Abnormal Glomerular Filtration Rate, Renal Plasma Flow, and Renal Protein Excretion in Recent and Short-term Diabetics

Ditzel, Jørn; Junker, Karsten

doi:10.1136/bmj.2.5804.13

Cited by 143 publications

(57 citation statements)

References 23 publications

(22 reference statements)

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“…Recently we found GFR and RPF elevated to nearly the same extent in another group of IDD patients comparable to the present group of patients -also with respect to metabolic control [13], (Table 3). Elevated GFR is a well established feature in short-term IDD [4,14]. The results regarding RPF in insulin-dependent juvenile diabetic patients with duration of diabetes less than 12 years have been conflicting.…”

Section: Discussionmentioning

confidence: 97%

“…The results regarding RPF in insulin-dependent juvenile diabetic patients with duration of diabetes less than 12 years have been conflicting. Ditzel and Junker found a reduced RPF [14]. The RPF was measured in the morning after the patients had received their usual insulin dose at 0700 h. Recent studies have demonstrated that insulin reduces RPF in short-term IDD [13,15].…”

Section: Discussionmentioning

confidence: 99%

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Increased kidney size, glomerular filtration rate and renal plasma flow in short-term insulin-dependent diabetics

et al. 1981

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Summary. Glomerular filtration rate (GFR), renal plasma flow (RPF) and kidney volume were measured in thirteen male subjects (mean age 30 years) with short-term insulin-dependent diabetes (mean duration of disease 2.4 years) and fourteen normal male subjects (mean age 29 years). GFR and RPF were measured by constant infusion technique using I125-iothalamate and 13q-hippuran. Kidney size was determined by means of ultrasound. GFR, RPF and kidney volume were increased in the diabetic patients compared to the normal controls, 144 versus 113 ml/ min • 1.73 m 2 (p < 0.0005), 627 versus 523 ml/ min x 1.73 m 2 (p < 0.0025) and 278 versus 224 ml/ 1.73 m 2 (p < 0.0005) respectively. Combining results from diabetic patients and controls revealed a positive correlation between kidney size and GFR (r = 0.70, p < 0.001) and between kidney size and RPF (r = 0.61, p < 0.001). Within the groups kidney size and RPF correlated significantly in the diabetics (p < 0.01) and the same was found for kidney size and GFR (0.025< p < 0.05), while no correlations were found in the normal group. GFR and RPF correlated in the diabetics when evaluated separately (r = 0.81, p < 0.001) and in the controls (r = 0.73, p < 0.001). The previous and present data suggest that the mechanisms of the elevated GFR in insulin-dependent diabetics are enhanced RPF, increased transglomerular hydrostatic pressure gradient and increased glomerular ultrafiltration coefficient. The increased kidney size is probably the main cause of the above alterations in the GFR determinants.

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Section: Discussionmentioning

confidence: 97%

Section: Discussionmentioning

confidence: 99%

Increased kidney size, glomerular filtration rate and renal plasma flow in short-term insulin-dependent diabetics

et al. 1981

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“…Microangiopathy is in fact a major cause of vascular beds are poorly understood, but an increase in intracapillary pressure and blood flow has been implicated (Tooke, 1986). These changes have been found in diverse vascular beds, including the kidney (Ditzel & Junker, 1972; l Author for correspondence.…”

Section: Introductionmentioning

confidence: 99%

Impaired endothelium‐dependent relaxation in isolated resistance arteries of spontaneously diabetic rats

