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

As angiotensin-converting enzyme inhibition is accompanied by a marked decrease in glomerular protein loss, the hypothesis was tested that an increase of the glomerular transcapillary hydraulic pressure difference by exogenous angiotensin II would increase microalbuminuria in patients with insulin (IDDM) and non-insulin-dependent diabetes mellitus (NIDDM). Acute effects of increasing doses of angiotensin II (1, 3 and 6 ng/kg/min) were studied on mean arterial pressure (MAP), glomerular filtration rate (GFR), effective renal plasma flow (ERPF), filtration fraction (FF), total renal vascular resistance (TRVR), and urinary albumin excretion rate (UAER) in 11 IDDM and 11 NIDDM microalbuminuric patients. Angiotensin II infusion changed MAP from 100 +/- 3 mmHg at baseline to 105 +/- 3, 111 +/- 3, and 116 +/- 3 mmHg (P < 0.001), ERPF from 542 +/- 29 to 478 +/- 24, 429 +/- 23, and 382 +/- 19 ml/min (P < 0.001), FF from 20.2 +/- 0.06 to 23.1 +/- 0.7, 27.1 +/- 1.1, and 29.8 +/- 1.2% (P < 0.001), and TRVR from 9454 +/- 809 to 11,158 +/- 930, 13,310 +/- 1206, and 15,538 +/- 1362 dyne s cm-5 (P < 0.001). GFR and UAER, however, did not change significantly. Therefore, during angiotensin II infusion ERPF decreased, while FF and TRVR increased. As UAER and GFR remained unchanged, the presumed rise in intraglomerular capillary pressure by exogenous angiotensin II did not increase UAER. We suggest that during manipulation of the renin-angiotensin system, as in other renal diseases with proteinuria, factors other than glomerular transcapillary hydraulic pressure determine the degree of urinary albumin loss in microalbuminuric IDDM and NIDDM patients.
Nephrol Dial Transplant 1997 Feb
PMID:Urinary albumin excretion rate during angiotensin II infusion in microalbuminuric patients with insulin and non-insulin-dependent diabetes mellitus. 913 45

This brief review will focus on the major factors leading to incipient diabetic nephropathy (i.e. microalbuminuria) progressing to overt nephropathy (i.e. macroalbuminuria) and particularly on the role of glycaemic control and hypertension. Both experimental and cohort studies support the role of hyperglycaemia in the development of diabetic nephropathy. Some recent long-term interventional studies in microalbuminuric patients show conflicting results regarding the role played by good metabolic control in reducing the incidence of overt nephropathy. However, strict metabolic control, which is fundamental in normoalbuminuric patients, is of little use even in microalbuminuric patients. In general, levels of glycosylated haemoglobin less than two standard deviations above the upper normal range, commonly <7.5-8%, seem to protect patients from developing nephropathy. The results of many cross-sectional studies have shown that the progression of renal damage regularly is accompanied by arterial hypertension both in insulin-dependent diabetes mellitus (IDDM) and non-insulin-dependent diabetes mellitus (NIDDM). Many long-term interventional studies have been performed in order to understand the effect of antihypertensive treatment on the incidence of proteinuria in both normotensive and hypertensive patients with IDDM or NIDDM. These data show a marked effect of antihypertensive therapy in preventing the onset of overt nephropathy, and suggest the superiority of angiotensin-converting enzyme (ACE) inhibitors. We believe that optimal blood pressure values are approximately 120/70-75 mmHg in younger patients and 125-130/80-85 mmHg in older patients. In conclusion, antihypertensive treatment, ACE inhibitors per se and possibly strict metabolic control reduce the development of nephropathy, thus playing a striking role in the secondary prevention of renal failure.
Nephrol Dial Transplant 1998
PMID:Diabetic nephropathy: from micro- to macroalbuminuria. 987 Apr 19

The onset of renal damage in diabetes mellitus may be influenced by several factors which largely result from genetic predisposition, hereditary factors and the early appearance of microalbuminuria and/or systemic hypertension. Most of these factors are also implicated in the progression of nephropathy from microalbuminuria to overt proteinuria and to end-stage renal failure (ESRF). Over the last few years, the role of hyperglycaemia has emerged as critical in mediating the progressive renal damage in diabetes. However, hyperglycaemia leads to increased formation of glycated proteins which may act as promoters of progression by localizing in renal tissue. In addition, hyperglycaemia may have a synergistic effect with some other risk factors, such as growth factors and the renin angiotensin system, in accelerating renal deterioration.
Nephrol Dial Transplant 1998
PMID:Progression of renal failure in diabetic nephropathy. 987 Apr 20

