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Aerobic conditioning exercises have been shown to be beneficial for maintenance hemodialysis patients, but biochemical changes during exhaustive exercise in these functionally anephric patients have been less thoroughly studied. We evaluated serum biochemical changes in 7 patients during and after treadmill exercise to patient exhaustion. Duration of exercise was limited by lower leg fatigue without claudication. At exhaustion, only mild changes from baseline rest values were noted in arterial pH (7.39 +/- 0.03-7.33 +/- 0.04) and lactate (0.94 +/- 0.3-5.73 +/- 2.68 mmol/l) despite normal exercise-induced intracellular fluid shifts as evidenced by albumin concentration increases (44.9 +/- 2.8-49.3 +/- 3.1 g/l). Increases in serum K+ concentrations are also modest (change in K from baseline = 0.87 +/- 0.22 mmol/l). An explanation for these minimal biochemical alterations at exhaustion is unclear, but could relate to exercise being limited well below estimated maximum cardiac output and muscle O2 extraction levels by early, unexplained muscle fatigue. Fatigue in hemodialysis patients does not appear to be due to muscle hypoxia.
Nephron 1987
PMID:Fatigue, acid-base and electrolyte changes with exhaustive treadmill exercise in hemodialysis patients. 360 Sep 12

The effect of hemodialysis (HD) on olfactory recognition and memory function was investigated in people receiving chronic HD treatment. Fifteen subjects were given an olfactory recognition task 0.5 h before and 0.5 h after a dialysis session in counterbalanced order. Ten dialysis patients received a verbal recall task twice. Ten age-matched normal subjects received the olfactory task twice. Results were: (1) olfactory scores in the HD group were significantly lower than control subjects scores; (2) within the dialysis sample, olfactory identification scores were significantly lower after treatment than before, and (3) there were no parallel decreases in memory performance of the dialysis group after a HD treatment. We therefore conclude that those subjects receiving HD treatment demonstrate acute and chronic deficits in olfactory recognition which are unlikely to be due to fatigue, cognitive disequilibrium, anticoagulant treatment or high levels of uremic toxins.
Nephron 1987
PMID:Olfaction and hemodialysis: baseline and acute treatment decrements. 369 14

137 patients on maintenance dialysis were studied. All but 2 patients were ambulatory, and all patients demonstrated good to normal strength on manual motor tests. With the exception of systemic lupus erythematosus, no correlation was found between primary diagnosis and patients' fatigue ratings. Laboratory studies of hematocrit, BUN, creatinine, calcium, and phosphorus did not correlate with fatigue ratings for the majority of patients. Fatigue appeared more problematic for patients who had been dialyzing for less than 4 years. Depression was pronounced among patients who reported feeling fatigued upon arising.
Nephron 1982
PMID:The problem of fatigue in dialysis patients. 711 Apr 64

We examined 58 patients (38 men, 20 women; mean age: 45 +/- 12 years; body mass index: 24 +/- 4 kg/m2) with a glomerular filtration rate (GFR) ranging from 3 to 32 ml/min, in order to determine the effects of a progressive decline in renal function on total hemoglobin (THb) and exercise capacity. The THb ranged from 185 to 759 g and the hemoglobin concentration ranged from 66 to 151 g/l. Maximal exercise capacity ranged from 50 to 260 W (40-143% of the expected norm). Nearly all the patients interrupted their exercise tests due to general fatigue, leg tiredness or a combination of these factors. There was a significant partial correlation between THb and GFR after sex and age had been accounted for (r = 0.39; p < 0.005). Maximal exercise capacity and THb showed a significant partial correlation after sex, age and GFR had been accounted for (r = 0.27; p < 0.05). Maximal exercise capacity showed a significant partial correlation with GFR after sex, age and THb had been accounted for (r = 0.30; P < 0.05). In conclusion, there is a gradual decline in THb and maximal exercise capacity as uremia progresses. Anemia appears to be a contributory cause responsible for the decrease in maximal exercise capacity along with other factors pertinent to uremia per se.
Nephron 1994
PMID:Progressive decline in renal function induces a gradual decrease in total hemoglobin and exercise capacity. 793 23