Heygate

Lawrence

Bennett

et al. 1995

British J Pharmacology

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1 Previous studies have shown that endothelium-dependent relaxation in the aorta of spontaneously diabetic bio bred rats (BB) is impaired. 2 We have investigated noradrenaline (NA) contractility, endothelium-dependent acetylcholine (ACh) and bradykinin (BK) relaxation, and endothelium-independent sodium nitroprusside (SNP) relaxation in mesenteric resistance arteries of recent onset BB rats and established insulin treated BB rats, compared to their age-matched non diabetic controls. 3 There was no significant difference in the maximum contractile response or sensitivity to noradrenaline in either of the diabetic groups compared to their age-matched controls. 4 Incubation with the nitric oxide synthetase inhibitor NG-nitro-L-arginine (L-NOARG) resulted in a significant increase in maximum contractile response to noradrenaline in the recent onset age-matched control group (P<0.05). Analysis of the whole dose-response curve (using ANOVA for repeated measures with paired t test) showed a significant left-ward shift following the addition of L-NOARG (P<0.001). A similar but less marked shift (P<0.01) was evident in vessels from recent onset diabetics. An overall shift in both sensitivity and maximum response was also evident in the age-matched non diabetic controls of the insulin-treated group (P<0.05). However, by contrast, there was no significant change in sensitivity in the insulin-treated diabetic rats. 5 ACh-induced endothelium-dependent relaxation was significantly impaired in the recent onset diabetic rats compared to their age-matched controls (47 ± 11% versus 92 ± 2%, P<0.05, n = 6), and in the insulin treated diabetic rats (34±5% versus 75 + 6%, P< 0.05, n = 6). The relaxation responses to BK also were significantly impaired in the diabetic rats compared to their age-matched controls (recent onset: 20+3% versus 72±7%, P<0.05, n=6; insulin treated: 12+9% versus 68+7%, P<0.05, n=7). 6 Incubation with either the nitric oxide synthetase substrate, L-arginine, or the free radical scavenging enzyme superoxide dismutase (150 jml1') failed to improve the attenuated response of acetylcholineinduced relaxation in the diabetic vessels. 7 Endothelium-dependent relaxation mediated by ACh and BK was significantly attenuated in both the diabetic and control vessels after incubation with L-NOARG. 8 Pretreatment with a cyclo-oxygenase inhibitor, indomethacin, significantly enhanced the relaxation to ACh in both the recent onset and insulin treated diabetic rats (42+10%, n=7 versus 64±7%, n=7, P<0.05, and 40±5%, n=7 versus 65+9%, n=6, P<0.05). 9 Following endothelium removal, there was a marked impairment in endothelium-dependent relaxation responses to ACh and BK in both the diabetic and control vessels. 10 Incubation with the thromboxane A2 receptor antagonist SQ29548, did not significantly improve the ACh endothelium-dependent relaxation response in the diabetic vessels. 11 Endothelium-independent relaxation to sodium nitroprusside was significantly impaired in the first group of diabetic vessels studied; however, subse...

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“…In diabetes, capillary endothelial cells and their basement membranes undergo major changes, particularly in the heart [10], retina [11,12], and kidney [13,14,15,16,17,18]. For the nervous tissue, the perineural [19,20,21] and endoneural capillaries [22,23] were reported as getting altered too during diabetes.…”

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confidence: 99%

Morpho-functional studies of the blood-brain barrier in streptozotocin-induced diabetic rats

Bouchard

Bendayan

2002

Diabetologia

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Aims/hypothesis. We undertook the characterization of the capillary bed of the rat frontal cortex and their permeability properties in short-term and long-term diabetic rats. Methods. Diabetes was induced by strepozotocin injection. Rats were maintained hyperglycaemic without insulin treatment during 4 to 5 months (short-term) and 8 to 13 months (long-term). Rats from an additional short-term hyperglycaemic group received an injection of exogenous dinitrophenylated albumin 15 min before being killed. Tissues were processed for electron microscopy and quantitative immunocytochemistry. Endogenous and dinitrophenylated exogenous albumin were revealed with high resolution over the capillary wall using specific antibodies and the protein A-gold complex. Morphometrical analyses were carried out. Results. Albumin is transported across endothelial cells by plasmalemmal vesicles or caveolae and larger vacuolar structures. This transport increased in diabetic rats by an increment in the number of vesicles. Albumin distribution across the capillary basement membrane showed that the restrictive properties of the basement membrane present in normoglycaemic rats are altered in the diabetic condition, as was its thickness. Similar alterations of the basement membrane structure and function were encountered in old normoglycaemic rats but to a lesser extent. Conclusion/interpretation. The results indicate that diabetes seems to accelerate the ageing process of the vascular wall and that the central nervous system capillary bed is also a target for diabetic microangiopathy.

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Abnormal Glomerular Filtration Rate, Renal Plasma Flow, and Renal Protein Excretion in Recent and Short-term Diabetics

Cited by 143 publications

References 23 publications

Increased kidney size, glomerular filtration rate and renal plasma flow in short-term insulin-dependent diabetics

Increased kidney size, glomerular filtration rate and renal plasma flow in short-term insulin-dependent diabetics

Impaired endothelium‐dependent relaxation in isolated resistance arteries of spontaneously diabetic rats

Morpho-functional studies of the blood-brain barrier in streptozotocin-induced diabetic rats

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