Differential effects of recombinant human growth hormone on glomerular filtration rate and renal plasma flow in chronic renal failure

1995 ◽  
Vol 9 (4) ◽  
pp. 458-463 ◽  
Author(s):  
Heather Maxwell ◽  
Devati R. Nair ◽  
R. Neil Dalton ◽  
Susan P. A. Rigden ◽  
Lesley Rees
Keyword(s):  
Growth Hormone ◽  
Renal Failure ◽  
Glomerular Filtration Rate ◽  
Chronic Renal Failure ◽  
Glomerular Filtration ◽  
Plasma Flow ◽  
Filtration Rate ◽  
Renal Plasma Flow ◽  
Recombinant Human Growth Hormone ◽  
Human Growth

scholarly journals Growth hormone and the kidney: the use of recombinant human growth hormone (rhGH) in growth-retarded children with chronic renal insufficiency.

1991 ◽  
Vol 1 (10) ◽  
pp. 1136-1145
Author(s):  
R N Fine
Keyword(s):  
Growth Hormone ◽  
Glomerular Filtration Rate ◽  
Plasma Flow ◽  
Growth Velocity ◽  
Filtration Rate ◽  
Renal Plasma Flow ◽  
Recombinant Human Growth Hormone ◽  
Human Growth ◽  
Growth Hormone Releasing Hormone ◽  
Rhgh Treatment

Hypothalamic production of growth hormone releasing hormone stimulates the anterior pituitary gland to release growth hormone (GH). The clinical manifestations of GH on tissues are either direct or are mediated by insulin-like growth factors (IGF). Both the somatic effects of GH and the renal manifestations of an increase in glomerular filtration rate and renal plasma flow are mediated by IGF. The increase in glomerular filtration rate/renal plasma flow that occurs with either exogenous or endogenous GH is not apparent in patients with chronic renal failure (CRF); therefore, it is unlikely that recombinant human growth hormone (rhGH) treatment of patients with CRF will result in glomerular hyperfiltration. Longitudinal studies are required to determine if the glomerulosclerosis and renal functional impairment occurring in GH and growth hormone releasing hormone transgenic mice occurs after rhGH treatment of growth-retarded uremic rats with GH resulted in an improvement in growth velocity. This led to preliminary studies in growth-retarded children with CRF by using rhGH. The acceleration of growth velocity was dramatic despite the fact that GH levels are elevated in uremia. The elevated IGF carrier proteins in uremic children may contribute to the growth retardation. Treatment with rhGH may be efficacious by stimulating a net increase in the free (unbound) IGF levels. Hyposecretion of GH may contribute to the failure to achieve optimal growth after successful renal transplantation. Treatment with rhGH may be efficacious in improving the growth velocity of renal allograft recipients.

Effects of IGF-I on renal function in patients with chronic renal failure

1993 ◽  
Vol 264 (5) ◽  
pp. F917-F922 ◽  
Author(s):  
M. H. O'Shea ◽  
S. B. Miller ◽  
M. R. Hammerman
Keyword(s):  
Renal Failure ◽  
Renal Function ◽  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Plasma Flow ◽  
Filtration Rate ◽  
Renal Plasma Flow ◽  
Kidney Volume ◽  
Igf I ◽  
Reduced Renal Function

Insulin-like growth factor I (IGF-I) has been shown to increase glomerular filtration rate and renal plasma flow in rats and humans with normal renal function. However, rats with reduced renal function are resistant to these effects. To determine whether IGF-I affects glomerular filtration rate and renal plasma flow in humans with reduced renal function, we administered recombinant human IGF-I (rhIGF-I) to patients with moderate chronic renal failure. Four patients whose baseline inulin clearances were 21.9, 23.2, 34.9, and 55.1 ml.min-1.1.73 m-2 were placed on a 1 g.kg-1.day-1 protein diet and studied over a 10-day period (0-10). On days 4-7, 100 micrograms/kg of rhIGF-I was subcutaneously administered twice daily to the patients. The effects of rhIGF-I on levels of circulating IGF-I, inulin clearance, p-aminohippurate (PAH) clearance, kidney volume, plasma glucose, plasma and urine calcium and phosphate, and urine sodium and protein were determined. Administration of rhIGF-I increased levels of circulating IGF-I, inulin clearances, PAH clearances, and kidney size in each of the four patients receiving the growth factor. IGF-I did not cause weight gain, natriuresis, proteinuria, or hypoglycemia. Plasma calcium and phosphate were not affected by rhIGF-I. However, the percent tubular reabsorption of filtered phosphate was increased. We conclude that administration of rhIGF-I can enhance glomerular filtration rate and renal plasma flow at least in some humans with moderately reduced renal function. The enhancement is associated with an increase in kidney volume.

