Renal Response to Intravenous Somatostatin in Insulin-Dependent Diabetic Patients and Normal Subjects

Abstract

The acute effects of iv somatostatin (SRIH; 100 micrograms/h) on the urinary flow (Uvol), effective renal plasma flow (RPF), and glomerular filtration rate (GFR) were compared with those of a control infusion of 0.15 M NaCl in nine insulin-dependent diabetic (IDD) patients of less than 10 yr disease duration and six normal subjects (NS). RPF and GFR were measured using a standard primed constant isotope infusion of [125I]iodohippurate and [51Cr]chromium EDTA. Uvol, RPF, and GFR were measured during 20-min clearance periods. During the NaCl infusion mean Uvol, RPF, and GFR were 14.1 +/- 0.2 (+/- SEM), 708 +/- 4, and 150 +/- 1 mL/min in the IDD group and 12.7 +/- 0.4, 568 +/- 5, and 110 +/- 2 mL/min in the NS group, respectively. In the IDD patients Uvol, RPF, and GFR decreased from 16.6 +/- 1.8, 670 +/- 30, 146 +/- 4 mL/min pre-SRIH to 9.2 +/- 1 (P less than 0.001), 553 +/- 25 (P less than 0.001), and 130 +/- 5 (P less than 0.001) mL/min, respectively, at 120 min during the SRIH infusion. Similarly, in the NS group mean Uvol, RPF, and GFR were 14.2 +/- 0.6, 552 +/- 15, and 112 +/- 5 mL/min pre-SRIH and decreased to 7.4 +/- 0.6 (P less than 0.001), 422 +/- 7 (P less than 0.001), and 93 +/- 3 (P less than 0.001) mL/min, respectively, after 120 min of the SRIH infusion. SRIH, therefore, had a profound effect on renal function in both IDD patients and NS, resulting in a reduction in RPF, GFR, and, as a consequence, Uvol.

Somatostatin receptor subtype 2-mediated uptake of radiolabelled somatostatin analogues in the human kidney

“…Table 5 summarises all human data on the effects of somatostatin or octreotide on kidney function. Somatostatin and octreotide have been described in healthy subjects and patients with diabetes mellitus and acromegaly to decrease renal plasma flow (RPF) and concomitantly decrease glomerular filtration rate (GFR) with an unchanged filtration fraction [25][26][27][28][29][30][31][32]. However, it should be noted that some of these studies administered supraphysiological doses of somatostatin [100-420 μg/h intravenously (IV) or 600 μg/day subcutaneously (SC)].…”

“…This, taken together with the reduced kidney uptake caused by both octreotide and LAR-octreotide, might provide a basis in the future for continuation of LAR-octreotide treatment during PRRT as it causes little reduction in tumour uptake but sustained kidney uptake reduction, enlarging the therapeutic window of PRRT. Larger studies that apply smaller intervals [26] Healthy (n=3) 6 μg/kg/h somatostatin IV, for 3 h Inulin clearance 131→124 ml/min Schmidt et al [27] Healthy (n=9) 6 μg/kg/h somatostatin IV, for 3 h Inulin clearance 138→119 ml/min Tulassay et al [28] Healthy (n=7) 250 μg somatostatin/h IV, for 2 h Inulin clearance 131→62 ml/min Vora et al [29] Healthy (n=6) and diabetics (n=9) Tc-DTPA clearance 79→72 ml/min Castellino et al [33] Healthy (n=18) 480 μg/h somatostatin IV, for 3 h No effect of somatostatin on inulin clearance Tulassay et al [34] Healthy (n=8) 100 μg octreotide SC, once Creatinine clearance 124→66 ml/min Krempf et al [35] Diabetics (n=5) 480 μg octreotide IV/h, for 10 h 99m Tc-DTPA clearance unchanged Malesci et al [36] Cirrhotics (n=11) T.i. Cr-EDTA clearance 120→114 ml/min (NS) Pomier-Layrargues et al [42] Hepatorenal syndrome (n=14) 50 μg/h IV, for 2 days Creatinine clearance unchanged between the scans are needed before such a strategy can be implemented in PRRT protocols, however.…”

Safety and efficacy of long-acting somatostatin treatment in autosomal-dominant polycystic kidney disease

“…First, somatostatin has been reported to depress GFR slightly and reversibly in human subjects [28][29][30][31][32]. Any tendency for improvement in GFR during treatment with somatostatin might be counteracted by this reversible functional effect.…”

Glucose and insulin exert additive ocular and renal vasodilator effects on healthy humans

“…It could well be, however, that the ability to inhibit insulin secretion contributes to reduced RPF during somatostatin administration. In addition, it has been suggested that somatostatin could have a direct effect on vascular smooth muscle through a calcium-dependent mechanism [46].…”