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Query: UMLS:C0730345 (microalbuminuria)
 4,018 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hypersecretion of growth hormone (GH) is a characteristic feature of Type 1 diabetic patients. In healthy subjects growth hormone is able to induce an increase in endothelial cell proteins such as fibrinogen and von Willebrand factor. Plasma concentrations of such proteins, which are markers of cardiovascular risk, are elevated in diabetic patients with microalbuminuria, suggesting endothelial cell dysfunction. In a randomized prospective study we therefore evaluated the possible effects of 1 year's treatment with a somatostatin analogue, octreotide, on lipoproteins and on endothelial function in Type 1 diabetes mellitus. Seven patients were allocated to treatment with a continuous subcutaneous infusion of 400 micrograms octreotide per day. Seven patients served as a control group. During treatment a decrease in plasma LDL-cholesterol (2.62 (2.17-3.11) (median (range] vs 2.00 (1.89-2.96) mmol l-1, p less than 0.05) and serum apolipoprotein A-I (1.47 (1.25-1.60) vs 1.23 (1.13-1.90) g l-1, p less than 0.05) was observed in the treated group. Furthermore a probable reduction during treatment in plasma concentrations of von Willebrand factor (1.72 (0.84-3.04) vs 1.24 (0.94-1.82) U ml-1, p = 0.08) and fibrinogen (11.3 (7.3-25.3) vs 8.1 (7.5-11.8) mumol l-1, p = 0.06) was found, and after withdrawal of treatment an increase towards the initial levels was seen. The platelet count declined (326 (301-612) vs 217 (206-400) x 10(9) l-1, p less than 0.01) during octreotide treatment and remained depressed 2 months after withdrawal.
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PMID:Effects of octreotide on lipoproteins and endothelial function of type 1 (insulin-dependent) diabetic patients. 214 88

Chronic hyperglycemia is the single most important pathogenic factor in the diabetic triad: retinopathy, glomerulopathy and neuropathy. But at equal serum glucose balance, diabetics are not equally at risk of microangiopathy. Hence the importance of timely screening of patients who should be convinced to accept the constraints and risk of perfect serum glucose balance or to whom specific therapy independent from serum glucose balance could be proposed. But at present, there is no genetic or immunologic marker allowing for the individual identification of at risk patients. Attention is thus directed towards factors which may be directly involved in the pathogenesis of diabetic microangiopathy: --Special sensitivity of vascular collagen to protein glycosylation which could be reflected in the involvement of tendon and aponeurotic collagen, --platelet abnormalities of which the exacerbating role appears to be confirmed by the significant efficacy of aspirin in the treatment of nonproliferative retinopathy in insulin-independent diabetics, --rheological abnormalities which might essentially be secondary to chronic hyperglycemia, --hormonal abnormalities, in particular hypersecretion of growth hormone and/or somatomedin C, whose role has long been suspected and could be established by therapeutic trials with new somatostatin analogues. But the most recent advances concern the study of hemodynamic factors. Irreversible organic diabetic microangiopathy is thought to be preceded by a phase of reversible functional microangiopathy, characterized by increased capillary blood flow, vascular dilatation, hyperpermeability and altered regulation of flow. Thus, diabetic glomerulopathy with decreased glomerular filtration is preceded by a phase of renal "hyperfunctioning" and irreversible proteinuria is the outcome of a progressive increase in microalbuminuria, reversible at least while the levels are not too high.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Screening of subjects at high risk for diabetic microangiopathies]. 264 89

Cardiovascular and Renal function were examined in two populations of long-term insulin-dependent diabetics, those with microalbuminuria, a sign of early, subclinical nephropathy and those with clinically manifest diabetic nephropathy. In addition, clinical variables of possible importance for the occurrence and prognosis of diabetic nephropathy were analyzed. Microalbuminuria - a mean of three over-night urinary albumin excretion rates greater than 20 micrograms/min - was found in 16% of Albustix-negative, normotensive, insulin-dependent diabetics. The microalbuminurics had higher supine blood pressures than normoalbuminurics. The albumin excretion rate in microalbuminurics correlated to blood pressure at rest but not to glycosylated haemoglobin. The cardiovascular responses to five different test manoeuvres revealed more evident signs of autonomic nerve dysfunction in microalbuminurics than in normoalbuminurics. The circulatory reactions during mental stress however, were almost identical in the two subgroups. Despite similar glomerular filtration rate and renal plasma flow the albumin excretion during mental stress increased in microalbuminurics, but remained unchanged in normoalbuminurics. It is postulated that a disturbance of glomerular basement membrane permeability is a pre-requisite for the elevated albumin excretion seen in microalbuminurics. Inability to regulate glomerular haemodynamics, due to autonomic nerve dysfunction, may also be a contributing factor. Such dysfunction perhaps even explains why microalbuminurics have higher blood pressures at rest compared with normoalbuminurics. In manifest diabetic nephropathy the rate of renal functional decline correlated to arterial blood pressure, while glycemic control showed no such relation. Patients with rapidly progressive nephropathy showed higher values of growth hormone than slow progressors. In patients with diabetic renal failure, cardiac catheterization revealed reduced stroke work and elevated left ventricular end-distolic pressure during exercise. Autonomic nerve dysfunction and arterial hypertension possibly contributed to the impaired cardiac performance. The existence of a specific diabetic cardiopathy must even be considered. There was a male predominance both in subclinical and manifest diabetic nephropathy. Age at onset of diabetes was lower in micro- as compared to normoalbuminurics. Duration of diabetes had no prognostic implication in subclinical or manifest nephropathy. The mortality rate was high in patients with manifest nephropathy.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Studies of cardiovascular and renal function in subclinical and manifest diabetic nephropathy. 316 65

