Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011881 (diabetic nephropathy)
 10,836 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In this study we investigated circulating atrial natriuretic factor (ANF) concentrations in patients with different stages of diabetic nephropathy. Type 1 diabetic patients with incipient or overt nephropathy had elevated plasma ANF concentrations when compared with nonnephropathic diabetics and normals. Patients having a hyperfiltration only, which might be a risk factor for the development of diabetic nephropathy, had also elevated ANF concentrations. No correlation could be found between ANF concentrations and blood pressure, diabetes duration, age, or parameters of metabolic control. These findings may indicate a role of ANF in the development of diabetic nephropathy. Long-term follow-up studies should be performed to assess the prognostic and diagnostic importance of plasma ANF determinations in diabetic patients.
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PMID:[Atrial natriuretic factor in patients with type 1 diabetes mellitus in various stages of diabetic nephropathy]. 297 Jan 65

Plasma concentrations of atrial natriuretic factor (ANF) were measured by radioreceptor assay in 148 insulin-dependent Type I diabetic patients with different stages of diabetic nephropathy. In patients with overt or incipient diabetic nephropathy as well as in patients with glomerular hyperfiltration only, ANF concentrations were elevated when compared with non-nephropathic diabetic and normal subjects. No correlations between ANF and blood pressure, age, diabetes duration, or parameters of metabolic control were found. These findings may indicate a pathophysiologic role of ANF in the development and progression of diabetic nephropathy.
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PMID:Atrial natriuretic factor in various stages of diabetic nephropathy. 297 64

This is a study about objective parameters of Syndrome Differentiation of diabetic nephropathy (DN) using radio immunoassay (RIA) technique. The result showed that beta 2-microglobulin (beta 2-mG), alpha 1-microglobulin (alpha 1-mG) in blood rose significantly in both groups. The group of Spleen-Kidney Deficiency and Qi-Blood Deficiency as well as the group of Yang Deficiency caused edema and upward gush of turbid Yin, there was significant difference between two groups, also there was significant difference between the two groups in measuring on atrial natriuretic factor (ANP), pancreatic glucagon (PG) in blood and beta 2-mG. Immunoglobulin G (IgG), albumin (Alb), secretory immunoglobulin A(SIg A) in urine. So above-mentioned parameters offered us some objective data on Syndrome Differentiation of DN. It is vital in guiding the Syndrome Differentiation and treatment of DN.
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PMID:[Study on objective parameters of syndrome differentiation of diabetic nephropathy]. 778 97

The early stages of diabetes mellitus are in some patients associated with renal haemodynamic changes resulting in increased glomerular filtration. This "diabetic hyperfiltration" is considered to be one of pathophysiological mechanisms and risk factors for the development of diabetic nephropathy. The aim of this paper is to review some contemporary views on pathophysiological mechanisms leading to this disorder with emphasis on the role impaired activity of humoral factors influencing renal haemodynamics. In addition to poor metabolic control due to insulinopenia there is a convincing experimental evidence suggesting the role of atrial natriuretic factor and endothelium-derived nitric oxide in mediating renal haemodynamic changes in diabetes. Enhanced renal activity of angiotensin I converting enzyme resulting in local overproduction of angiotensin II and accelerated degradation of kinins may be another factor contributing to the genesis of diabetic hyperfiltration. Hyperglycaemia induces changes in cellular signalling of these vasoactive systems. Furthermore, diabetes is a state of decreased capability of renal vascular bed to autoregulate blood flow likely due to altered activity of tubuloglomerular feedback and ion channels.
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PMID:[Pathophysiologic mechanisms of early changes in renal hemodynamics in diabetes mellitus]. 868 53

