20 research outputs found
Kidney function and size in normal subjects before and during growth hormone administration for one week
Renal Hemodynamics and Limitations of Creatinine Clearance in Determining Filtration Rate in Glomerular Disease
Growth Hormone Treatment in Short Children with Chronic Renal Failure and after Renal Transplantation: Combined Data from European Clinical Trials
Renal Function before and after Urography and Angiography with Large Doses of Contrast Media
RENAL RESERVE FILTRATION CAPACITY IN GROWTH-HORMONE DEFICIENT SUBJECTS
In normal subjects, the glomerular filtration rate (GFR) and effective renal plasma flow (ERPF) acutely increase in response to infusion of amino acids and to low doses of dopamine. It is uncertain whether circulatory growth hormone (GH) is a permissive factor for these stimulatory effects. GFR and ERPF (constant infusion technique using I-125-iothalamate and I-131-hippuran, respectively) were measured before and during the infusion of dopamine and amino acids in 8 GH deficient subjects. The clearance study was repeated during concomitant administration of octreotide to investigate whether this somatostatin analogue would modify the amino acid and dopamine-induced renal haemodynamic changes. Dopamine increased baseline GFR from 89 +/- 3 (mean +/- SEM, n = 8) to 102 +/- 4 ml min-1 1.73 m-2 and ERPF from 352 +/- 19 to 476 +/- 26 ml min-1 1.73 m-2, p <0.001 for both. During amino acid infusion GFR and ERPF increased to 108 +/- 3 and 415 +/- 23 ml min-1 1.73 m-2, respectively, P <0.001 for both. Octreotide did not significantly decrease baseline and dopamine-stimulated renal haemodynamics but lowered the amino acid-stimulated GFR (98 +/- 4 ml min-1 1.73 m-2, P <0.05) and ERPF (381 +/- 18 ml min-1 1.73 m-2, P <0.05). Basal plasma glucagon concentrations were not suppressed by octreotide, whereas the amino acid-induced increments in plasma glucagon were partially inhibited. It is concluded that GH is not a necessary factor for the stimulatory effects of amino acids and dopamine on renal haemodynamics. The renal reserve filtration capacity in GH deficiency was at least as large as previously documented in normal subjects. It is likely that there is a functional antagonism between the effects of amino acids and octreotide on renal haemodynamics in GH deficiency