The progressively growing number of patients with end-stage renal failure (ESRF) associated with diabetes mellitus and requiring renal replacement therapy (RRT) stimulated both nephrologists and diabetologists to investigate the mechanisms linking hyperglycaemia to diabetic renal failure and to set up measures to prevent the onset and slow the progression of diabetic nephropathy. Over the last few decades, a large number of studies have investigated both the incidence of diabetic nephropathy and the relationship between metabolic control and the development of diabetic nephropathy. Chronologically, the first type of diabetes and diabetic nephropathy to be studied was type I, and it is only in recent years that metabolic control has been proven to be a contributor to the development of nephropathy in such patients. Recently, the DCCT demonstrated that metabolic control in the prealbuminuric phase was effective in reducing the incidence of microalbuminuria, even if it was unable to reduce the incidence of overt proteinuria in patients with type I diabetes and established proteinuria. On the other hand, in type II diabetes, the number of studies demonstrating a favourable effect of metabolic control on onset and progression of diabetic nephropathy is only slightly greater than those that failed to show a favourable effect. This feature may suggest that in type II patients, genetic and ethnic differences, nutritional aspects, lifestyle and other confounding factors may play a relevant role in the course of the disease. However, the trials performed and the retrospective analyses generally agree that glycated haemoglobin two standard deviations greater than the mean is related to a worsening in progression of diabetic nephropathy and to an enhanced risk of other complications. In general, a glycated haemoglobin < or =8% seems advisable. Moreover, in both type I and type II, greater emphasis should be placed on the major risk factors such as hypertension, smoking habits and hyperlipidaemia.
Nephrol Dial Transplant 1998
PMID:The effect of metabolic control on development and progression of diabetic nephropathy. 987 Apr 24

Throughout the industrialized (well-fed) world, diabetes mellitus is the most prevalent cause of end-stage renal disease (ESRD). Diabetic nephropathy is as likely to develop in long-duration non-insulin-dependent diabetes (type 2) as in insulin-dependent diabetes mellitus (type 1). Nephropathy in diabetes follows a well outlined course, starting with microalbuminuria through proteinuria, azotaemia and culminating in ESRD. Renal functional decline in diabetic nephropathy is slowed by establishment of euglycaemia and normalization of hypertensive blood pressure. Diabetic ESRD patients, compared with other causes of ESRD, sustain greater mortality and morbidity due to concomitant systemic disorders, especially coronary artery and cerebrovascular disease. A central role for glucose toxicity, especially the adverse impact of accumulated advanced glycosylated end-products (AGEs), appears likely from experimental data generated both in induced diabetic rodents and diabetic individuals. Treatment with aminoguanidine raises the possibility of blocking end-organ damage in diabetes without the necessity for correcting hyperglycaemia.
Nephrol Dial Transplant 1999
PMID:Advanced glycation end-products in diabetic nephropathy. 1038 74

The prevalence of type 2 diabetes is rising in all Westernized societies. Presumably as a consequence of diminishing cardiovascular mortality, end-stage renal failure (ESRF) in patients with diabetes (mostly type 2) as a co-morbid condition has risen dramatically in the past decade. This constellation has become the single most common cause of ESRF in most countries. Such an epidemiological trend is particularly regrettable, since in uraemic diabetic patients, medical rehabilitation and survival are remarkably poor. Recent studies indicate that an interplay between genetic predisposition and factors, some of them susceptible to intervention, such as hyperglycaemia, blood pressure, smoking, age, gender and ethnicity, predispose to the development and progression of nephropathy. It has also become clear that trace albuminuria ('microalbuminuria') provides unique opportunities to recognize incipient renal involvement early on, although it is less specific in type 2 as compared with type 1 diabetes. Factors that promote progression include hypertension, proteinuria, smoking, glycaemic control and, less certainly, dietary protein intake and hyperlipidaemia. Cumulating evidence indicates that early intervention delays progression of nephropathy. The most important strategies to combat the medical catastrophe of increasing numbers of diabetic patients with ESRF include: (i) prevention of diabetes (mainly type 2); (ii) glycaemic control to prevent onset of renal involvement; and (iii) meticulous antihypertensive treatment to avoid progression of nephropathy.
Nephrol Dial Transplant 2001
PMID:Renal disease in type 2 diabetes. 1150 79

