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Query: UMLS:C0035078 (renal failure)
 31,970 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Recombinant human growth hormone (rhGH) has been widely used to improve growth in children with chronic renal failure (CRF). However, there has been great concern that GH may aggravate renal disease and hasten the progression to end-stage renal failure. We therefore investigated the effect of prolonged administration of rhGH at various doses on somatic growth and renal function and structure in rats with CRF, divided into four groups based on rhGH dose (vehicle, 0.4, 2.0, and 10.0 IU/day). rhGH was administered subcutaneously daily for 8 weeks. The mean growth was significantly greater in rats treated with high-dose rhGH (10.0 IU) than those treated with low-dose rhGH (P = 0.0089) or vehicle (P = 0.0011). Body weight gain increased in parallel with body length (Creatinine clearance at the end of the experiment was significantly lower in rats on high or medium-dose rhGH than those on low-dose rhGH and controls (P < 0.05). The glomerular sclerosing index was greater in rats treated with higher doses of rhGH. There were significant differences between rats treated with high-dose rhGH and controls (P = 0.0144) and also between rats on medium-dose rhGH and controls (P = 0.0065). Although there was no significant difference, rats treated with higher doses of rhGH tended to excrete more protein. Renal insulin-like growth factor-I (IGF-I) content and circulating IGF-I and IGF-II levels did not significantly differ among groups. We conclude that: (1) GH improves somatic growth failure in rats with CRF, but prolonged administration of GH dose-dependently induces deterioration in renal function and structure and (2) this effect was induced neither via circulating IGF-I and IGF-II nor by local production of IGF-I, but seems to be direct.
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PMID:Somatic and renal effects of growth hormone in rats with chronic renal failure. 920 73

Growth failure is an important problem in children with renal failure. Even after renal transplantation their growth rates may be lower than normal, and "catch-up" growth does not occur. Therefore there is great interest in giving growth hormone (GH) after transplantation. Clinical observations and theoretic considerations call into question whether GH after transplantation is safe. Studies have shown a more rapid than normal decline in renal function after the initiation of GH therapy. This result could be explained by the effects of GH on the immune response. Growth hormone is known to modulate (usually upregulate) the immune response and could be a reason for the increased loss of renal function caused by rejection. It could also be explained by the long-term effects of GH on the injured kidney. Experimental data (generally not in the transplantation model) suggest that exogenous GH given after renal injury or reduced renal mass leads to a more rapid development of glomerular sclerosis and reduced renal function. GH should not be administered to children after renal transplantation until all safety questions have been answered in prospective clinical trials.
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PMID:Growth hormone is not safe for children with renal transplants. 925 23

The goal of treatment of end-stage renal failure in pediatric patients is a functioning transplant. Due to the serious shortage of cadaver kidneys, we have to consider living related donor transplantation (tpl) more frequently. Certain features are characteristic of pediatric patients before transplantation: underlying disease (over 2/3 are congenital or hereditary), the form of dialysis (automated peritoneal dialysis at home in young children) and the frequent need for tube feeding and treatment with growth hormone. Patients weighing 10 kg or more can be given an adult kidney. Young recipients are at risk for vascular thrombosis and hence the CVP should be kept high to allow good circulation, and continuous heparinization (10 units per kg and hour) is advocated. Minor rejection episodes may be overlooked in the presence of a large graft in a small child. Bladder dysfunction is a problem in many children with obstructive uropathy. Later on, viral infections (CMV, EBV) may pose serious problems since most children have not previously been exposed to them. Further problems are pyelonephritis in the graft and recurrence of the underlying disease. Long-term results are very satisfactory in terms of survival and quality of life including later social integration.
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PMID:[Kidney transplantation in the child]. 928 31

