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Query: UMLS:C0011881 (diabetic nephropathy)
 10,836 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A total of 116 patients with various degrees of chronic renal insufficiency were studied. The most frequent cause that led to its development was the chronic pyelinephritis, followed by chronic glomerulonephritis, and the other chronic renal disease, as--renal polycystosis, diabetic nephropathy, endemic nephropathy, etc. The dynamic and static pulmonary volumes volumes and capacities were investigated in order to achieve the task set and on their base--the type of ventilation disorder was determined. Certain changes of the indices were found in parallel with the intensification of the chronic renal insufficiency. They were best manifested in the patients with advanced renal insufficiency from II and IV group. Ventilation disorders were present in 50% of the patients examined. The restrictive type ventilation insufficiency was most often found (22.4%), second--the mixed type of ventilation defect (16.4%) and third--the obstructive type ventilation insufficiency (11.2%).
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PMID:[Types of ventilatory insufficiency in chronic kidney insufficiency]. 738 5

A number of changes in intrarenal hemodynamics and morphology are characteristic of diabetic nephropathy. These changes include: increases in intraglomerular pressure and volume, glomerular capillary permeability to macromolecules, and mesangial matrix expansion. Most antihypertensive drugs attenuate some of the increases in these parameters. Certain antihypertensive agents, however, have effects on all these parameters. Studies in animal models of diabetes demonstrate that the angiotensin-converting enzyme (ACE) inhibitors reduce both intraglomerular volume and pressure, mesangial matrix expansion, and albuminuria. The calcium antagonists TA-3090 (diltiazem-like) and verapamil recently have been shown to have most of these effects. Conversely, the dihydropyridine calcium antagonists (nifedipine, felodipine, nitrendipine) do not attenuate increases in most of these parameters. In several clinical studies, nifedipine either did not affect or increased urinary albumin excretion in diabetic patients with renal insufficiency. Moreover, in animal models of diabetes, most dihydropyridine compounds do not prevent progression of glomerulosclerosis in spite of blood pressure control. Although the majority of clinical studies support the concept that reduction of arterial pressure preserves renal function, recent long-term clinical studies show that ACE inhibitors and heart-rate-lowering calcium antagonists (diltiazem, verapamil) attenuate progression of diabetes to a greater extent than most other agents do.
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PMID:Antihypertensive therapy and progression of diabetic renal disease. 751 95

Urokinase (u-PA) dissolves and removes fibrin deposits in the renal secretory pathways in various renal diseases. During pregnancy nephropathy creates a problem in preeclampsia and diabetes, but the underlying mechanism of glomerular damage is different. Preeclamptic nephropathy is characterized as 'glomerular endotheliosis' with hypertrophy of the intracapillary cells, and diabetic nephropathy as 'glomerulosclerosis' with hyaline deposits. The role of fibrin deposition for the etiology of renal damage in preeclampsia is controversial. Changes of the urinary secretion of u-PA may reflect the type of glomerular damage. Our hypotheses were that renal insufficiency is associated with a low u-PA activity in both conditions, and that severe disease is parallel to declining concentrations of u-PA. We compared the glomerular filtration rate, S-Creatinine and S-Urate with urinary u-PA excretion in 24 hypertensive and 20 diabetic pregnant women. In diabetic patients, a low u-PA concentrations was associated with an impaired renal function. In hypertensive pregnancy, the u-PA excretion did not reflect the severity of the hypertensive disease or renal function. No association was found between u-PA excretion and renal function post partum in any group. We conclude that renal urokinase activity plays a role for renal function in diabetic but not in hypertensive pregnancy.
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PMID:Renal function and urinary urokinase in hypertensive and diabetic pregnancies. 782 57

Proteinuria and progressive renal insufficiency are the primary manifestations of diabetic nephropathy. Accumulating evidence suggests that these clinical features can be linked, at least in part, to pathologic changes in the glomerular extracellular matrix. Most evidence suggests that glomerular basement membrane thickening and mesangial matrix expansion consist of at least three elements. These are (1) an accumulation of normal extracellular components; (2) an increase in the novel peptide chains of the normal components of Type IV collagen; and (3) an increase in matrix elements not normally expressed in the glomerulus. The pathogenetic features underlying these changes include increased synthesis and decreased degradation of matrix. Abnormal physico-chemical interactions among these matrix elements likely contribute to alterations in three-dimensional structure, leading to proteinuria and loss of glomerular basement membrane filtering surface area. Many of these changes may be explained in whole or in part by direct or secondary effects of hyperglycemia, as well as by hemodynamic changes.
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PMID:Structure-function relationships associated with extracellular matrix alterations in diabetic glomerulopathy. 787 25