1. In diabetes mellitus a selective increase in the excretion of albumin generally precedes the occurrence of demonstrable loss of glomerular size-selectivity. However, even in this (microalbuminuric) phase of diabetic nephropathy a defect in glomerular barrier function can be demonstrated during infusion of atrial natriuretic peptide. 2. The aim of this study was to investigate whether angiotensin-converting enzyme inhibition could prevent the proteinuric response to atrial natriuretic peptide in these patients. We performed infusions of atrial natriuretic peptide (0.01 microgram min-1 kg-1) in 10 patients with insulin-dependent diabetes mellitus and microalbuminuria (urinary albumin excretion 90 +/- 44 mg/day), both before and after 1 month of treatment with enalapril (20 mg once daily). 3. Despite a 40% reduction in proteinuria, angiotensin-converting enzyme inhibition did not prevent the atrial natriuretic peptide-induced increase in protein excretion. Both before and during angiotensin-converting enzyme inhibition, atrial natriuretic peptide infusion resulted in a significant increase in the fractional excretion of large dextran molecules, which is compatible with an increase in flow through large unrestrictive 'shunt' pores. Atrial natriuretic peptide infusion also induced an increase in the transcapillary escape rate of albumin and angiotensin-converting enzyme inhibition also failed to prevent this effect of atrial natriuretic peptide on peripheral capillary permeability. 4. We conclude that angiotensin-converting enzyme inhibition during 1 month does not correct the capillary barrier function defect in patients with diabetes mellitus and microalbuminuria that is unmasked by atrial natriuretic peptide infusion.
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PMID:Angiotensin-converting enzyme inhibition does not correct early defects in renal and vascular permeability in diabetes mellitus. 953 25

Approximately 30% of diabetic patients develop nephropathy, the appearance of which is partially under genetic control. Atrial natriuretic peptide (ANP) has associated physiologic effects on the kidney. This study was conducted to examine the relationship between a newly identified and known polymorphism at the pronatriodilatin (PND) gene locus and renal involvement in type 1 diabetic subjects. Of 454 type 1 diabetic patients (219 men, 235 women), 323 showed no sign of nephropathy, 79 had incipient renal involvement, and 52 established nephropathy; 58 healthy control subjects were examined for comparison. Allele frequencies (C708 versus T708) were: 0.95 and 0.05 in normoalbuminuric patients, respectively; 0.88 and 0.12 in microalbuminuric patients; 0.96 and 0.04 both in those with overt nephropathy and in healthy control subjects (P = 0.011). Patients with incipient nephropathy were in disequilibrium compared with the total diabetic cohort (P = 0.02). In the same populations, an additional genotype for ScaI polymorphism of the PND gene was tested. The A1 and A2 allele frequencies were: 0.21 and 0.79 in normoalbuminuric patients; 0. 13 and 0.87 in microalbuminuric patients; 0.06 and 0.94 in type 1 diabetic subjects with overt nephropathy; and 0.20 and 0.80 in healthy control subjects, respectively (P < 0.0001). A subset of 55 normotensive patients with type 1 diabetes, well matched for clinical features, plasma ANP levels, and microvascular permeability to macromolecules, was investigated on the basis of the C708/T and A2/A1 polymorphisms. Both transcapillary escape rate of albumin (TERalb) and plasma ANP levels were significantly lower in patients with the T708 than with C708 allele, as well as in the A1 than in A2 allele (TERalb: T708 versus C708: 5.5+/-1.7 versus 7.8+/-2.0%/h, P = 0.0001; plasma ANP levels: 8.3+/-3.9 versus 15.3+/-7.7 pg/ml, P = 0.0003; A1 versus A2: 6.05+/-2.2 versus 7.3+/-2.1%/h, P = 0.044; 8.53+/-4.6 versus 14.5+/-7.4 pg/ml, P = 0.0024, respectively). Thus, in a large ethnically homogeneous cohort of diabetic subjects, our data show: (1) a significant association of C708/T polymorphism with microalbuminuria in long-term diabetes and with both lower plasma ANP levels and widespread albumin leakage; and (2) a strong association between ScaI polymorphism and both diabetic nephropathy and plasma ANP concentrations. These results suggest a possible role of PND gene in conferring protection from nephropathy and microvascular damage in type 1 diabetes.
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PMID:Pronatriodilatin gene polymorphisms, microvascular permeability, and diabetic nephropathy in type 1 diabetes mellitus. 1040 9

