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)

Hypothalamo-hypophysial-thyroid function has been studied in twenty-five patients with chronic renal failure. Eight were receiving conservative treatment, nine peritoneal dialysis and eight haemodialysis. All were clinically euthyroid. Total thyroxine (T4) and triiodothyronine (T3) levels were reduced but free T4 levels were normal, while free T3 was reduced in patients with the most severe renal failure. It is suggested that the binding of thyroid hormones by the transport proteins is reduced and that peripheral conversion of T4 to T3 is impaired in renal failure. The thyrotrophin response to thyrotrophin-releasing hormone (TRH) is reduced in renal failure but this reduction is probably independent of alterations in thyroid hormone metabolism. Growth hormone was released by TRH in seven of the patients studied, possibly as a result of protein malnutrition.
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PMID:Function of the hypothalamo-hypophysial-thyroid axis in chronic renal failure. 11 57

Administration of recombinant human growth hormone stimulates protein synthesis, decreases urea generation, and improves nitrogen balance in individuals with normal renal function. However, little information is available concerning the effects of growth hormone in patients with renal disease. This pilot study evaluated urea kinetics and clinical/metabolic responses to short-term growth hormone administration in five clinically stable adult patients requiring maintenance hemodialysis for end-stage renal failure. The dialysis prescription, medications, and oral calorie and protein intake of each patient remained constant during an initial control week and a subsequent 2-wk growth hormone treatment period. During treatment, growth hormone (5 or 10 mg) was administered s.c. immediately after each dialysis session. Protein and calorie intake, vital signs, body weight, and other clinical parameters remained stable throughout the 3-wk study. BUN values fell significantly (approximately 20 to 25%) during growth hormone administration compared with control week values. Similarly, urea kinetic modeling demonstrated a significant reduction in urea generation and the protein catabolic rate during each week of growth hormone treatment. Plasma insulin-like growth factor I levels rose significantly, and serum phosphorus and intact parathyroid hormone levels fell significantly during growth hormone administration. Serum glucose and other blood values remained stable. This preliminary study suggests that growth hormone administration reduces urea generation and improves the efficiency of dietary protein utilization in stable adult hemodialysis patients. Growth hormone may be a useful adjunctive therapy to diminish body protein catabolism in this patient population.
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PMID:Effects of recombinant human growth hormone in adults receiving maintenance hemodialysis. 177 93

Growth hormone increases renal plasma flow and glomerular filtration rate and reduces total renal vascular resistance. Evidence presented in this paper indicates that these effects of growth hormone are mediated by insulin-like growth factor I (IGF-I). Published literature indicates that growth hormone and IGF-I have a number of other physiological and morphological effects on the kidney. Further studies are indicated to evaluate under which conditions growth hormone and IGF-I are regulators of kidney function, and to identify the mechanisms of action. In addition, the role of both hormones, if any, in the development of progressive glomerular sclerosis and renal failure needs to be explored.
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PMID:Physiological effects of growth hormone and insulin-like growth factor I on the kidney. 218 98

Although in recent years experimental work on growth in uremia has clarified many issues, many key questions cannot be answered with available experimental data. In our own studies on subtotally nephrectomized rats, uremic animals consumed less food and grew less. However, although low energy intake diminishes growth, it has not been established that high protein energy intake will normalize growth. We showed that uremia reduced growth (and net protein synthesis) even under conditions of controlled food intake. In renal failure the optimal dietary protein level for growth or for efficiency of utilization has not been established, particularly since protein intake has an independent injurious effect on long-term renal function. Calcium and vitamin D supplements improved growth in uremic rats, but the data cannot easily be extrapolated to humans. The growth-promoting action of 1,25(OH)2D3 was not superior to that of equipotent doses of vitamin D3. Correction of anemia and physical exercise did not improve growth. Diminished stimulation of growth cartilage cyclic AMP with PTH and augmented stimulation with calcitonin was noted in uremic animals. Growth hormone in supraphysiological doses improved growth and raised IGF carrier protein in uremic animals. Spermine, a potential uremic toxin, inhibited growth cartilage 3H-thymidine incorporation, but only in concentrations higher than that encountered in uremia.
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PMID:Skeletal growth in experimental uremia. 636 50