We investigated the role of measurement of serum and urinary type IV collagen (IV-C) levels in monitoring diabetic microangiopathy. Furthermore, we compared these levels in diabetic nephropathy and non-diabetic renal disease (NDRD). A one-step sandwich enzyme immunoassay was used to measure IV-C levels in 82 diabetic patients, 33 NDRD patients and 20 healthy non-diabetic control subjects. The diabetic patients were classified into four groups according to urinary albumin/creatinine index (ACI) (mg/g) and serum creatinine (s-Cr) (mg/dl): normoalbuminuria (ACI < 30), microalbuminuria (ACI 30-300), albuminuria (ACI > 300, s-Cr < 1.99 mg/dl) and renal insufficiency (s-Cr > 1.99 mg/dl). Serum and urinary IV-C levels were significantly elevated even in diabetic patients without clinical evidence of microangiopathy compared with control subjects (p < 0.05 and p < 0.01, respectively). Both levels were significantly higher in normoalbuminuric patients than in the control subjects, and in patients with microalbuminuria, albuminuria or renal insufficiency than in normoalbuminuric patients, with significant differences between these groups (serum and urinary IV-C, both p < 0.0001 by ANOVA). Urinary IV-C and albumin levels were significantly correlated, even in normo- and microalbuminuric patients (r = 0.55, p < 0.0001). Serum IV-C in normoalbuminuric patients rose significantly as the degree of retinopathy progressed from background to proliferative stages (p < 0.05). Neither serum nor urinary IV-C levels were influenced by glycemic control. Albuminuric diabetic patients (with and without renal insufficiency) had significantly higher levels of serum IV-C compared with those in proteinuric NDRD patients (p < 0.005), though there was no significant difference in the urinary IV-C level. However, the urinary IV-C/albumin ratio was significantly higher in albuminuric diabetic patients than in proteinuric NDRD patients, even after adjusting for s-Cr and creatinine clearance (p < 0.0001). In conclusion, we suggest that measured serum and urinary IV-C concentrations may serve as new markers for monitoring the development and progression of diabetic microangiopathy, particularly nephropathy. Furthermore, the measurement of serum IV-C concentrations and urinary IV-C/albumin ratios in diabetic patients may allow diabetic nephropathy and non-diabetic renal disease to be differentiated.
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PMID:Serum and urinary type IV collagen concentrations in the assessment of diabetic microangiopathy. 788 78

Since the metabolic changes in normal pregnancy are diabetogenic, pregnancy imposes a severe stress on the metabolic milieu of diabetic patients. Moreover, many patients with long-standing diabetes have vascular complications, including retinopathy, renal insufficiency, nephrotic syndrome and hypertension, all representing separate risk factors for optimal fetal development. Recent experience has suggested that maternal hyperglycaemia, and associated fetal hyperinsulinaemia, may represent an important factor in the development of fetal complications. During the past two to three decades the incidence of perinatal deaths in all categories of diabetics has been reduced to a level that approaches the rate in healthy gravidas when severe congenital anomalies are excluded. Fetal and neonatal morbidity have also been reduced, although rates of congenital anomalies, hydramnios and respiratory distress syndrome remain high. Although the morbidity associated with oedema formation and hypertension is elevated, with meticulous management of patients with diabetic nephropathy, especially in the absence of severe renal insufficiency and/or severe hypertension, pregnancy performance and outcome can be similar to that of other insulin-dependent diabetic patients.
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PMID:Managing diabetic patients with nephropathy and other vascular complications. 792 15

Increased plasma activity of plasminogen activator inhibitor 1 (PAI-1) is considered as a risk factor for thrombosis associated with atherosclerosis by reduction of fibrinolysis. Since nephropathic patients with non-insulin-dependent diabetes mellitus (NIDDM) are a cardiovascular high-risk group, which has yielded only controversial results as to the regulation of PAI-1, we compared 19 overt nephropathic NIDDM patients (mean age 63 years, serum creatinine 1.9 mg/dl, proteinuria 4.2 g/day) to 17 nondiabetic nephropathic patients with various causes of renal insufficiency (mean age 63 years, serum creatinine 2.8 mg/dl, proteinuria 3.9 g/day). We found normal PAI-1 levels for patients with diabetic nephropathy and significantly elevated PAI-1 levels within the upper normal range for nondiabetic nephropathic patients. Common risk factors in both groups were very high levels of fibrinogen, lipoprotein(a), serum cholesterol, and LDL cholesterol.
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PMID:Plasminogen activator inhibitor 1 activity and lipoprotein(a) in nephropathic patients with non-insulin-dependent diabetes mellitus versus patients with nondiabetic nephropathy. 795 56