Forty percent of patients with insulin-dependent diabetes will develop nephropathy during the course of their disease, thus being the most important single disorder leading to end-stage renal failure (ESRF). Intensive metabolic control delays onset of diabetic nephropathy, the first omen of which is appearance of subclinical albuminuria, also termed microalbuminuria. Moreover, it is now established that intensive treatment of hypertension reduces rate of decline in GFR and thus postpones ESRF. When uremia eventually sets in, a range of biochemical and endocrine abnormalities can be included among those characteristics of diabetes mellitus per se. These include elevated plasma levels of growth hormone, glucagon and free fatty acids, which may participate in the uremic insulin resistance superimposed on the preexisting diabetic carbohydrate intolerance. Hemodialysis (HD) and continuous ambulatory peritoneal dialysis (CAPD) are two established modalities of renal replacement therapy in diabetes mellitus. Controlled clinical trials for comparison of CAPD versus HD treatment of diabetics are, however, still needed. The survival rate is approximately 80 and 65-95% in insulin-dependent diabetic patients at 1 year during treatment with HD and CAPD, respectively. However, it is general experience that diabetics on CAPD exhibit a glycemic control, superior to that attained during HD. It has not been proved that patient survival after cadaveric renal transplantation is better than on dialysis. The degree of vascular heart disease seems to be the major determinant for survival of kidney-transplanted diabetic patients.
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PMID:End-state renal failure in diabetic nephropathy: pathophysiology and treatment. 391 47

Glomerular hyperfiltration is a characteristic feature of acromegaly but it is uncertain whether albuminuria is elevated in this disease. To investigate the role of abnormal growth hormone (GH) and insulin-like growth factor I (IGF-I) levels on urinary protein excretion, we measured the overnight urinary albumin excretion rate (UalbV) and creatinine clearance in 14 acromegalic patients with metabolically active disease (fasting GH > 5 micrograms/l and IGF-I > 2.2 kU/l), 8 GH-deficient patients and 20 control subjects. The UalbV was higher in the acromegalic patients (median 8.4 (range 4.2-68.2) micrograms/min) than in the GH-deficient patients (2.0 (0.9-5.9) micrograms/min, p < 0.001) and control subjects (3.3 (1.0-7.8) micrograms/min, p < 0.01). Five acromegalic patients had UalbV levels above the normal upper normal limit of 10 micrograms/min. Only one patient with concomitant untreated hypertension had persistent microalbuminuria. Creatinine clearance also was higher in the acromegalic patients (p < 0.05) and lower in the GH-deficient patients (p < 0.05) than in the control subjects. In 11 of these acromegalic cases, the lowering of GH by 63% and of IGF-I by 48%, following treatment with the somatostatin analogue (N = 10) or spontaneous pituitary infarction (N = 1), reduced the UalbV by 29% to 4.9 (3.1-45.2) micrograms/min (p < 0.01). Among the acromegalic patients (25 observations), the UalbV was related to GH (r = 0.61, p < 0.01), IGF-I (r = 0.57, p < 0.01) and creatinine clearance (r = 0.54, p < 0.01). In conclusion, circulatory GH and IGF-I levels influence albuminuria.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of growth hormone and insulin-like growth factor I on urinary albumin excretion: studies in acromegaly and growth hormone deficiency. 837