To determine if exercise intolerance and fatigue in chronic heart failure could be exacerbated by an abnormal metabolic response to exercise, we studied 12 patients with stable chronic heart failure and 12 normal volunteers during symptom-limited maximal treadmill exercise. Peak VO2 was 17.2 (15.1-19.2) ml.kg-1 x min-1 in patients and 29.9 (26.3-33.5) in controls (mean and 95% confidence intervals; P < 0.0001, t-test). Overall, levels in peripheral venous blood of glucose, glycerol and free fatty acids were greater in patients, although the differences became less marked with increasing exercise intensity. Noradrenaline was elevated in patients at rest, but the peak exercise response was similar to controls. Responses of adrenaline, insulin and glucagon were similar in both groups. We conclude that depletion of the levels of circulating substrates is not contributory to exercise intolerance and fatigue in chronic heart failure. Greater levels of glycerol and free fatty acids may be mediated by excess sympathetic nervous system activity, reflected in elevated noradrenaline levels.
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PMID:Metabolic responses to graded exercise in chronic heart failure. 829 29

A disease-specific questionnaire to assess the quality of life of renal transplant recipients was developed. A list of items of potential relevance to these patients was created and 50 transplant recipients rated the importance of each item. A combination of factor analysis and clinical judgment was then used to create the final questionnaire which consists of 25 questions in 5 dimensions (physical symptoms, fatigue, uncertainty/fear, appearance and emotions). The physical symptoms dimension is patient specific. All questions are scored on a 7-point Likert scale. The reproducibility of the questionnaire when it was administered to stable transplant recipients was high (intraclass correlation coefficients between 0.82 and 0.91 for the 5 dimensions). The scores of all dimensions except appearance improved 6 months after transplantation, when compared to pretransplantation scores. Patients who had a well-functioning graft (creatinine < 250 mmol/l) had higher scores than those with poorly functioning grafts. This questionnaire is easy to administer and is valid, reproducible in stable patients and responsive to change.
Nephron 1993
PMID:Disease-specific questionnaire for patients with a renal transplant. 832 55

Norepinephrine (NE), a vital neurotransmitter in both the central and peripheral nervous systems, is synthesized by dopamine beta-hydroxylase (DBH) through the oxidation of dopamine (DA) to NE. DBH deficiency is a congenital disorder characterized by severe orthostatic hypotension, ptosis, and retrograde ejaculation. Biochemical features of the syndrome include elevated levels of dopamine, undetectable levels of DBH, undetectable tissue and circulating levels of NE and epinephrine. Molecular genetic analysis studies suggested that DBH deficiency is a Mendelian recessive disorder attributable to heterogenous mutations at the DBH locus. DBH deficiency has been treated effectively with L-threo-3,4-dihydroxyphenylserine (DOPS). DOPS is converted directly to NE through decarboxylation by L-aromatic amino acid decarboxylase (AADC), thereby bypassing DBH. Orthostatic intolerance is a syndrome characterized by lightheadedness, fatigue, altered mentation, syncope, and postural tachycardia. Biochemical features may include plasma NE concentration that is disproportionately high in relation to sympathetic outflow, decreased NE clearance with standing, resistance to the NE-releasing effect of tyramine, and increased sensitivity to adrenergic agonists. A subset of OI patients has pathophysiologic features that have been associated with a genetic polymorphism. The coding mutation, A457P, occurs in one of the alleles of norepinephrine transporter gene of a proband with OI and her family. Alpha-methyl dopa, beta blockers and clonidine, a partial agonist of alpha2-adrenoceptor that acts centrally to reduce sympathetic outflow and lower blood pressure, have been effective in the treatment of this condition. The identification of the genetic polymorphisms involved in the synthesis, transport, storage, and metabolism of the catecholamines may provide new insights into the diagnosis and management of autonomic, cardiovascular, endocrine and psychiatric disorders.
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PMID:The broader view: catecholamine abnormalities. 1210 62

