Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:Q9BZE4 (chronic renal failure)
 13,583 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 19-yr-old female lynx (Lynx canadensis) presented for an acute onset of anorexia and reluctance to move. Physical examination, radiography, hematology, and serum biochemistry revealed evidence of renal failure, presumptive uremic gastritis, chronic intervertebral disk disease at T13-L1, and markedly low serum levels of total thyroxine (1.54 nmol/L) and total triixodothyronine (0.55 nmol/L). Twenty-five hours after its original presentation, the lynx exhibited horizontal nystagmus, which has been suggested as a clinical sign associated with hypothyroidism in domestic dogs. The lynx was euthanatized because of poor prognosis, and medical management concerns related to its chronic renal failure. Necropsy examination substantiated that the lynx had true hypothyroidism with 60-90% of the thyroid gland replaced with adipose tissue. Although feline adult-onset hypothyroidism may have low incidence, it should still be considered as a cause of nonspecific signs of disease in cats, as well as signs suggestive of hypothyroidism. Routine monitoring of baseline exotic felid thyroid levels throughout life would help to identify normal values and diagnose a potential disease that has obscure clinical signs.
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PMID:Adult-onset hypothyroidism in a lynx (Lynx canadensis). 1458 93

Malnutrition is prevalent in patients with end-stage renal disease (ESRD). Elevated serum leptin levels were thought to contribute to the anorexia and poor nutrition in renal failure. However, studies of the relationship between nutritional status and leptin concentration in chronic renal failure have yielded conflicting results. Plasma insulin-like growth factor I (IGF-I) level has been used as an indicator of nutritional status in patients with renal failure. The relationship between leptin and IGF-I is controversial. The present study was conducted with the aim of assessing the relationship between nutritional status, hyperleptinemia, and serum IGF-I. Seventeen ESRD patients (8 male, 9 female), aged 8-18 years (mean 15.3+/-3.3 years) and undergoing standard hemodialysis for 58.8+/-23.1 months were enrolled. Nine age-matched healthy children served as controls. In all patients, energy and protein intakes were 40-70 kcal/kg per day and 1-1.54 g/kg per day, respectively. Predialysis serum leptin and IGF-I levels were measured by radioimmunoassay. Body mass index was decreased in 13 (76%) patients. Triceps skinfold thickness (TST) was reduced (below the 5th percentile) in 7 (41%), whereas mid arm circumference and mid arm muscle circumference were reduced in 14 (82.5%) and 13 (76.5%), respectively. The median serum leptin level was significantly higher in patients than in controls [13.7 interquartile range (IQR) 30.50 pg/ml vs. 6.50 IQR 8.65 pg/ml, P=0.01]. The median serum IGF-I level was lower in the patients (205.1 ng/ml IQR 194.4 ng/l) than controls (418.0 ng/l IQR 310.5 ng/ml) ( P=0.01). IGF-I levels were more decreased in patients with severe malnutrition, defined according to TST (145.0 ng/ml IQR 125.5 ng/l) than patients without malnutrition (301.2 ng/l IQR 218.8 ng/ml) ( P=0.03) and healthy children ( P=0.002). Although statistically not significant, IGF-I levels tended to be decreased, while leptin levels were increased. The median plasma insulin concentration was 15 microU/ml (1.63-45.80) and did not correlate with leptin and IGF-I levels. In conclusion, the results of this study confirm the presence of high circulating plasma leptin levels, which may be one of the many factors involved in the pathogenesis of the malnutrition in children on hemodialysis.
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PMID:Relationship of leptin and insulin-like growth factor I to nutritional status in hemodialyzed children. 1458 83

Hyperparathyroidism is a disease characterized by hypercalcemia with hypophosphoremia resulting from increased secretion of parathyroid hormone (PTH). The disease may be divided into 3 forms: a) primary, b) secondary, c) tertiary (secondary refractory form). Primary hyperparathyroidism is rare in children; hyperplasia is more frequent during the early years of life (neonates and infants) and is difficult to distinguish from adenoma in children. The disease may be asymptomatic; elevated calcemia levels (>12 <13.5 mg/dl) are accompanied by anorexia, asthenia and persistent stipsis; severely elevated concentrations (>13.5 mg/dl) are accompanied by nausea, vomiting, polyuria due to osmosis, with dehydration and progressive onset of lethargy, stupor and coma. Osteopenia or osteitis fibrosa cystica may be present due to augmented bone resorption. Height and weight increases are altered due to anorexia and dehydration. Differential diagnosis includes iatrogenic causes of hypercalcemia (excessive vitamin D intake, prolonged immobilization, etc.) and idiopathic familial hypercalcemia. Emergency treatment is required in cases of extremely elevated hypercalcemia (Ca >13.5-14 mg/dl), due to risk of injury to the heart, the central nervous system, the gastrointestinal tract and the kidneys. The 4 cardinal points of treatment are: hydration, calciuresis, inhibition of bone calcium resorption, treatment of the cause underlying hyperparathyroidism. Secondary hyperparathyroidism is found in cases where chronic hypocalcemia is present, particularly in chronic renal failure, untreated deficiency rickets, chronic intestinal malabsorption, hepatobiliary disease, types I and II vitamin D-dependent rickets, tubular acidosis or Fanconi's syndrome. The tertiary form is distinguished by the autonomous nature of the parathyroid glands which have become hypertrophic/hyperplastic due to uncontrollable, chronic severe renal failure. It can also be of iatrogenic origin due to excessive intake of inorganic phosphates in familial hypophosphatemic rickets or chronic vitamin D deficiency.
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PMID:Hyperparathyroidism. 1524 24

