Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0235394 (wasting)
 8,040 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Maximal tubular phosphate reabsorption capacity corrected for changes in glomerular filtration rate (TmP/GFR) was taken as a measure of renal phosphate handling in patients with good and stable functioning kidney allografts. TmP/GFR values were within the normal range in only one-fifth of the patients. Eighty per cent had an abnormally low renal phosphate threshold concentration. Persistent hyperparathyroidism was the causative factor of this diminished tubular reabsorption in less than half of these patients, the majority of them showing an iPTH independent phosphate leak. Although glucocorticoids, azathioprine and tubular damage of the graft in the perioperative phase may contribute to this iPTH independent phosphate wasting, no single causative factor could be identified. Cases with hypophosphataemia should be treated in order to avoid symptoms of phosphate depletion. Active Vitamin D metabolites would be the therapy of choice by suppressing the parathyroid glands ("chemical PTX") and by directly enhancing tubular phosphate reabsorption. In persistent hyperpathyroidism with hypercalcaemia, surgical parathyroidectomy must be considered. Therapy with phosphate salts is only symptomatic and should be used only as an adjunct.
Proc Eur Dial Transplant Assoc 1979
PMID:Handling of phosphate by the transplanted kidney. 39 23

Inadequate control of serum chemistries and extracellular fluid volume may result in patients being changed from continuous ambulatory peritoneal dialysis (CAPD) to another form of dialysis. We report 2 patients in whom apparent inadequacy of CAPD resulted from dialysate dumping. The first patient could not control her fluid intake and required frequent hypertonic exchanges. She felt too full with these exchanges and drained a substantial portion of each exchange 30 to 60 min after infusion. Patient 2 had similar complaints but simply drained a large portion of each fresh bag directly into the drain bag at the start of the flush-before-fill step. Both patients had improved results from CAPD once they stopped their dialysate dumping. Partial wasting of each exchange because of abdominal discomfort should be added to the causes of inadequate dialysis in CAPD.
Perit Dial Int 1989
PMID:Dialysate dumping: a novel cause of inadequate dialysis in continuous ambulatory peritoneal dialysis (CAPD) patients. 248 88

Uricosuric and antiuricosuric drugs have been utilised widely for the study of tubular urate transport in humans. A normal suppression of urate excretion after pyrazinamide is usually taken as evidence of normal presecretory reabsorption. However, in patients with reduced presecretory reabsorption, during pyrazinamide inhibition of urate secretion unreabsorbed urate might still undergo reabsorption along postsecretory sites, allowing for a normal pyrazinamide suppression of urate excretion. To test this possibility, we have performed the pyrazinamide test both alone and after pretreatment with probenecid, which should block postsecretory urate reabsorption. The test was performed in 8 controls, in 9 patients with 'low-excretory' hyperuricaemia, and in 7 patients with tubular urate wasting. Pyrazinamide-non-suppressible urate excretion after pretreatment with probenecid did not differ from the excretion obtained after pyrazinamide alone in hyperuricaemic patients (mean difference 1.33 +/- 2.3% of filtered urate; P = NS); it was slightly higher in controls (3.4 +/- 3.4; P less than 0.05), but was much higher in patients with tubular urate wasting (19.6 +/- 12.7; P less than 0.005). The pyrazinamide test, performed alone, was normal in three patients with tubular urate wasting, but it was abnormal in all patients after pretreatment with probenecid. These results are consistent with the possibility that, during maximal pyrazinamide effect, some uric acid escaping reabsorption at presecretory sites may undergo reabsorption along postsecretory sites, leading to a quantitative overestimation of presecretory reabsorption. This phenomenon appears to have clinical relevance, especially in patients with abnormal urate reabsorption.(ABSTRACT TRUNCATED AT 250 WORDS)
Nephrol Dial Transplant 1987
PMID:Pharmacological evaluation of urate renal handling in humans: pyrazinamide test vs combined pyrazinamide and probenecid administration. 251 73

