by renal bone disease. The complex nature of renal, bone, and cardiovascular diseases was renamed as mineral and bone disorder of chronic kidney disease to encompass how bone disease drives vascular calcification and contributes to the development of long-term cardiovascular disease, and recent data suggest that managing bone disease well can augment and improve cardiovascular disease status. Pediatric nephrologists have additional obstacles in optimal mineral and bone disorder of chronic kidney disease management such as linear growth and skeletal maturation. In this article, we will discuss cardiovascular and bone diseases in chronic kidney disease and end-stage kidney disease patients with a focus on pediatric issues and concerns.

Gaining insight into the complex cycle of renal programming and its early-life clinical associations is essential to understand the origins of kidney disease. Prematurity and intrauterine growth restriction are associated with low nephron endowment. This increases the risk of developing hypertension and chronic kidney disease later in life. There is appreciable evidence to support mechanistic links between low nephron endowment secondary to intrauterine events and kidney size, kidney function, and blood pressure in postnatal life. A clear understanding of the cycle of developmental programming and consequences of fetal insults on the kidney is critical. In addition, the impact of events in the early postnatal period (accelerated postnatal growth, development of obesity, exposure to nephrotoxins) on the cardiovascular system and blood pressure of individuals born prematurely or with low birth weight is discussed. In summary, this review draws attention to the concepts of renal programming and nephron endowment and underscores the associations between intrauterine growth restriction, prematurity, and its clinical consequences in adult life.

Hypertension (HTN) is an important cause of morbidity and mortality in children as well as adults. HTN and related adverse cardiovascular health develop and progress on a continuum across an individual's life course. Pediatric HTN, or even isolated elevated blood pressure as a child, increases the risk of sustained HTN and cardiovascular disease in later adulthood. Transitioning the care of adolescents and young adults who have HTN is an important but unmet health care need that could potentially have a dramatic effect on mitigating the risk of cardiovascular disease in adulthood. However, very little has been published about the transition process in this population, and considerable gaps in the field remain. We discuss the epidemiology, etiology, and management approach in youth with HTN and how they differ from adults. We contextualize HTN and cardiovascular health on a continuum across the life course. We discuss key considerations for the transition process for adolescents and young adults with HTN including the major barriers that exist. Finally, we review key immediate health care needs that are particularly important around the time of the transfer of care.

The pediatric patient with end-stage kidney disease who transitions to the adult dialysis unit or nephrology center requires a unique nutritional focus. Clinicians in the adult center may be faced with complex issues that have often been part of the patient's journey since early childhood. The causes of kidney disease in children are often quite different than those which affect the adult population and may require different nutritional priorities. Abnormal growth including severe short stature, underweight, overweight or obesity, and poor musculature may affect the long-term health and psychosocial well-being of these patients. Nutritional assessment of these patients should include a focus on past growth and anthropometric data, dietary information, including appetite, quality of diet, and assessment of biochemical data through a pediatric lens. This review discusses the unique factors that must be considered when transitioning pediatric patients and notes major recommendations from a compilation of pediatric guideline statements.