The angiotensin converting enzyme inhibitors constitute a major treatment modality for cardiovascular diseases, including congestive heart failure and hypertension. In addition to their beneficial hemodynamic effects, they offer other advantages, such as a relative lack of adverse effects on other cardiovascular risk factors. When used judiciously, the angiotensin converting enzyme inhibitors may also contribute to improved renal function. These agents induce vasodilation of both efferent and afferent renal vessels, which may facilitate improved renal blood flow and glomerular filtration rate in individuals whose renal insufficiency results from hyperadrenergic activity. Improvements in renal function may also be observed when angiotensin converting enzyme inhibitors are employed in other clinical conditions, such as diabetic nephropathy or proteinuric renal disease. Although the renal protective effects of the angiotensin converting enzyme inhibitors are well recognized, their use in certain circumstances may actually contribute to renal dysfunction. The factors which may predispose an individual to angiotensin converting enzyme inhibitor-induced renal dysfunction must be recognized by the clinician and appropriate interventions taken to prevent this potentially deleterious effect. This article reviews those factors which increase risk for angiotensin converting enzyme inhibitor-induced renal dysfunction and provides recommendations for prevention.
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PMID:Angiotensin converting enzyme inhibitor-induced renal dysfunction: recommendations for prevention. 800 61

Infection has been recognized as an important cause of morbidity and mortality in children with nephrotic syndrome. However, the incidence and severity of infection and the mechanisms responsible for the increased susceptibility to infection are still unclear in adults. We studied 86 consecutive adult patients with nephrotic syndrome but no diabetic nephropathy. Risk factors for infection were evaluated by logistic regression analysis. Infections were found in 16 patients (19%), of whom six died of infection and two developed end-stage renal failure associated with infection. The relative risk for bacterial infection among patients with serum immunoglobulin G (IgG) levels below 600 mg/dL was 6.74 compared with that for patients with serum IgG levels over 600 mg/dL (95% confidence interval, 1.22 to 36.32; P = 0.029). In patients with serum creatinine levels over 2.0 mg/dL, the relative risk of bacterial infection was 5.31 compared with patients with serum creatinine levels below 2.0 mg/dL (95% confidence interval, 1.08 to 26.09; P = 0.040). Intravenous immunoglobulin (10 to 15 g) was administered prospectively every 4 weeks to 18 patients with serum IgG levels below 600 mg/dL until serum IgG levels increased to over 600 mg/dL. Administration of immunoglobulin resulted in a decreased rate of bacterial infections to a level equal to that in patients with endogenous levels over 600 mg/dL. These data indicate that hypogammaglobulinemia and renal insufficiency are independent risk factors for bacterial infection in adult patients with nephrotic syndrome. The effects of intravenous immunoglobulin suggest that maintenance of serum IgG levels over 600 mg/dL may reduce the risk of infection.
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PMID:Risk factors for infection and immunoglobulin replacement therapy in adult nephrotic syndrome. 807 68

To assess whether moderate dietary protein restriction can delay the progression of overt diabetic nephropathy, 22 subjects with insulin-dependent diabetes mellitus were randomly assigned to an unrestricted protein diet (> 1.6 g.kg body wt-1.d-1) or a moderately protein-restricted diet (0.8 g.kg body wt-1.d-1) and followed prospectively for six mo. Direct isotope methods were used to assess renal function. Protein intake was assessed by measurement of urinary urea nitrogen. The two groups were well-matched for age, sex, duration of diabetes, glycemic control, blood pressure, and degree of renal insufficiency. Patients consuming the unrestricted protein diet (n = 11) showed a progressive decline in glomerular filtration rate of 1.3 mL.min-1.mo-1 with no change in proteinuria. Patients consuming the moderately protein-restricted diet showed a marked decrease in the degree of proteinuria (2.15-1.13 g/d, P = 0.036) and a stabilization of glomerular filtration rate. This occurred independently of changes in blood pressure or glycemic control. Moderate dietary protein restriction can ameliorate progression of overt diabetic nephropathy.
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PMID:Effect of moderate dietary protein restriction on the progression of overt diabetic nephropathy: a 6-mo prospective study. 809 94


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