Proximal tubular dysfunction may be implicated in the pathogenesis of diabetic nephropathy. An investigation of proximal tubular function was carried out by assessing proximal tubular sodium-reabsorption and low molecular weight protein excretion in a group of patients with type 1 diabetes mellitus. Normoalbuminuric [group A, n = 6, albumin excretion rate (AER) mean (range) 4 (0-10) micrograms/min], and microalbuminuric [group B, n = 6, AER 88 (35-198) micrograms/min] patients with type 1 diabetes were compared with matched controls. Simultaneous lithium and growth hormone (GH) clearance and urinary beta 2-microglobulin excretion were assessed. Fasting plasma glucose at the start of the study was [median (range)] 13 (10.2-15.1), 9.3 (5.9-15) and 4.1 (4.0-5.0) mmol/l in groups A, B and controls, respectively, with a mean coefficient of variation during the study of 3.9% (group A) and 5.2% (group B). There was no significant difference in plasma glucose levels between patients in groups A and B. Urinary GH excretion was raised in the patients with microalbuminuria (group B; P < 0.05), although there was no difference in serum GH clearance rate between the patient groups and controls. Urinary GH correlated with B 2-microglobulin in the diabetic subjects (r = 0.665, P < 0.05) and with the degree of microalbuminuria in group B patients (r = 1, P < 0.01). Urinary GH was also greater than 10 microU, the median value observed in the controls, in 5 of 6 (83%) patients in group A. Glomerular filtration rate (GFR) and effective renal plasma flow (ERPF) measured by constant infusion of 51Cr-ethylene diamine tetra-acetic acid (EDTA) and I125-para-amino hippuric acid (PAH), respectively, showed relative hyperfiltration in the normoalbumiruric group compared with controls (P < 0.05) and group B (P < 0.05). Absolute proximal reabsorption of sodium and of water (APRNa and APRH2O) was significantly higher in group A patients (P < 0.05). Although GFR was significantly higher in group A patients, no differences were found in fractional proximal reabsorption of sodium and water (FPRNa+H2O) or end proximal delivery between the patient groups and controls. Therefore, the measurement of protein reabsorptive capacity provides a more sensitive marker of renal tubular impairment in type 1 diabetes than sodium/fluid reabsorptive capacity. In patients with microalbuminuria, both glomerular and tubular damage may coexist. Our results stress the usefulness of markers of renal tubular function in monitoring the course of diabetic nephropathy. This study also shows that assessment of GH clearance has promise as a marker of renal tubular protein reabsorptive capacity.
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PMID:Proximal tubular reabsorption of growth hormone and sodium/fluid in normo- and microalbuminuric insulin-dependent diabetes mellitus. 913 54

The albumin excretion rate (AER), insulin-like growth factor-I (IGF-I) levels, glomerular filtration rate (GFR) and glycosylated hemoglobin (HbA1c) levels were studied in 49 diabetic children and 49 controls. The duration of diabetes varied from newly diagnosed to 17.5 years. Diabetics exhibited a wide range of AER values and had significantly higher AER and IGF-I levels compared to controls. At puberty elevated circulating growth hormone (GH) concentrations were found with a parallel increase in the levels of IGF-I. High IGF-I levels were found in 10-12 year-old girls and 15-16 year-old boys in both diabetic and control groups. Positive correlations were found between IGF-I and GFR in girls of both groups (p < 0.05) and in control girls between IGF-I, GFR and microalbuminuria (p < 0.05). The diabetic boys also showed microalbuminuria with respect to controls at high HbA1c levels and when their testis volume exceeded 8 ml (p < 0.05). We concluded that the prominent change in GH release at puberty, reflected by IGF-I, is in pulse amplitude, and that this is increased in diabetes but it is not a very important factor when determining the abnormal levels of urinary albumin excretion.
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PMID:Albumin excretion rate, serum insulin-like growth factor-I and glomerular filtration rate in type I diabetes mellitus at puberty. 936 55

