1. The renal effects of insulin may play a central role in the association between insulin resistance, hypertension and hyperuricaemia. After a 2-h baseline period, we investigated the effects of exogenous insulin for 4 h (50 m-units h-1 kg-1) on fractional renal sodium and urate excretion in 13 healthy subjects, using the euglycaemic clamp and lithium clearance technique, and performed a control experiment in eight of the subjects. 2. Insulin caused a decline in both fractional renal sodium excretion, from 1.13 +/- 0.41% to 0.88 +/- 0.58% (control study: 0.81 +/- 0.35 to 1.35 +/- 0.49%; P < 0.001, insulin versus control), and fractional renal urate excretion, from 6.72 +/- 1.87% to 5.71 +/- 2.02% (control study: 7.03 +/- 2.06 to 7.05 +/- 1.94%; P = 0.085, insulin versus control). The changes in fractional renal sodium and urate excretion were positively correlated (r = 0.71, P < 0.01). Estimated fractional distal sodium reabsorption increased during insulin infusion from 93.7 +/- 2.8% to 96.7 +/- 1.9% (control study: 95.7 +/- 1.5% to 93.6 +/- 1.1%; P < 0.001, insulin versus control). Estimated fractional proximal tubular sodium reabsorption fell from 81.0 +/- 0.5% to 73.7 +/- 4.7% during insulin infusion, but less in the control study (81.5 +/- 4.3% to 79.3 +/- 4.8%; P = 0.056, insulin versus control). The changes in fractional proximal tubular sodium reabsorption and fractional distal sodium reabsorption during insulin infusion were inversely correlated (r = -0.59, P = 0.03). 3. During the course of the insulin infusion experiment an inverse correlation between the changes in fractional sodium and urate excretion, and the insulin-mediated glucose disposal, became gradually evident (r = -0.73, P < 0.01, and r = -0.71, P < 0.01, respectively; fourth hour of the insulin infusion period). 4. We conclude that exogenous insulin acutely decreases renal sodium and urate excretion, and that this effect is probably exerted at a site beyond the proximal tubule.
125Iothalamate and 131I-hippuran clearances, sodium excretion and plasma renin activity (PRA) before and during indomethacin administration in an oral dose of 3 × 50 mg/day were studied in volunteers with a normal or reduced kidney function, as well on non-sodium-restricted as on sodium-restricted diet. Indomethacin induced a temporary sodium and water retention and a decrease in glomerular filtration rate. It also lowered PRA. The latter phenomenon did not depend on sodium retention and was present within 2 h after an oral dose of 50 mg. The results may be explained by indomethacin-induced inhibition of prostaglandin synthesis.
1. Renal and cardiovascular effects of three dosages of insulin [50 (Ins I), 300 (Ins II) and 500 (Ins III) m-units h-1 kg-1] were investigated in healthy males by using a euglycaemic clamp technique. On separate days, control experiments were carried out to correct for any circadian variation in the variables studied. 2. All three insulin dosages resulted in a marked decline in fractional sodium excretion (actual experiments: basal, 0.95 +/- 0.15%, Ins I, 0.79 +/- 0.10%, Ins II, 0.80 +/- 0.12%, Ins III, 0.84 +/- 0.08%; control experiments: basal, 0.96 +/- 0.10%, Ins I, 1.20 +/- 0.12%, Ins II, 1.53 +/- 0.15%, Ins III, 1.43 +/- 0.10%; means +/- SEM, P less than 0.005, analysis of variance). With the highest insulin dosage, the reduction in fractional sodium excretion tended to be less striking. This coincided with a rise in heart rate, pulse pressure and pulse rate-systolic blood pressure product (double product). Although blood pressure itself did not change, systolic blood pressure also tended to increase (actual experiments: basal, 133 +/- 5 mmHg, Ins I, 132 +/- 5 mmHg, Ins II, 139 +/- 5 mmHg, Ins III, 143 +/- 4 mmHg; control experiments: basal, 128 +/- 3 mmHg, Ins I, 129 +/- 3 mmHg, Ins II, 130 +/- 3 mmHg, Ins III, 133 +/- 3 mmHg; means +/- SEM, P = 0.09, analysis of variance). There was a positive correlation between the change in fractional sodium excretion and the change in systolic blood pressure over control values (r = 0.696, P less than 0.028).(ABSTRACT TRUNCATED AT 250 WORDS)
Objective: Protein restriction delays the progression of non-diabetic and type 1 diabetic renal disorders. This study assessed whether protein restriction delays the onset or early progression of renal disorders in type 2 diabetes. Design: Randomized controlled trial. Outcomes were albuminuria (mg=24 h) and, as an estimate of the glomerular filtration rate, cimetidine-influenced creatinine clearance. Setting: Primary care. Subjects: Patients with type 2 diabetes and microalbuminuria or at least detectable albuminuria, or a diabetes duration > 5 y. Interventions: The experimental group received dietary counselling on protein restriction (n ¼ 63); a control group (n ¼ 68) received the usual dietary advice. The duration of intervention and follow-up was 28 AE 7 months. Results: After 6 months, protein intake differed only by 0.08 g=kg=day between the study groups. Subsequently, this difference decreased and eventually disappeared. An initial effect of protein restriction on albuminuria in favor of the experimental group was not sustained, and the glomerular filtration rate decreased in the experimental group at a 1.6 AE 2.2 ml=min=1.73 m 2 y lower rate than in the control group (P ¼ 0.5). Comparison of patients in the experimental group with a decrease in protein intake of at least 0.20 g=kg=day, with controls with no decrease, indicated a similarly small and insignificant effect on glomerular filtration rate. Conclusions: It is concluded that, in the longer term prevention or delay of renal damage in patients with type 2 diabetes, protein restriction is neither feasible nor efficacious.
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