The aim of this clinical trial was to study the participation of plasma atrial natriuretic factor (ANF) in the risk of developing diabetic nephropathy by increasing the intraglomerular pressure. The effect of glibornuride on the plasma ANF levels and natriuresis was estimated in 10 newly diagnosed NIDDM patients and 10 control subjects. At base line, plasma ANF levels (15.05+/-2.32 pg/ml and 11.13+/-0.85 pg/ml) and the urinary sodium and potassium excretion rates were similar in patients and control subjects, respectively. Similarly, intravenous saline infusion (2 mmol/kg/60 min) resulted in remarkable elevation of plasma ANF levels in patients and in controls (28.89+/-4.72 pg/ml and 20.18+/-2.48 pg/ml, respectively) and in increased urinary sodium and potassium excretion rates in both groups. In contrast, after a single dose of 50 mg glibornuride p.o. the saline infusion did not increase ANF levels (15.13+/-1.00 pg/ml), while natriuresis but not kaliuresis persisted. All tests were performed during euglycemic clamp. It was suggested that glibornuride, with its natriuretic effect through the ATP sensitive potassium channels on the apical membrane of the thick ascending limb of loop of Henle and cortical collecting duct cells might inhibit the elevation of plasma ANF levels in response to extracellular fluid volume expansion. Similarly, with its natriuretic effect, it protects the diabetic patients against possible sodium retention. This result is considered noteworthy, since the inhibition of plasma ANF elevation in early diabetes by glibornuride may prevent glomerular hypertension and subsequent development of nephropathy.
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PMID:The Effect of Glibornuride on Plasma Atrial Natriuretic Factor Levels in Patients with Newly Diagnosed NIDDM. 1040 67

Diabetes mellitus (DM) shows a markedly increased incidence of cardiovascular pathology that leads to hypertension, endothelial macro- and microangiopathy, diabetic nephropathy, and myocardial infarction. Atrial natriuretic peptide (ANP), is a 28 amino acid peptide hormone synthesized mainly by the heart atria and ventricles. It has potent diuretic and natriuretic properties. In this article the effect of long-term DM on blood plasma, kidney, and heart atrial and ventricular ANP concentrations were evaluated in streptozotocin (STZ)-induced 8-month diabetic and control rats by using radioimmunoassay (RIA). Moreover, ANP receptors in STZ-induced, 8-month diabetic rat kidneys were studied by receptor autoradiography. In addition, the expression of ANP concentrations in the kidney of diabetic and control rats was evaluated by means of immunohistochemistry. Body weight loss and increased blood glucose levels were used as indices of DM in the STZ-induced diabetic rats. Our results showed significantly higher ANP concentrations in diabetic plasma (P < 0.05), kidney (P < 0.01), heart atria (P < 0.05), and ventricles (P < 0.01) compared to controls. We also demonstrated a significant decrease in ANP receptors in the outer cortex (P < 0.05), juxtaglomerular medulla (P < 0.05), and papilla (P < 0.05) of 8-month diabetic rat kidneys compared to controls. The observed increase in ANP levels in plasma and kidney could play a role in the development of diabetic nephropathy: probably by reducing the levels of ANP receptors in diabetic kidney. Furthermore, the role of ANP in the STZ-induced diabetic heart merits additional study.
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PMID:Alterations in atrial natriuretic peptide and its receptor levels in long-term, streptozotocin-induced, diabetes in rats. 1715 4

The incretin hormone, glucagon-like peptide-1 (GLP-1), stimulates insulin secretion and forms the basis of a new drug class for diabetes treatment. GLP-1 has several extra-pancreatic properties which include effects on kidney function. Although renal GLP-1 receptors have been identified, their exact localization and physiological role are incompletely understood. GLP-1 increases natriuresis through inhibition of the sodium-hydrogen ion exchanger isoform 3 in the proximal tubule. This may in part explain why GLP-1 receptor agonists have antihypertensive effects. Glomerular filtration rate is regulated by GLP-1, but the mechanisms are complex and may depend on e.g. glycaemic conditions. Atrial natriuretic peptide or the renin-angiotensin system may be involved in the signalling of GLP-1-mediated renal actions. Several studies in rodents have shown that GLP-1 therapy is renoprotective beyond metabolic improvements in models of diabetic nephropathy and acute kidney injury. Inhibition of renal inflammation and oxidative stress probably mediate this protection. Clinical studies supporting GLP-1-mediated renal protection exist, but they are few and with limitations. However, acute and chronic kidney diseases are major global health concerns and measures improving renal outcome are highly needed. Therefore, the renoprotective potential of GLP-1 therapy need to be thoroughly investigated in humans.
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PMID:Effects of GLP-1 in the kidney. 2479 75