To study anorexia in chronic renal failure (CRF) patients, we measured appetite-related hormones in seven CRF patients and four controls. Plasma concentrations and fractional changes from baseline (values from day 1, 0800) are listed as control vs. CRF (means +/- SE). Leptin, although higher in CRF (5.6 +/- 1.7 and 34 +/- 17 ng/ml), was suppressed after fasting; decrements were -51 +/- 9 and -55 +/- 8%. Nocturnal surge present during feeding was abolished upon fasting in both groups. Neuropeptide Y (NPY) was elevated in CRF (72 +/- 12 vs. 304 +/- 28 pg/ml, P = 0.0002). NPY rhythm, reciprocal to that of leptin, was muted in CRF. Basal cortisol was similar in both groups (17 +/- 3 and 17 +/- 2 microg/dl). In the controls, cortisol peaked in the morning and declined in the evening. CRF showed blunted cortisol suppression. Decrements were -61 +/- 3 and -20 +/- 9% at 1800 on day 1 (P = 0.008) and -61 +/- 8 and -26 +/- 8% at 2000 on day 2 (P = 0.02). Basal ACTH (25 +/- 5 and 54 +/- 16 pg/ml) as well as diurnal pattern was not statistically different between the groups. Baseline insulin was 6 +/- 1 and 20 +/- 9 microU/ml. During fasting, insulin was suppressed to -64 +/- 10 and -51 +/- 9%, respectively. Upon refeeding, increments were 277 +/- 96 and 397 +/- 75%. Thus, in our CRF patients, anorexia was not due to excess leptin or deficient NPY. Impaired cortisol suppression should favor eating. Insulin suppression during fasting and secretion after feeding should enhance both eating and anabolism. The constant high NPY suggests increased tonic hypersecretion.
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PMID:Hormonal responses to fasting and refeeding in chronic renal failure patients. 1530 76

Hypoalbuminemia is the result of the combined effects of inflammation and inadequate protein and caloric intake in patients with chronic disease such as chronic renal failure. Inflammation and malnutrition both reduce albumin concentration by decreasing its rate of synthesis, while inflammation alone is associated with a greater fractional catabolic rate (FCR) and, when extreme, increased transfer of albumin out of the vascular compartment. A vicious cascade of events ensues in which inflammation induces anorexia and reduces the effective use of dietary protein and energy intake and augments catabolism of the key somatic protein, albumin. Hypoalbuminemia is a powerful predictor of mortality in patients with chronic renal failure, and the major cause of death in this population is due to cardiovascular events. Inflammation is associated with vascular disease and likely causes injury to the vascular endothelium, and hypoalbuminemia as two separate expressions of the inflammatory process. Albumin has a myriad of important physiologic effects that are essential for normal health. However, simply administering albumin to critically ill patients with hypoalbuminemia has not been shown to improve survival or reduce morbidity. Thus the inference from these clinical studies suggests that the cause of hypoalbuminemia, rather than low albumin levels specifically, is responsible for morbidity and mortality.
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PMID:Serum albumin: relationship to inflammation and nutrition. 1566 May 73

Chronic renal failure (CRF) is a polymorphic disease whose management need frequently multiple drugs administration and multidisciplinary approach. Thirteen years after the beginning of haemodialysis treatment in Senegal, we aimed to evaluate the management of chronic renal failure in Dakar University Hospital Internal Medicine Department. We analysed retrospectively 243 CRF in patients managed during the last three years in this department. Most of these patients (43.6%) were under 46 years old. The sex ratio (M/F) was 1.31. The clinical symptoms were distributed as follow: high blood pressure (85.6%), anorexia (61.73%), anaemia (83.9%) and pruritus (12.3%). More than one third (37.04%) of patients had a clearance of creatinine under 10 ml/mn, at the diagnosis, and therefore required chronic haemodialysis. Only 8.23% of cases had the opportunity to get a medical treatment. Five machines ware available at this unity). The deficience of dialysis and nephrology personal is obvious in our practice. The majority of CRF patients can not afford the treatment cost. Therefore, medical training, prevention and screening of renal diseases seem to be the best way to solve this public health problem in developing countries.
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PMID:[Chronical renal failure in one Dakar Hospital Department]. 1577 28