Growth hormone (GH) secretion persists during adulthood with mostly metabolic effects, stimulating lipolysis and protein synthesis. Besides GH-deficient patients, other adult patients might in the future benefit from recombinant GH (rhGH) therapy. These conditions would mainly include: 1. Highly catabolic states in intensive-care patients (conflicting results); 2. Osteoporosis, because of significant, although moderate improvement in bone density; 3. Aging: compensating for age-related GH-deficiency has yielded positive results concerning nutritional status; in the elderly however, the risk of side-effects, above all hypervolemia, should not be overlooked; 4. Uremia, frequently associated with poor nutritional status: preliminary results in hemodialysis patients are certainly encouraging; rhGH coupled with intradialytic parenteral nutrition might be particularly efficient. Treatment of uremic patients before end-stage renal failure seems also to be contemplated since, in spite of hyperfiltration and glomerulosclerosis observed in rats receiving high doses of rhGH, no case of worsened renal failure has ever been reported in pre-dialysis children treated for stunted growth.
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PMID:[Possible indications for human recombinant growth hormone in adults: current data and future perspectives]. 781 66

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

Chronic renal failure modifies the morphology and dynamics of the growth plate (GP) of long bones. In young uremic rats, the height of cartilage columns of GP may vary markedly. The reasons for this variation are unknown, although the severity and duration of renal failure and the type of renal osteodystrophy have been shown to influence the height of GP cartilage. Expansion of GP cartilage is associated with that of the hypertrophic stratum. The interference of uremia with the process of chondrocyte differentiation is suggested by some morphological features. However, analysis by immunohistochemistry and/or in situ hybridization of markers of chondrocyte maturation in the GP of uremic rats has yielded conflicting results. Thus, there have been reported normal and reduced mRNA levels for collagen X, parathyroid hormone/parathyroid hormone-related peptide receptor, and matrix metalloproteinase 9, as well as normal mRNA and protein expression for vascular endothelial growth factor and chondromodulin I, peptides related to the control of angiogenesis. In addition, a decreased immunohistochemical signal for growth hormone receptor and low insulin-like growth factor I mRNA in the proliferative zone of uremic GP are supportive of reduced chondrocyte proliferation. Growth hormone treatment improves chondrocyte maturation and activates bone metabolism in the primary spongiosa.
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PMID:Alterations of the growth plate in chronic renal failure. 1554 11

Growth hormone (GH) improves growth in children with chronic renal failure. The response to GH may be affected by the degree of secondary hyperparathyroidism and concurrent treatment with vitamin D. Forty-six rats underwent 5/6 nephrectomy (Nx) and were given a high-phosphorus diet (Nx-Phos) to induce advanced secondary hyperparathyroidism and divided into the following groups: (1) Nx-Phos (n = 10) received saline, (2) GH at 10 IU/kg per d (Nx-Phos+GH; n = 9), (3) GH and daily calcitriol (D) at 50 ng/kg per d (Nx-Phos+GH+daily D; n = 8), (4) GH and intermittent D (three times weekly) at 350 ng/kg per wk (Nx-Phos+GH+int D; n = 9), and (5) intact-control (n = 10). Serum parathyroid hormone (PTH) levels were elevated in Nx-Phos, but IGF-I levels did not change with growth hormone. Body length, tibial length, and growth plate width did not increase with either GH or calcitriol. Proliferating cell nuclear antigen staining, PTH/PTHrP receptor, bone morphogenetic protein-7, and fibroblast growth factor receptor-3 expression increased with GH alone or with intermittent calcitriol but were slightly diminished during daily calcitriol administration. GH enhanced IGF-I, IGF binding receptor-3, and GH receptor but declined with daily and intermittent calcitriol. Overall, there was no improvement in body length, tibial length, and growth plate width at the end of GH therapy, but selected markers of chondrocyte proliferation and chondrocyte differentiation increased, although these changes were attenuated by calcitriol. The combination of GH and calcitriol that is frequently used in children with renal failure and secondary hyperparathyroidism require further studies to evaluate the optimal dose and frequency of administration to increase linear growth and prevent bone disease.
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PMID:Daily or intermittent calcitriol administration during growth hormone therapy in rats with renal failure and advanced secondary hyperparathyroidism. 1572 89