Recent clinical studies have demonstrated an increase of urinary albumin excretion (UAE) at rest in acromegalic patients and, on the other hand, a reduced UAE in patients with growth hormone (GH) deficiency. Physical exercise is known to induce abnormal UAE in patients with diabetes, probably unmasking early glomerular alterations. The effect of exercise on UAE in acromegaly is not known. Moreover, the effect of acute but sustained GH inhibition in acromegaly on UAE at rest and after exercise has never been studied. The aim of our study was to evaluate the acute short-term effects of slow-release lanreotide (SR-L), a long-acting somatostatin analog, on UAE and alpha1-microglobulinuria (A-1-M), a marker of renal tubular damage, at rest and after exercise in 7 normotensive patients with active acromegaly and normal renal function (4 males and 3 females; mean age, 53 +/- 3.1 years; body mass index [BMI], 27.3 +/- 1.1 kg/m2) at baseline and 7 and 14 days after SR-L injection (30 mg). Two of the acromegalic patients were microalbuminuric at rest, and in other 3 cases, UAE was in the borderline range (10 to 20 microg/min). At baseline in the acromegalic subjects, we found a significant increase in UAE at rest with respect to 7 normal subjects considered as a control group. GH and insulin-like growth factor-1 (IGF-1) were also reduced compared with baseline 7 and 14 days after SR-L injection (GH, 13.4 +/- 7.3 and 13.61 +/- 7 v 18.5 +/- 9.3 microg/L, P < .05; IGF-1, 230 +/- 53 and 255 +/- 54 v 275 +/- 64 microg/L). Concomitantly, we observed a significant decrease of UAE at rest and after exercise and 7 and 14 days after SR-L injection as compared with baseline values (27.3 +/- 20.5 and 18.2 +/- 13.7 v 35.3 +/- 12.8 microg/min, P < .05; exercise, 48.5 +/- 24.1 and 18.6 +/- 6.8 v68.3 +/- 39.7 microg/min, P < .05). A-1-M always remained in the normal range (< 12 mg/L) both at rest and after exercise. We can thus conclude that in acromegaly, submaximal exercise induces abnormal increases in microalbuminuria. We hypothesize that this phenomenon may be due to the functional glomeruler involvement. SR-L can significantly reduce UAE at rest and after exercise in the short-term in acromegaly, probably via a decrease in circulating GH levels.
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PMID:Exercise-induced microalbuminuria in patients with active acromegaly: acute effects of slow-release lanreotide, a long-acting somatostatin analog. 1083 Nov 75

Circulating levels of insulin-like growth factor-I (IGF-I) and its principal binding protein IGFBP-3 are reduced, whereas those of the inhibitory binding protein, IGFBP-1, tend to be high in children and adolescents with type 1 diabetes mellitus (T1DM). These abnormalities are thought to arise because of relative portal hypoinsulinaemia and partial resistance at the hepatic growth hormone (GH) receptor. During adolescence, reductions in IGF-I and IGF bioactivity lead to feedback for GH hypersecretion and the elevated GH and low IGF-I levels lead to an increase of the normal insulin resistance encountered during puberty. Low IGF-I levels, but in particular elevated GH levels, have been implicated in the pathogenesis of diabetic microangiopathic complications, in particular, renal hypertrophy, glomerular hyperfiltration and the development of microalbuminuria. Early study of IGF-I replacement with recombinant human IGF-I (rhIGF-I) demonstrated, in the short term, reductions in GH hypersecretion with improved insulin sensitivity and, in the longer term, reductions in insulin requirements and improvements in HbA1c levels. However, larger doses of rhIGF-I were associated with retinopathy either due to rapid improvements in glycaemic control or direct effects of high levels of 'free' IGF-I. More recently, pilot studies using the combination of rhIGF-I/rhIGFBP-3 have confirmed the physiological efficacy of IGF-I replacement in T1DM. The combined treatment is better tolerated and may result in reduced tissue exposure to high levels of 'free' IGF-I. Longer term clinical studies with this IGF-I/IGFBP-3 combination are needed.
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PMID:Childhood and adolescent diabetes. 1587 93

Diabetes is currently one of the leading causes of end-stage renal failure requiring renal replacement therapy in the Western World. About 15% to 20% of type 1 diabetic patients and 30% to 40% of type 2 diabetic patients will eventually develop end-stage renal failure. To prevent the development or progression of diabetic kidney disease, good glycaemic control remains the cornerstone in the management of diabetic patients. Beyond glycaemic control, other metabolic factors have been shown to be involved in the development of diabetic kidney disease, i.e. advanced glycation endproducts (AGEs) and the aldose reductase pathway. Furthermore, an adequate control of high blood pressure and treatment of microalbuminuria are major therapeutic targes. To achieve adequate blood pressure control, a combination therapy with different classes of antihypertensive agents is often necessary, especially including angiotensin-converting enzyme inhibitors and angiotensin receptor blockers. Other vasoactive factors involved in diabetic nephropathy such as endothelin and nitric oxide will be covered briefly. Besides hyperglycaemia and high blood pressure, other risk factors have been identified in the development or progression of diabetic kidney disease: smoking, hyperlipidaemia, obesity and high protein intake. Their impact on renal function will be highlighted. Finally, recent research has also identified intracellular pathways such as the diacylglycerol-protein kinase C pathway and several growth factors, such as growth hormone, insulin-like growth factor, transforming growth factor-beta, vascular endothelial growth factor, and platelet derived growth factor as players in diabetic kidney disease.
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PMID:Novel insights in the treatment of diabetic nephropathy. 1822 60


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