Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0035078 (renal failure)
 31,970 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The renal growth hormone--insulin-like growth factor-I system in acute ischemic renal failure. Recovery from acute tubular necrosis (ATN) is accelerated by IGF-I therapy. Furthermore, the local renal growth hormone-IGF-I system may participate in the natural repair. We examined the IGF-I system in rat kidneys subjected to 60 minute ischemia compared to sham operated controls. Two days after injury, growth hormone receptor mRNA and IGF-I mRNA levels fell approximately 9 to 33% of control values. This was associated with a reduction in kidney immunoreactive IGF-I levels. In contrast, IGF-I receptor mRNA abundance was unchanged. However, plasma membrane IGF-I receptor binding on day 2 and day 7 was near double the control values (P < 0.01). Scatchard analysis revealed a near twofold increase in receptor number. Since receptor mRNA levels were unchanged, this implies receptor protein up-regulation. In contrast to unchanged IGF-I receptor mRNA levels, the abundance of mRNA levels of insulin-like growth factor binding proteins (IGFBP) -2, -3, -4 and -5 fell approximately 14 to 62% of control levels day 2 after injury (P < 0.05), suggesting reduced IGFBP production. Thus, the renal response to ischemic ATN, namely, low IGFBP mRNA levels and high IGF-I receptor number, may function to increase IGF-I bioavailability and thereby enhance the reparative actions of local and circulating IGF-I in ischemic ATN.
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PMID:Renal growth hormone--insulin-like growth factor-I system in acute renal failure. 754 60

The interrelationships of hypercholesterolemia, progression of renal disease to renal failure, and to risks of nephrotic syntrouse are emerging. Both hypercholesterolemia and growth hormone are progression factors, and, in the chronically nephrotic patient, these factors may help to explain the progression to renal failure. Treatment of such patients with growth hormone even though growth retarded should be approached with caution.
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PMID:Hypercholesterolemia and growth hormone in renal diseases. 757 65

Progressive glomerulosclerosis is associated with decreasing kidney function, eventuating in end-stage renal failure. There are multiple components of the extracellular matrix, and the exact composition in various renal diseases is not known. Thus, we examined some of the major components of the extracellular matrix (ECM) in murine and human glomerular diseases. We studied matrix synthesis and degradation at the level of gene expression and ECM composition in the intact glomerulus. To determine whether the composition of sclerosis was similar among diseases, we examined a normal mouse strain and compared it with strains which spontaneously developed glomerulosclerosis. The baseline levels of matrix components varied between different mouse strains, and this level correlated with their propensity to develop glomerulosclerosis. In addition, when glomerulosclerosis was induced, the baseline ECM mRNA level predicted the subsequent outcome. We studied mice transgenic for bovine growth hormone, since they develop progressive glomerulosclerosis. Treatment with heparin substantially decreased the lesions without changes in type IV collagen mRNAs. However, there was an up-regulation of both the mRNA and enzyme activity for the 92 kD matrix metalloproteinase. In contrast, when these mice were treated with either angiotensin converting enzyme inhibitors or angiotensin II (Ang II) receptor antagonists, the glomerulosclerosis was accentuated histologically and the ECM synthetic and degradative mRNAs were elevated. These data suggest that the mRNA levels reflect response to therapy.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Collagen and collagenase mRNAs in normal and sclerotic glomeruli: predictors of progression and response to therapy. 767 91