Clinical Renal Function Testing by External Double Isotope Monitoring Technique

1971 ◽  
Vol 10 (01) ◽  
pp. 16-24
Author(s):  
J. Fog Pedersen ◽  
M. Fog Pedersen ◽  
Paul Madsen
Keyword(s):  
Renal Function ◽  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Plasma Flow ◽  
Filtration Rate ◽  
Renal Plasma Flow ◽  
Correlation Coefficients ◽  
Feedback System ◽  
Effective Renal Plasma Flow ◽  
Advantages And Disadvantages

SummaryAn accurate catheter-free technique for clinical determination simultaneouslyof glomerular filtration rate and effective renal plasma flow by means of radioisotopes has been developed. The renal function is estimated by the amount of radioisotopes necessary to maintain a constant concentration in the patient’s blood. The infusion pumps are steered by a feedback system, the pumps being automatically turned on when the radiation measured over the patient’s head falls below a certain preset level and turned off when this level is again readied. 131I-iodopyracet was used for the estimation of effective renal plasma flow and125I-iothalamate estimation of the glomerular filtration rate. These clearances were compared to the conventional bladder clearances and good correlation was found between these two clearance methods (correlation coefficients 0.97 and.90 respectively). The advantages and disadvantages of this new clearance technique are discussed.

Influence of nifedipine on cyclosporin A nephrotoxicity after unilateral nephrectomy in the spontaneously hypertensive rat

1991 ◽  
Vol 81 (2) ◽  
pp. 271-279 ◽  
Author(s):  
P. G. McNally ◽  
F. Baker ◽  
N. Mistry ◽  
J. Walls ◽  
J. Feehally
Keyword(s):  
Body Weight ◽  
Glomerular Filtration Rate ◽  
Renal Impairment ◽  
Cyclosporin A ◽  
Glomerular Filtration ◽  
Plasma Flow ◽  
Filtration Rate ◽  
Renal Denervation ◽  
Renal Plasma Flow ◽  
Spontaneously Hypertensive

1. Nifedipine ameliorates cyclosporin A-induced renal impairment in surgically intact (two-kidney) rats. This study investigates the effect of nifedipine on cyclosporin A nephrotoxicity in spontaneously hypertensive rats after either uninephrectomy or uninephrectomy with contralateral renal denervation. 2. Fourteen days after uninephrectomy pair-fed rats were injected for 14 days with cyclosporin A (25 mg/kg body weight) via the subcutaneous route and with nifedipine (0.1 mg/kg body weight) via the intraperitoneal route. Renal and systemic haemodynamics were measured in conscious unrestrained rats. 3. Whole-blood levels of cyclosporin A did not differ between groups (overall 352 ± 22 ng/ml, means ± sem). After uninephrectomy, cyclosporin A decreased the glomerular filtration rate (olive oil versus cyclosporin A: 0.96 ± 0.04 versus 0.70 ± 0.06 ml min−1 100 g body weight, P < 0.02) and effective renal plasma flow (1.94 ± 0.10 versus 1.38 ± 0.13, P < 0.01), and increased renal vascular resistance {(20.2 ± 1.8) × 104 versus (31.6 ± 3.3) × 104 kPa l−1 s [(20.2 ± 1.8) × 103 versus (31.6 ± 3.3) × 103 dyn s cm−5], P < 0.02} and mean arterial pressure (146.7 ± 6.7 versus 167.3 ± 2.9 mmHg, P < 0.05). Neither renal denervation nor nifedipine prevented the reduction in glomerular filtration rate or effective renal plasma flow induced by cyclosporin A. 4. This study infers that the sympathetic nervous system does not play an active role in cyclosporin A nephrotoxicity and demonstrates that the concomitant administration of nifedipine to rats with reduced renal mass does not ameliorate cyclosporin A-induced renal impairment.

Effect of Proportional Reduction of Sodium Intake on the Adaptive Increase in Glomerular Filtration Rate/Nephron and Potassium and Phosphate Excretion in Chronic Renal Failure in the Rat

1975 ◽  
Vol 49 (3) ◽  
pp. 193-200 ◽  
Author(s):  
C. H. Espinel
Keyword(s):  
Renal Failure ◽  
Glomerular Filtration Rate ◽  
Chronic Renal Failure ◽  
Glomerular Filtration ◽  
Sodium Excretion ◽  
Filtration Rate ◽  
Sodium Intake ◽  
Dietary Sodium ◽  
Control Group ◽  
Phosphate Excretion

1. The influence of dietary sodium intake on the glomerular filtration rate (GFR/nephron) and potassium and phosphate excretion was examined at three stages of progressive chronic renal failure produced in rats by sequential partial nephrectomies. 2. The adaptive increased sodium excretion per nephron in the control group receiving a constant sodium intake did not occur in the experimental group that had a gradual reduction of dietary sodium in direct proportion to the fall in GFR. 3. Despite the difference in sodium excretion, the increase in GFR/nephron, the daily variation in the amount of potassium and phosphate excreted, the increase in potassium and phosphate excretion per unit nephron, and the plasma potassium and phosphate concentrations were the same in the two groups. 4. The concept of ‘autonomous adaptation’ in chronic renal failure is presented.

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