Notes

Doxycycline-induced cholestatic hard working liver damage.
Over the past 40 years there has been a steady rise in the number of people with chronic kidney disease due mainly to a significant increase in the number of people with diabetic kidney disease (DKD). Current treatments (blood pressure control, blood sugar control, and renin-angiotensin-aldosterone system inhibitors) have had a significant impact on slowing progression of DKD. But the continued rise illustrates that there is a great need for new medications. Recently, a number of potentially reno-protective medicines have been studied. In this review, these new medications are discussed with respect to both their reported benefits and possible risks.Obesity has a fundamental role in driving the global kidney disease burden. The perplexing relationship of obesity with chronic kidney disease remains debated. However, a thorough understanding of the interplay of obesity in conjunction with chronic kidney disease and appropriate management options is lacking, leading to further increases in morbidity and mortality. Moreover, underutilization of bariatric procedures and unrealistic expectations of weight reduction based on body mass index, leading to poor access to kidney transplantation, are fueling the fire. In this review, we summarize the available data related to the obesity and chronic kidney disease association and its novel management options.The kidneys are responsible for maintaining our bodies' homeostasis through excretion, biodegradation, and synthesis of different hormones. Therefore, a decline in renal function often results in significant derangements in hormone levels. The most common metabolic and endocrine abnormalities seen in patients with chronic kidney disease include deficiencies in erythropoietin, calcitriol, triiodothyronine, testosterone, and estrogen. In addition, accumulation of hormones such as adiponectin, leptin, triglycerides, and prolactin also is seen. Subsequently, this can lead to the development of a wide range of clinical consequences including but not limited to anemia, hyperparathyroidism, insulin resistance, anorexia-cachexia, infertility, bone disorders, and cardiovascular diseases. These disorders can negatively affect the prognosis and quality of life of patients with chronic kidney disease, and, thus, early diagnosis, nutritional intervention, and pharmacologic treatment is imperative.Bone disease after kidney transplantation is associated with an increased risk of fractures, morbidity, and mortality. Its pathophysiology is complex, involving multiple contributors including pretransplant bone disease, immunosuppressive medications, and changes in the parathyroid-bone-kidney axis. Risk scores, bone turnover markers, and noninvasive imaging modalities are only able to partially predict the fracture risk in kidney transplant recipients. The optimal management of bone disease after kidney transplantation has not yet been established, with only a limited number of randomized clinical trials evaluating the efficacy of treatment regimens in kidney transplant recipients. This review focuses on the pathophysiology, evaluation, prevention, and treatment of post-kidney transplant mineral and bone disease as guided by recent evidence.Prolactin levels are increased in chronic kidney disease (CKD) as a result of reduced clearance and increased secretion. Hyperprolactinemia manifests as galactorrhea and hypogonadism. Treatment of hyperprolactinemia should focus on improving bothersome galactorrhea or hypogonadism by using dopamine agonists and/or replacement of sex hormone(s). DEG-77 Changes in the hypothalamic-pituitary-adrenal axis in CKD are characterized by increases in adrenocorticotropic hormone (ACTH) and cortisol levels, largely preserved circadian rhythms of ACTH and cortisol, and a normal response of cortisol to ACTH, metyrapone, and insulin-induced hypoglycemia. However, the hypothalamic-pituitary-adrenal axis is less inhibited by 1 mg dexamethasone but retains normal suppression by higher-dose dexamethasone. Diagnosis of adrenal insufficiency in CKD patients, as in normal subjects, usually is made by finding a subnormal cortisol response to ACTH. The mainstay of treatment of adrenal insufficiency is to replace glucocorticoid hormone. Cud kidney disease until kidney transplantation. Diagnosis of the syndrome of inappropriate antidiuretic hormone is similar in mild or moderate kidney disease as in normal subjects, but is challenging in patients with advanced kidney disease owing to the impairment in urine dilution.Growth hormone (GH) has become a critical therapy for treating growth delay and failure in pediatric chronic kidney disease. Recombinant human GH treatment is safe and significantly improves height and height velocity in these growing patients and improved growth outcomes are associated with decreased morbidity and mortality as well as improved quality of life. However, the utility of recombinant human GH in adults with chronic kidney disease and end-stage renal disease for optimization of body habitus and reducing frailty remains uncertain. Semin Nephrol 41x-xx © 2021 Elsevier Inc. All rights reserved.Hypothyroidism is a highly prevalent endocrine complication in chronic kidney disease (CKD) patients. A large body of evidence has shown that there is a bidirectional relationship between thyroid dysfunction and kidney disease, yet there are many remaining gaps in knowledge in regards to the clinical management of CKD patients with hypothyroidism, including those receiving hemodialysis and peritoneal dialysis. Given that hypothyroidism has been associated with many deleterious outcomes including a higher risk of (1) mortality, (2) cardiovascular disease, (3) impaired health-related quality of life, and (4) altered body composition in both non-CKD and CKD patients, future research is needed to establish the appropriate screening, diagnosis, and treatment approaches in these populations.Sexual and reproductive function are impacted negatively in individuals with chronic kidney disease and end-stage renal disease. Disruption of the hypothalamic-pituitary-gonadal axis plays a pivotal role in contributing to these manifestations as a result of decreasing kidney function and the development of uremia. Early menopause is encountered commonly in women with reduced kidney function, and treatment is problematic as a result of reduced kidney function changing the half-life of medications. Kidney transplantation corrects some of these abnormalities, but medications required after transplantation as well as the persistence of other comorbidities are barriers to normal restoration of gonadal dysfunction.
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