A case of a renal transplant recipient with colchicine-induced myopathy is presented. He was on colchicine therapy for 10 months. He was hospitalized for investigation of fatigue, severe myalgia in the lower extremities and elevated serum aminotransferase levels. His viral markers and other factors that may cause myalgia and that may increase the serum aminotransferase levels were either normal or negative. Creatine phosphokinase (CK) levels were normal. Electrophysiological findings indicated myopathy and muscle biopsy was consistent with vacuolar myopathy. After withdrawal of colchicine, the symptoms disappeared gradually and serum aminotransferase levels were normalized. We suggest that colchicine myopathy should be taken into account in patients who have been on colchicine therapy and had unexplained myalgia as well as elevated aminotransferase levels even with normal CK levels.
Nephron 2002 Dec
PMID:Colchicine-induced myopathy with normal creatine phosphokinase level in a renal transplant patient. 1239 40

Being awake, alert, and able to function in our 24-7 world is a challenge in the face of the fatigue and sleepiness engendered by long work hours, unusual work schedules, sickness, and other factors. Development of effective treatments to combat fatigue and sleepiness requires an understanding of the neurobiology of wakefulness. In this brief review, we examine the neuroanatomical, neurochemical, and molecular basis of the wakeful state to provide a framework for understanding current and future pharmacologic approaches to modification of wakefulness. The spontaneously awake state can be defined as a natural state of vigilance or arousal differing from natural sleep in both behavior and neural activity. These differences have long intrigued researchers and largely have been characterized in the brain areas and neurochemical systems affecting the sleep and wake states. Many of the strategies for promoting the awake condition involve manipulation or modulation of specific neurochemical systems with the ultimate goal of enhancing wakefulness, diminishing sleepiness, or both. Wakefulness is an important cortical function that depends on the coordinated effort of multiple brain areas including the thalamus, hypothalamus, and basal forebrain to integrate and relay information from the brainstem to the cortex. Norepinephrine and serotonin-long considered arousal-enhancing transmitters as well as glutamate, acetylcholine, histamine, and the neuromodulators hypocretin-orexins and adenosine, are known to affect the signal transduction in these brain areas and initiate, promote, or enhance wakefulness. Use of molecular tools to evaluate the awake, asleep, and sleep-deprived state has revealed novel insights concerning the gene expression events associated with wakefulness. Understanding wakefulness at this level undoubtedly will contribute to the development of pharmacologic approaches to promote or enhance the wakeful state. We caution, however, that sleep may have a necessary, restorative function for the brain; therefore, prolonging wakefulness for long periods through artificial means could have unexpected and perhaps detrimental consequences on brain health.
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PMID:The pharmacology of wakefulness. 1697 20

Patients with advanced chronic kidney disease (CKD), especially those on long-term dialysis, often suffer from muscle wasting and excessive fatigue. It is known that inactivity, muscle wasting and reduced physical functioning are associated with increased mortality in CKD. Known causes include uraemic myopathy and neuropathy, inactivity, and anaemia. Exercise in patients receiving regular dialysis treatment for end-stage renal disease was first introduced 3 decades ago, but is still only offered in a minority of renal units around the world, despite a significant body of evidence to support its use. Work is needed to increase awareness of the potential benefits of increased physical activity for patients with advanced CKD. This review summarizes the mechanisms of exercise intolerance and debility in advanced CKD patients, the methods used for the estimation of functional capacity, the options currently available for exercise training, and their influence on the well-being of this group of patients.
Nephron Clin Pract 2010
PMID:Physical exercise in patients with severe kidney disease. 2017 44


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