In 44 adult patients, 16 men and 28 women, with chronic renal failure who were dialysed under uniform conditions (Dialyser area 1.2 m2, blood flow 200 ml/min, dialysate flow 500 ml/min, dialysis fluid acetate concentration 35 mmol/l) we determined the plasma acetate concentration after 1 h of haemodialysis (1H-Ac) and 3 h of dialysis (3H-Ac). 1H-Ac was significantly lower than 3H-Ac in both male and female patients, and both mean values were significantly greater in males than in females. 3H-Ac showed a negative correlation with body surface area, serum creatinine before dialysis, and serum albumin, respectively. Using multivariate analysis, body surface area and serum creatinine showed the strongest significant combination of independent variables (R = 0.66), and accounted for 43% of the total variance in 3H-Ac. Sex, age, serum albumin and haematocrit did not further contribute to explaining the variance in 3H-Ac independently of body surface area and serum creatinine. Assuming that serum creatinine to some extent reflects the generation rate of creatinine and thus the muscle mass of the patients, our findings suggest that the rate of metabolism of acetate is proportional to the body size and that acetate is metabolised to a large extent in skeletal muscle. Accordingly, malnutrition with muscle-wasting may lead to slow metabolism of acetate and possibly to exaggerated acetate-related side-effects.
Nephrol Dial Transplant 1987
PMID:Patient-related factors influencing the plasma acetate concentration during haemodialysis. 312 53

Cyclosporin treatment is often accompanied by hypomagnesaemia and renal magnesium wasting, but it is unknown whether cyclosporin induces tissue magnesium depletion. Magnesium status is best evaluated by measurement of skeletal muscle magnesium content. The purpose of the present study was to evaluate whether skeletal muscle magnesium content was reduced during cyclosporin treatment. In two groups of renal transplant recipients treated with either cyclosporin and prednisolone (group Cy, n = 13) or azathioprine and prednisolone (group Az, n = 17) skeletal muscle content of magnesium, serum magnesium, and urinary excretion of magnesium were determined, and the relationships between skeletal muscle magnesium content, serum magnesium and urinary magnesium were analysed. Skeletal muscle magnesium content did not differ significantly between groups; 7.93 mumol/g wet weight (median) in group Cy versus 8.38 mumol/g wet weight in group Az. Serum magnesium was significantly (P < 0.01) lower in group Cy (0.71 mmol/l) than in group Az (0.82 mmol/l). The urinary excretion of magnesium did not differ between the groups. Skeletal muscle magnesium did not correlate with either serum magnesium or urinary magnesium excretion in group Cy or group Az. Thus the present study indicates that cyclosporin-treated patients are not magnesium depleted, and serum magnesium in these patients does not reflect the skeletal muscle content of magnesium.
Nephrol Dial Transplant 1993
PMID:Skeletal muscle magnesium content during cyclosporin and azathioprine treatment in renal transplant recipients. 838 43

It is increasingly apparent that end-stage renal disease (ESRD) patients carry an inflammatory burden, which may play a pivotal role in the evolution of not only wasting, but also the massive increase in the relative risk of cardiovascular disease (CVD). Thus wasting is strongly associated with a persistent systemic inflammatory response, CVD, and impaired patient survival in end-stage renal disease (ESRD), as well as in other chronic diseases. Evidence suggests that a facilitative interaction between inflammatory cytokines and other factors such as poor appetite, comorbidity, acidosis, anemia, and hormonal derangements may cause wasting in this patient group. Clearly, isolated interventions in the form of nutritional energy and protein supplementation have seldom proven to be very effective in improving nutritional status and outcome in ESRD patients, presumably because of the need to attack other causative factors. Therefore, new treatment strategies must be evaluated. Strategies such as multiple appetite stimulants, various "anti-inflammatory diets," and new potentially useful anti-inflammatory pharmacologic agents may be tested alone, or in combination, to evaluate if these new therapeutic modalities can improve the outcome of ESRD patients. As the etiology of wasting in ESRD is multifactorial, we propose that its treatment must include not one, but a number of concomitant measures to provide an integrated therapy against this devastating complication.
Semin Dial
PMID:Novel approaches in an integrated therapy of inflammatory-associated wasting in end-stage renal disease. 1566 May 82

