“Uremic sarcopenia” refers to a progressive decrease in muscle mass, strength, and function despite normal skeletal muscle physiology in patients with chronic kidney disease (CKD). Sarcopenia involves multiple risk factors, comprising immunological changes, hormonal, metabolic acidosis, reduced protein intake, and physical inactivity. All these risk factors, along with complex pathophysiological mechanisms including ubiquitin, insulin/IGF-1, myostatin, and indoxyl sulfate, activate downstream pathways that ultimately increase muscle degradation while reducing muscle regeneration. Uremic sarcopenia not only affects the quality of life but also increases the risk of morbidity and mortality in patients with CKD. Of all the treatment modalities, aerobic and resistance exercise have shown prevention and reduced rate of muscle degeneration. A variety of pharmacological agents have been tried to target different steps in the known pathogenetic pathways, including the use of androgens and anabolic steroids, correction of vitamin D deficiency, use of growth hormone supplementation, and suppression of the ubiquitin pathway. Though some of these techniques have had beneficial results in animal experiments, human trials are still sparse. This review article relates to recent publications that describe the abnormalities in skeletal muscle that primarily leads to muscle wasting and its consequences in patients with CKD.
Background: The presence of comorbidities and relative immunosuppression in chronic kidney disease patients on hemodialysis raises concerns that these patients may have an increased risk of severe COVID-19. We aimed to examine the presentation and in-hospital outcomes of COVID-19 patients with end stage renal disease requiring hemodialysis. Methods:To examine presentation and in-hospital outcomes of COVID-19 in patients with end stage renal disease requiring hemodialysis. The study was conducted in a tertiary care centre from June 2020 to December 2020. We collected clinical & laboratory data of 126 COVID-19 positive in-patients requiring hemodialysis. CKD patients referred to our centre for hemodialysis patients were also included. Patients requiring invasive ventilation and management in intensive care units were excluded. Patients were categorised into two groups based on their outcomes; survivors and non-survivors. Detailed history & biochemistry results were recorded and analysed using SPSS 20.0. Results: A total of 126 patients were included in our study, with male predominance, n=91(72.2%). The median age of our study population was 53 years. The main presenting complaints were fever, n=78(61.9%); cough, n=69(54.8%), dyspnea, n= 62(49.2%), fatigue, n=102(81%) and myalgia, n=51(40.5%). Eighty nine(70.6%) patients were hypertensives, 48 (38.1%) known diabetics and 13 (10.3%) had pre-existing chronic obstructive pulmonary disease. Lung involvement in CT imaging at the time of admission, were found in 93(85.5%) patients. On comparison between survivor and non-survivors, there was no statistical difference in the biochemical prole, however there was signicant chest imaging ndings (p<0.001) and requirement of ventilator (p<0.001) in the non-survivor group. Conclusion: In our study, mortality was high in patients showing chest imaging ndings and also in those requiring non-invasive ventilation even in non-intensive care setting, at admission. The high mortality in CKD patients on hemodialysis emphasizes the need of dedicated COVID hemodialysis units,to prevent interruption in routine outpatient stable dialysis patients.
Acute porphyrias are metabolic disorders resulting from deficiency of a specific enzyme involved in heme biosynthetic pathway. These deficiencies also affect normal renal physiology, as kidneys are also involved in heme synthesis. Sometimes, this could even lead to end stage renal disease. Acute Intermittent Porphyria, an autosomal dominant disorder arising from half-normal activity of hydroxymethylbilane synthase, is characterized by occurrence of vague neurovisceral attacks (abdominal pain, nausea, vomiting, constipation and neuropsychiatric symptoms), with urinary excretion of porphyrin precursors, such as 5-Amino-levulinic acid (ALA) and Porphobilinogen (PBG). Acute attacks are triggered by dehydration, diarrhea, steroids, low calorie diets. Treatment includes avoidance of precipitating factors, adequate hydration, high carbohydrate diet and heme replacement. Here, we present an adolescent female who had presented with recurrent abdominal pain, dyselectrolyemia with associated seizures, was diagnosed with Acute Intermittent Porphyria and recovered well with symptomatic management.
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