Growth retardation is one of the major problem in children with chronic and terminal renal failure. The growth hormone-insulin-like growth factor axis is altered in uraemia, resulting in peripheral resistance. This insensitivity seems to be overcome in an experimental study by supraphysiological doses of recombinant human growth hormone (rhGH). Several clinical studies have confirmed that rhGH increases growth velocity in children with chronic renal failure with and without dialysis and after renal transplant, without significant side-effects. The improvement of growth is more marked in prepubertal patients and during the first year of rhGH treatment. Also in our experience prepubertal children showed an increase of height standard deviation score and growth velocity during rhGH treatment; the pubertal patients failed to improve their statural growth. GH, as the prototype of an anabolic hormone, has also great potential in improving catabolic conditions of various origin, particularly those due to renal failure. RhGH can improve nitrogen balance and the nutritional parameters with an increase of muscle mass and a decrease of fat mass. Prospectively, rhGH could be utilized to improve the hypercatabolic condition of acute renal failure. The following analysis will discuss the recent studies employing rhGH in renal diseases and will attempt to give some guide lines to rhGH treatment in these illnesses.
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PMID:[Indications for recombinant growth hormone (rhGH) treatment in kidney diseases]. 773 21

Perhaps the liver in renal failure significantly alters its pH in order to attempt to maintain homeostasis. This alteration might explain the growth hormone resistance found in children with chronic renal failure.
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PMID:A possible explanation for growth hormone resistance in chronic renal failure. 783 99

It has been claimed that low protein diets slow deterioration of chronic renal failure (CRF) by reducing renal solute load. The anabolic effect of recombinant human growth hormone (rhGH) also has potential to reduce renal solute load and thereby slow progression of renal failure. The aim of this study was to determine the effect of rhGH on growth, renal solute load and renal function in children with CRF. Seven prepubertal children, aged 2-14 years, with moderately severe CRF (creatinine clearance 7.7-23.4 mL/min per 1.73m2) were treated with daily subcutaneous rhGH, 1 U/kg per week for 10-12 months. As expected, mean height velocity standard deviation scores (SDS) increased, from -2.87 before treatment to +3.39 on rhGH, and mean height increased from -3.1 to -2.4 SDS. Serum urea concentrations decreased in most patients during the first month of growth hormone treatment from a mean of 20.0 +/- 7.7 mmol/L to 14.8 +/- 5.8 mmol/L (P = 0.006). The serum urea then returned to pretreatment levels over the next few months. In the 12 months before treatment with growth hormone, mean creatinine clearance decreased from 19.3 mL/min per 1.73 m2 to 16.7 mL/min per 1.73 m2. In the next 12 months on rhGH mean creatinine clearance decreased further to 13.5 mL/min per 1.73 m2. Therefore the rate of deterioration of renal function was unaffected during treatment with growth hormone. Initial treatment with rhGH is associated with decrease in serum urea concentrations in children with CRF, probably mediated by stimulation of anabolic incorporation of dietary nitrogen into body protein.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The effect of growth hormone on growth and blood urea levels in children with chronic renal failure. 786 79

Growth failure continues to be a problem in the management of children with renal failure. Children have improved growth after successful renal transplantation, but seldom have "catch-up" growth, or normal adult height. In this study we report the findings of an open label pilot study to determine the safety and efficacy of the use of recombinant human growth hormone (rhGH) in children with growth failure after successful renal transplantation. Eleven children completing at least 1 year of treatment had a mean age of 11.5 years (+/- 3.3) and mean bone age of 8.4 years (+/- 2.4), and were significantly growth-retarded (mean standard deviation score of -3.18 [+1.1]). After receiving rhGH (0.05 mg/kg) subcutaneously each day the height velocity increased from 5.2 cm/year to 8.4 cm/year (P = 0.003), and the standard deviation score improved from -3.18 to -2.23 (P = 0.004). Treatment was associated with advancement in Tanner stage from 1 to 2.8 (P = 0.004), increased bone age from 8.4 years to 10.9 years (P = 0.0002), and although it was not at the point of statistical significance, moderate decrease in creatinine clearance from 75 ml/1.73m2/min to 60 ml/1.73m2/min (P = 0.1). The advancement in Tanner stage and bone age was not out of proportion to the advancement in height age. These data suggest that children with functioning renal allografts have improved growth with supraphysiologic doses of rhGH.
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PMID:Treatment of growth failure in children after renal transplantation. 843 81