Thirteen cases of feline primary hyperaldosteronism were diagnosed based on clinical signs, serum biochemistry, plasma aldosterone concentration, adrenal imaging and histopathology of adrenal tissue. Two cases presented with blindness caused by systemic hypertension, whilst the remaining 11 cases showed weakness resulting from hypokalaemic polymyopathy. Elevated concentrations of plasma aldosterone and adrenocortical neoplasia were documented in all cases. Seven cases had adrenal adenomas (unilateral in five and bilateral in two) and six had unilateral adrenal carcinomas. Three cases underwent medical treatment only with amlodipine, spironolactone and potassium gluconate; two cases survived for 304 and 984 days until they were euthanased because of chronic renal failure, whilst the third case was euthanased at 50 days following failure of the owner to medicate the cat. Ten cases underwent surgical adrenalectomy following a successful stabilisation period on medical management. Five cases remain alive at the time of writing with follow-up periods of between 240 and 1803 days. Three cases were euthanased during or immediately following surgery because of surgical-induced haemorrhage. One cat was euthanased 14 days after surgery because of generalised sepsis, whilst the remaining cat was euthanased 1045 days after surgery because of anorexia and the development of a cranial abdominal mass. It is recommended that primary hyperaldosteronism should be considered as a differential diagnosis in middle-aged and older cats with hypokalaemic polymyopathy and/or systemic hypertension and should no longer be considered a rare condition.
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PMID:Primary hyperaldosteronism in the cat: a series of 13 cases. 1592 24

Patients with chronic renal failure are often characterized by clinical and laboratory signs of protein and calories malnutrition, which is associated with a significant increase in the total morbidity and mortality risk. The loss of muscle mass is often multifactorial. If the patient is consuming a low protein diet the risk of protein calories malnutrition is increased. Among the various factors that can affect protein metabolism the role of calories and protein intake as well the influences of concomitant conditions as increased leptin levels and uncontrolled metabolic acidosis are evaluated. Hemodialysis treatment induces a transient increase in proteolysis which is associated with a significant loss of amino acid in the dialysis fluid. Subclinical inflammation contributes to malnutrition increasing both muscle proteolysis and anorexia. Albumin levels are often reduced in dialysis patients, this decline is associated with an increase in morbidity and mortality. Various factors as protein intake, acidosis and inflammation can affect albumin levels via a reduction in hepatic albumin synthesis.
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PMID:[Protein metabolism in renal failure]. 1634 50

Malnutrition is a major problem in patients with chronic renal failure, especially in children in the first three years of life. Meeting high energy needs in these patients may be difficult because of anorexia and vomiting, which are common in predialysis renal failure. Nutritional support for children with chronic renal failure often involves the use of nasogastric tubes or gastrostomy feeding. We describe an infant with pre-dialysis renal failure and severe malnutrition in whom only insertion of percutaneus endoscopic gastrostomy provided adequate caloric intake and satisfactory weight gain.
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PMID:[Percutaneus endoscopic gastrostomy (PEG) in an infant with chronic renal failure]. 1689 22

Anorexia is possibly one of the most important causes of malnutrition in uremic patients. The cause of this abnormality is still unknown. Considering that: (a) NPY is one of the most important stimulants of food intake; (b) eating is a central nervous system regulated process and (c) NPY is expressed in hypothalamus, we hypothesized that the decrease of NPY gene expression in the hypothalamus could be an important factor contributing to anorexia associated with uremic state. In contrast to the prediction, the results presented in this paper indicate that the NPY gene expression in the hypothalamus of chronic renal failure (CRF) rats was significantly higher than in the hypothalamus of control (pair-fed) rats. Moreover, we found that serum NPY concentration in CRF rats was higher than in control (pair-fed) animals. The increase of plasma NPY concentration in CRF rats may be due to the greater synthesis of the neuropeptide in liver, since higher level of NPY mRNA was found in liver of CRF rats. The results obtained revealed that experimental chronic renal failure is associated with the increase of NPY gene expression in hypothalamus and liver of rats.
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PMID:Up-regulation of NPY gene expression in hypothalamus of rats with experimental chronic renal failure. 1701 Nov 71


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