To evaluate the impact of uremia and associated caloric restriction on physiologically pulsatile growth hormone (GH) release, we used deconvolution analysis of spontaneous plasma GH profiles in 5/6-nephrectomized male rats (NX, N = 9). Three different normal renal function sham-operated groups were used: rats fed a normal diet ad libitum (SAL, N = 9); NX pair-fed rats (SPF, N = 6); NX rats pair-fed for protein ingestion but calorically supplemented up to the energy intake of SAL (SPF+, N = 8). Severe renal failure was confirmed by much higher (P < 0.001) BUN in NX than sham groups. NX rats were growth retarded as shown by reduced (P < 0.01) weight and length gains as compared with sham animals. Deconvolution analysis (mean +/- SEM) of plasma samples obtained every 10 minutes over 6 hours, and 14 to 16 days after second stage nephrectomy showed that NX rats had a longer GH t(1/2) (17.0 +/- 1.8 vs. 11.6 +/- 0.8 min), less GH mass secreted per burst (48 +/- 15 vs. 95 +/- 16 ng/ml/pulse), lower secretory pulse amplitude (1.9 +/- 0.5 vs. 5.8 +/- 0.9 ng/ml/min), and a reduced total GH secretion (240 +/- 69 vs. 400 +/- 56 ng/ml/6 hr) than SAL rats. Corresponding data were not significantly different between NX and SPF, or between SAL and SPF+ groups. In summary, stunted rats with chronic renal failure exhibit a prolonged GH t(1/2) and suppression of GH secretory pattern burst mass. Control data from rats with normal renal function suggest that the amplitude-specific depression of GH secretion may be attributed, at least in part, to chronic renal failure-associated calorie deficiency.
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PMID:Impaired secretion of growth hormone in experimental uremia: relevance of caloric deficiency. 929 Nov 83

Chronic renal failure is rare in children. About one child per year per million population reaches terminal renal insufficiency. The breakdown of the excretory and incretory renal function leads to a damage of nearly all organ systems. Growth retardation and renal osteodystrophy are the most important manifestations in childhood. In the predialytic stage, therapy consists in a low protein, high caloric diet with calcium and vitamin D supplementation as well as the parenteral application of erythropoetin and growth hormone. In terminal renal failure, artificial kidney support is necessary either as hemodialysis or peritoneal dialysis. The ultimate aim is a successful transplantation for full rehabilitation. The multiple medical and psychological problems need a good cooperation between family physician and the center of pediatric nephrology.
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PMID:[Chronic renal failure in childhood]. 931 27

Insulin-like growth factor-I (IGF-I) is a nutrient-regulated growth factor. In malnutrition, serum IGF-I levels fall despite normal or elevated growth hormone (GH) levels and this is caused by resistance to GH, defects in IGF-I gene transcription and translation and mRNA instability. Because IGF-I production is sensitive to protein and energy deficiencies serum IGF-I levels may be valuable in the assessment of the nutritional status of patients with wasting diseases, including advanced renal failure. It should be recognized, however, that serum or tissue IGF-I peptide levels do not always reflect IGF-I gene expression. For example, in the K-deficient rat, kidney IGF-I levels are increased even though IGF-I mRNA levels are low. This appears to be due in part to increased sequestration by IGF-binding proteins and by decreased kidney IGF-I degradation. The increase in kidney IGF-I may contribute to the exaggerated renal growth that occurs in hypokalemia.
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PMID:Nutrient regulation of insulin-like growth factor-I. 938 7

The use of (costly) growth hormone (GH) treatment in short children is often justified by the assumption that short stature considerably reduces quality of life in adults. We tested this assumption in 5 groups of short adults: 25 patients with isolated GH deficiency; 17 male patients with childhood onset renal failure; 25 women with Turner syndrome and 26 patients who were presented as a child to a paediatrician for idiopathic short stature. A group of 44 short individuals with presumably idiopathic short stature, who had not been presented to a paediatrician for short stature, was sampled from the general population ('normal shorts'). We measured quality of life in terms of socio-economic variables, the Nottingham Health Profile and time trade-off. The mean height of most groups was close to the 3rd percentile. The chance of having a partner was low for all groups, except for the normal shorts. Problems with job application were only reported in Turner syndrome. The scores on the Nottingham Health Profile were all within the normal range, but GH-deficient adults had a higher score on the domain energy than normal shorts. Women with Turner syndrome, individuals with renal failure, and those with idiopathic short stature had a wish to be taller, with an estimated reduction in quality of life of 2-4% (time trade-off). As the normal shorts did not show any sign of a reduced quality of life, we falsify the assumption of a direct relation between short stature and quality of life. The complaints of patients with idiopathic short stature around the 3rd percentile seem to be the result of unsuccessful coping strategies.
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PMID:Quality of life in short adults. 943 83