Although traditional risk factors for cardiovascular disease are common in dialysis patients, they alone cannot explain the unacceptably high prevalence of vascular disease in this patient group. Much recent interest has therefore focused on the role of various nontraditional cardiovascular risk factors, such as inflammation, wasting, obesity, vascular calcification, and oxidative stress. In addition, genetic factors such as single nucleotide polymorphisms (SNPs) may significantly influence the immune response, the levels of inflammatory markers and body composition, as well as the prevalence of vascular calcification in this patient group. While genetic variations in the tumor necrosis factor (TNF)-alpha-308 and interleukin (IL)-10 -1082 SNPs seem to be consistently associated with adverse clinical outcome in end-stage renal disease (ESRD) patients, the results regarding genetic variations in the IL-6 gene have been conflicting. To elucidate the respective role of DNA polymorphisms in the IL-6 and C-reactive protein (CRP) genes, as well as genes that encode vascular calcification inhibitors (such as fetuin-A, matrix Gla protein, and osteoprotegerin), sufficiently powered studies are needed in which both the protein product and the specific phenotype are determined. In addition, polymorphisms in genes related to body composition may be excellent candidates for analysis in the ESRD population, since nutritional parameters are strongly associated with adverse events in these patients. It seems conceivable that in the future, prognostic or predictive multigene DNA assays (which allow a simultaneous and rapid assessment of multiple genetic variants) will provide nephrologists with a more precise approach for the identification of "high-risk" ESRD patients and the development of accurate individualized treatment strategies.
Semin Dial
PMID:Gene polymorphism association studies in dialysis: the nutrition-inflammation axis. 1607 56

Uremic wasting is strongly associated with increased risk of death and hospitalization events in patients with advanced chronic kidney disease (CKD). Recent evidence indicates that patients with advanced chronic kidney disease are prone to uremic wasting due to several factors, which include the dialysis procedure and certain comorbid conditions, especially chronic inflammation and insulin resistance or deficiency. While the catabolic effects of dialysis can be readily avoided with intradialytic nutritional supplementation, there are no established alternative strategies to avoid the catabolic consequences of comorbid conditions other than treatment of their primary etiology. To this end, there is no indication that simply increasing dietary protein and energy intake above the required levels based on level of kidney disease is beneficial in patients with advanced chronic kidney disease. However, aside from the potential adverse effects such as uremic toxin production, dietary protein and energy intake in excess of actual needs might be beneficial in maintenance dialysis patients as it may lead to weight gain over time. Clearly, the role of obesity in advanced uremia needs to be examined in detail prior to making any clinically applicable recommendations, both in terms of ''low'' and ''high'' dietary protein and energy intake.
Semin Dial
PMID:Protein and energy intake in advanced chronic kidney disease: how much is too much? 1724 11

Protein-energy malnutrition (PEM) is highly prevalent among peritoneal dialysis (PD) patients and is a strong predictor of morbidity and mortality. A wide range of factors can lead to PEM and associated wasting (PEM/W) in PD patients, but persistent inflammation and the presence of diabetes have been identified as the two main reasons. An important body of literature has been reporting studies of methods suitable for detecting malnutrition in its early phase so that appropriate intervention can be provided. Although assessment of nutrition status has been substantially improved, no definitive single method of assessing nutrition status has been decided. Rather, several different markers of nutrition should be evaluated together. Because of the complexity of treating malnutrition in PD patients, nontraditional strategies such as appetite stimulants, anti-inflammatory diets, and anti-inflammatory pharmacologic agents are recommended to be combined with more traditional forms of nutritional support, so as to provide a better chance of recovery. The present review briefly discusses the causes of PEM/W, the methods most commonly used to identify the condition, and the new management strategies available.
Perit Dial Int 2007 Jun
PMID:Identifying and managing malnutrition stemming from different causes. 1755 12

Complex abnormalities of body composition occur in peritoneal dialysis (PD). These abnormalities reflect changes in hydration, nutrition, and body fat, and they are of major clinical significance. Clinical assessment of these body compartments is insensitive and inaccurate. Frequently, simultaneous changes of hydration, wasting, and body fat content can occur, confounding clinical assessment of each component. Body composition can be described by models of varying complexity that use one or more measurement techniques. "Gold standard" methods provide accurate and precise data, but are not practical for routine clinical use. Dual energy X-ray absorptiometry allows for measurement of regional as well as whole-body composition, which can provide further information of clinical relevance. Simpler techniques such as anthropometry and bioelectrical impedance analysis are suited to routine use in clinic or at the bedside, but may be less accurate. Body composition methodology sometimes makes assumptions regarding relationships between components, particularly in regard to hydration, which may be invalid in pathologic states. Uncritical application of these methods to the PD patient may result in erroneous interpretation of results. Understanding the foundations and limitations of body composition techniques allows for optimal application in clinical practice.
Perit Dial Int 2007 Jun
PMID:Body composition analysis techniques in adult and pediatric patients: how reliable are they? How useful are they clinically? 1755 13


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