A growing body of evidence indicates that the renal proximal tubular epithelial cell (PTEC) plays an important role in the pathogenesis of diabetic nephropathy (DN). Microalbuminuria that intensifies over time to overt proteinuria, a hallmark of DN, is already known to activate the PTEC to induce tubulointerstitial inflammation. In addition to proteins, a number of diabetic substrates including high glucose per se, advanced glycation end-products and their carbonyl intermediates, angiotensin II, and ultrafiltered growth factors activate a number of signaling pathways including nuclear factor kappa B, protein kinase C, extracellular signal-regulated kinase 1/2, p38, signal transducer and activator of transcription-1 and the generation of reactive oxygen species, to culminate in tubular cell hypertrophy and the accumulation in the interstitium of a repertoire of chemokines, cytokines, growth factors and adhesion molecules capable of orchestrating further inflammation and fibrosis. More recently, the kallikrein-kinin system (KKS) and toll-like receptors (TLRs) in PTECs have been implicated in this process. While in vitro data suggest that the KKS contributes to the progression of DN, there are conflicting in vivo results on its precise role, which may in part be strain-dependent. On the other hand, there are both in vitro and in vivo data to suggest a role for both TLR2 and TLR4 in DN. In this review, we offer a critical appraisal of the events linking the participation of the PTEC to the pathogenesis of DN, which we believe may be collectively termed diabetic tubulopathy.
Nephrol Dial Transplant 2012 Aug
PMID:The pathogenic role of the renal proximal tubular cell in diabetic nephropathy. 2273 10

Over 140 million people live at high altitude, defined as living at an altitude of 2400 m or more above sea level. Subjects living under these conditions are continuously living under hypoxic conditions and, depending on the population, various adaptations have developed. Interestingly, subjects living chronically at high altitude appear to have a decreased frequency of obesity, diabetes and coronary artery disease. However, these benefits on health are balanced by the frequent development of systemic and pulmonary hypertension. Recently, it has been recognized that subjects living at high altitude are at risk for developing high-altitude renal syndrome (HARS), which is a syndrome consisting of polycythemia, hyperuricemia, systemic hypertension and microalbuminuria, but with preserved glomerular filtration rate. More studies should be performed to characterize the mechanisms and etiology of HARS; as such studies may be of benefit not only to the high-altitude population, but also to better understanding of the renal consequences of acute and chronic hypoxia.
Nephrol Dial Transplant 2012 Dec
PMID:Cardiovascular and renal effects of chronic exposure to high altitude. 2325 4

Diabetes mellitus (DM) is increasingly recognized as a heterogeneous condition. The individualization of care and treatment necessitates an understanding of the individual patient's pathophysiology of DM that underpins their DM classification and clinical presentation. Classical type-2 diabetes mellitus is due to a combination of insulin resistance and an insulin secretory defect. Type-1 diabetes is characterized by a near-absolute deficiency of insulin secretion. More recently, advances in genetics and a better appreciation of the atypical features of DM has resulted in more categories of diabetes. In the context of kidney disease, patients with DM and microalbuminuria are more insulin resistant, and insulin resistance may be a pathway that results in accelerated progression of diabetic kidney disease. This review summarizes the updated classification of DM, including more rarer categories and their associated renal manifestations that need to be considered in patients who present with atypical features. The benefits and limitations of the tests utilized to make a diagnosis of DM are discussed. We also review the putative pathways and mechanisms by which insulin resistance drives the progression of diabetic kidney disease.
Nephrol Dial Transplant 2016 Feb
PMID:Diabetes mellitus, a complex and heterogeneous disease, and the role of insulin resistance as a determinant of diabetic kidney disease. 2555 Apr 48

Diabetic nephropathy (DN) is one of the major microvascular complications of diabetes mellitus and the leading cause of end-stage kidney disease. Both diabetes and chronic kidney disease are risk factors for cardiovascular disease, and diabetic patients with renal involvement are three times more likely to eventually die of cardiovascular disease than diabetic patients without signs of renal failure. In type 2 diabetes, microalbuminuria is a marker of renal dysfunction and a crucial predictor of cardiovascular disease. Inhibitors of angiotensin II synthesis/activity, while preventing micro- or macroalbuminuria, also reduced cardiovascular events in diabetic patients. However, the effectiveness of renin angiotensin system blocking agents depends on the time when treatment is started, and imperfect renoprotection may occur if therapy begins at an advanced disease phase. This raises the need to identify novel multidrug approaches that simultaneously inhibit additional pathways other than angiotensin II for those diabetic patients who remain at high risk of both poor renal and cardiovascular outcomes. Studies in animal models of diabetes have contributed to defining relevant cellular mechanisms underlying the pathogenesis of DN that could represent possible targets for therapies. The pathogenesis of DN is multifactorial, involving a complex series of molecular processes. In this review, we report evidence obtained in experimental models of DN on some specific processes and pathways implicated in DN that may be crucial for managing this disease.
Nephrol Dial Transplant 2015 Aug
PMID:Key pathways in renal disease progression of experimental diabetes. 2620 38


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