A 26-year-old man with Graves' hyperthyroidism associated with central diabetes insipidus (DI), initially showed hypercalcemic crisis. Initially, very low serum levels of intact parathyroid hormone (PTH) and 1,25-dihydroxy vitamin D3 and a moderate rise of serum C-terminal PTH related protein (C-PTHrP) were observed which strongly suggested a humoral hypercalcemia of malignancy due to PTHrP. However, the serum C-PTHrP level later became normal. Mild hyperprolactinemia, no responses of growth hormone (GH) to insulin-induced hypoglycemia despite a normal growth hormone releasing hormone (GRH) test and mild thickening of the pituitary stalk on magnetic resonance imaging were observed. Thus, an autoimmune nature of his central DI is considered; it is noteworthy that the serum C-PTHrP level may be elevated by renal failure in patients with hypercalcemia due to causes other than PTHrP.
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PMID:Development of hypercalcemic crisis in a Graves' hyperthyroid patient associated with central diabetes insipidus. 858 May 71

Secretion of growth hormone (GH) is excessive in acromegaly, but also in a number of other pathological states such as anorexia nervosa, insulin-dependent diabetes mellitus (IDDM), liver cirrhosis, depression, renal failure and GH-insensitivity syndrome. Abnormalities in the neuroendocrine control of GH secretion and/or a state of insensitivity to GH contribute to hypersecretion of GH in these states, with the possible exception of acromegaly, which appears to be a primary pituitary disease. GH hypersecretion may also occur in neonates or adolescents with tall stature, thus reflecting particular physiological or paraphysiological conditions. In the cohort of brain neurotransmitters, catecholamines and acetylcholine reportedly play a major role in the control of neurosecretory GH-releasing hormone (GHRH) and somatostatin (SS)-producing neurons, and hence GH secretion. Activation of alpha 2-adrenoceptors or of muscarinic cholinergic receptors in the hypothalamus stimulates GH release, probably through stimulation of GHRH and inhibition of SS release, respectively. Activation of dopamine receptors likewise stimulates GH release, while activation of beta-receptors inhibits GH release through stimulation of hypothalamic SS function. This review discusses the involvement of brain catecholamines and acetylcholine in GH hypersecretory states, including anorexia nervosa, acromegaly, IDDM, liver cirrhosis, depression, renal failure and GH insensitivity syndrome, with a view to providing a fuller understanding of their pathophysiology and, whenever possible, diagnostic and therapeutic implications.
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PMID:Involvement of brain catecholamines and acetylcholine in growth hormone hypersecretory states. Pathophysiological, diagnostic and therapeutic implications. 858 28

The pathogenesis of growth retardation in children with chronic renal failure (CRF) is clearly multifactorial. A major breakthrough in the understanding of the pathogenesis of uremic growth failure was achieved only recently by a more detailed analysis of the growth hormone (GH)/insulinlike growth factor (IGF) axis. Uremia is characterized by an insensitivity to the somatotropic action of GH. The mechanisms that account for this insensitivity include reduced hepatic GH receptor expression, decreased production of IGF-I, and inhibition of IGF bioactivity by increased binding of IGFs to their specific binding proteins. Recombinant human growth hormone (rhGH) in supraphysiological doses is able to overcome the partial GH resistance and to stimulate longitudinal growth under both experimental and clinical conditions. One possible mechanism of action of rhGH in uremia is the restoration of circulating IGF bioactivity, which results from the differential regulatory effect of rhGH on circulating IGF-I and IGFBP-3 concentrations. RhGH has proven to be an effective, safe, and well-tolerated new treatment modality for growth-retarded children at all stages of CRF. There is strong evidence that final height will increase in these children. Other than a modest chronic stimulation of insulin secretion, no frequent side effects have been observed; in particular, no acceleration in loss of residual renal function has been seen in children treated before the onset of end-stage renal failure. In children after transplantation, rhGH is also effective, but the potential risk of interference with graft function is not yet sufficiently defined.
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PMID:Recombinant human growth hormone for children with renal failure. 862 Mar 67


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