Microencapsulated genetically engineered cells have the potential to treat a wide range of diseases. For example, in experimental animals, implanted microencapsulated cells have been used to secrete growth hormone to treat dwarfism, neurotrophic factors for amyotrophic lateral sclerosis, beta-endorphin to decrease pain, factor XI for hemophilia B, and nerve growth factors to protect axotomized neurons. For some applications, microencapsulated cells can even be given orally. They can be engineered to remove unwanted molecules from the body as they travel through the intestine, and are finally excreted in the stool without being retained in the body. This application has enormous potential for the removal of urea in kidney failure, ammonia in liver failure and amino acids such as phenylalanine in phenylketonuria and other inborn errors of metabolism.
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PMID:Therapeutic uses of microencapsulated genetically engineered cells. 961 2

Growth and psychological functioning were studied in 30 patients with renal failure over a two year period following the offer of growth hormone treatment for significant short stature. Parents' concerns about growth decreased significantly during the study. Twenty eight parents (93%) accepted growth hormone treatment; most (74%) were satisfied with it and would opt for it again (89%). The views of these parents were unrelated to growth outcome in their child. This suggests that the positive responses were related more to the effort to improve growth than to any objective treatment success. In contrast children's reduction in concern about growth, satisfaction with treatment (36%), and decision to opt for growth hormone again (50%) were all significantly related to improvement in growth. Parents' reports of non-compliance increased significantly from 41% at 1 year to 91% at 2 years in the group as a whole. No significant changes were identified in maternal mental distress and no additional costs to the psychological health of the children seem to have resulted from the introduction of growth hormone treatment. A group of children was identified who accepted treatment but had continued poor growth. These appeared to be at particular risk of both physical problems and associated or consequent psychological difficulties.
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PMID:Growth in renal failure: a longitudinal study of emotional and behavioural changes during trials of growth hormone treatment. 961 51

The quality of life of patients with end-stage renal disease (ESRD) has become an area of intensive investigation because of the high costs of renal-replacement therapy (dialysis or renal transplantation) and the rising prevalence of renal failure. Studies comparing quality of life of patients using different forms of renal-replacement therapy are flawed by deficiencies in study design, such as lack of randomisation. Nevertheless, in both retrospective and prospective studies, transplantation has been shown to offer the highest levels of functional ability, employment and subjective quality of life. After case-mix adjustment, there is little difference between peritoneal dialysis and haemodialysis in terms of quality-of-life (QOL) outcomes. Vocational rehabilitation is an important aim of therapy; for patients below retirement age, pre-dialysis education and counselling are important in maintaining employment. The elderly comprise the fastest-growing group of dialysis recipients; multiple comorbidities add to functional impairment in these patients. Subjective quality of life remains surprisingly high in many elderly patients, despite poor objective quality of life. The quality of life of patients with diabetes mellitus and ESRD is lower than that of nondiabetic patients with ESRD. For selected patients with insulin-dependent diabetes mellitus, combined renal and pancreatic transplantation offers the advantage of freedom from insulin injections. Unfortunately, available evidence suggests only small improvements in quality of life with combined transplantation versus kidney-only transplantation, probably because many patients have developed multiple diabetic complications by the time of transplantation. Epoetin alfa (erythropoietin) has been shown to improve quality of life in a number of trials. The optimal target haematocrit is a subject of controversy, but on current evidence, a target of 34 to 37% is reasonable. The degree of improvement in quality of life must be balanced against the additional costs of achieving a higher haematocrit. Further study is necessary to clarify the optimal target haematocrit for epoetin alfa therapy, as well as the possible effects of nutritional support, growth hormone in paediatric patients, and combined renal and pancreatic transplantation in improving quality of life.
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PMID:A review of quality of life in chronic renal failure. 1016 67


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