Growth hormone and IGF-1 have been suggested to have tissue-protective effects. Ghrelin is a stomach-derived growth hormone secretagogue. The effects of ghrelin on ischemia/reperfusion-induced renal failure in mice were examined. Ischemic acute renal failure was induced by bilateral renal artery clamping for 45 min and reperfusion for 24 h. Ghrelin (100 microg/kg mouse) or vehicle was injected subcutaneously six times before surgery and three times after surgery every 8 h. Twenty-four hours after reperfusion, the right kidney was isolated and perfused. Acetylcholine (ACh)- and adrenomedullin-induced endothelium-dependent vasorelaxation of renal vessels significantly improved in ghrelin-pretreated mice (%Delta renal perfusion pressure by 10(-7) M ACh -63.5 +/- 3.7 versus -41.2 +/- 5.5%; P < 0.05). This change was associated with significant increases of nitric oxide release in the kidneys of ghrelin-treated mice (10(-7) M ACh 35.5 +/- 5.8 versus 16.9 +/- 3.5 fmol/g kidney per min; P < 0.05). Serum concentration of urea nitrogen (53 +/- 7 versus 87 +/- 15 mg/dl; P < 0.05) and renal injury score were significantly lower in the ghrelin group (2.5 +/- 0.8 versus 5.3 +/- 1.5; P < 0.01). Tubular apoptotic index was significantly lower in the ghrelin group (5 +/- 5 versus 28 +/- 4; P < 0.05). Furthermore, the survival rate after the 60-min ischemic period was higher in the ghrelin group (80 versus 20%; P < 0.05). Ghrelin treatment significantly increased the serum level of IGF-1. However, such renal protective effects of ghrelin on ischemia/reperfusion injury were not observed in insulin receptor substrate-2 knockout mice. These results suggest that ghrelin may protect the kidneys from ischemia/reperfusion injury and that this effect is related to an improvement of endothelial function through an IGF-1-mediated pathway.
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PMID:Ghrelin improves renal function in mice with ischemic acute renal failure. 1630 69

Growth hormone (GH) insufficiency is difficult to identify especially in adults, because its clinical manifestations overlap with metabolic syndrome and diabetes mellitus. We experienced a case of a 38-year-old woman who abruptly gained weight from the age of five, and was diagnosed as type 2 diabetes mellitus (DM) during her 20s. When the patient visited JA Toride Medical Center at age 38, her renal function had been severely damaged, and caused congestive heart failure. Hemodialysis (HD) therapy was introduced, and GH insufficiency was identified, based on her obesity profile since her childhood and hormone surveillance. GH supplementation was initially avoided, because of her concurrent problems of DM and advanced renal failure. However, because of her restricted activities in daily living (ADL) and frequent hypotension episodes, a decision was taken to start supplementary administration of GH, which consequently succeeded in stabilizing blood pressure and extended her ADL. Although GH supplementation has recently been reported to be effective in improving protein energy malnutrition in dialysis patients without GH insufficiency, there is no report concerning GH insufficiency in dialysis patients. This is the first case report of GH insufficiency, in which GH supplementation enabled the patient to continue HD.
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PMID:[Successful maintenance hemodialysis therapy with supplemented growth hormone in a diabetic patient with growth hormone insufficiency]. 2381 88


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