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

Between 1988 and 1992, 565 type 2 diabetic patients were examined for nephropathy and diabetes-associated diseases during hospital treatment. Stages of nephropathy were defined as no clinical sign of nephropathy (N = 280), microalbuminuria (N = 38), overt proteinuria (N = 105), impaired renal function (N = 55), and chronic dialysis therapy (N = 87). In dialyzed patients, HbA1c averaged 6.8%, and, in the other groups, HbA1c was between 7.6% and 8.3% (normal range, 3.8%-6.1%). Cataract was not associated with the severity of nephropathy. Stroke was most common in the stage of renal insufficiency (34%). The following complications, as found in medical history or as current event, showed a significant association with the stage of nephropathy and occurred most frequently in dialysis patients (percentage is displayed for patients with nephropathy in comparison to diabetic dialysis patients): hypertension (53%-89%), left ventricular hypertrophy (39%-81%), myocardial infarction (14%-36%), peripheral vascular disease (27%-77%), foot lesions (7%-75%), minor or major amputations (3%-23%), proliferative retinopathy (6%-46%), blindness (2.9%-16.1%), and internal carotid artery stenosis (15%-36%). In this preselected cohort of diabetic patients, a high morbidity was found already without nephropathy that increased several-fold in the course of the development of nephropathy. Our data identify patients with diabetic nephropathy as a high-risk group for excess morbidity.
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PMID:Morbidity in 565 type 2 diabetic patients according to stage of nephropathy. 955 88

The prevalence of abnormally elevated albumin excretion rate (> 30 mg/24 h) is approximately 40% in insulin-dependent (IDDM) and non-insulin-dependent (NIDDM) diabetic patients. Diabetes has become the leading cause of end-stage renal failure in the US, Japan and Europe. Approximately 90% of the direct and indirect cost of caring for diabetic patients are spent on the complications of diabetes. Identification of patients at high risk of developing diabetic nephropathy is possible by screening for microalbuminuria (30-300 mg/24 h). Elevated urinary albumin excretion rate indicates a substantially increased mortality risk in diabetic patients. Randomised controlled trials in normotensive IDDM and NIDDM patients with persistent microalbuminuria indicate that ACE inhibitors diminish urinary albumin excretion rate, postpone it and may even prevent progression to clinical overt nephropathy. These findings indicate that screening and intervention programs are likely to have life saving effects and lead to considerable economic savings. Systemic blood pressure elevation to a hypertensive level is an early and frequent phenomenon in diabetic nephropathy. Furthermore, nocturnal blood pressure elevation (non-dippers) occurs more frequently in patients with nephropathy. Systemic blood pressure elevation and to a lesser degree albuminuria accelerate the progression of diabetic nephropathy. Effective blood pressure reduction with non-ACE-inhibitors and/or ACE-inhibitors frequently in combination with diuretics: (a) reduces albuminuria; (b) delays the progression of nephropathy; (c) postpones renal insufficiency; and (d) improves survival in IDDM and NIDDM patients with diabetic nephropathy. A specific renal protective effect of ACE-inhibitors in diabetic nephropathy has been demonstrated in IDDM patients with moderately reduced kidney function (s-creatinine > 133 mumol/l) while the data conflict with NIDDM patients. Antihypertensive treatment for diabetic nephropathy simultaneously extends life and saves money. Finally, reduced risk of fatal and non-fatal cardiovascular events have been demonstrated when diabetic patients with isolated systolic hypertension are treated with blood pressure lowering agents. Absolute risk reduction with active treatment compared to placebo was twice as great for the diabetic versus non-diabetic patients (101/1000 versus 51/1000 randomised participants at the 5-year follow-up), reflecting the higher risk of diabetic patients. In conclusion, early detection and aggressive treatment of arterial hypertension with ACE-inhibitors, long acting calcium antagonist and low dose diuretics as first line drugs are highly warranted in diabetic patients with or without diabetic renal disease.
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PMID:Is antihypertensive treatment the same for NIDDM and IDDM patients? 964 59

Diabetic nephropathy is a serious microangiopathic complication of type 1 and 2 diabetes and accounts in a major way for the high morbidity and invalidity of diabetics. Although progression is inevitable when the disease is advanced, there are ways how to prevent its development and retard its progress. Because reliable prediction of diabetic nephropathy is impossible, primary prevention is essential in all diabetic patients. As soon as the diagnosis of diabetes is established, the blood sugar level should be checked systematically and permanent satisfactory compensation of diabetes should be ensured (HbA1c less than 6.5%) which is the main principle throughout the subsequent course of the disease. The principle of secondary prevention the objective of which is to prevent the development of manifest nephropathy with permanent proteinuria, is to monitor microalbuminuria and maintenance of a normal blood pressure. With regard to pathophysiological circumstances in therapy angiotensin converting enzyme inhibitors are preferred. The objective of tertiary prevention is retardation of renal insufficiency by fortified hypotensive therapy, correction of hyperlipoproteinaemia, dietary protein restriction and adequate compensation of diabetes. In case of renal failure dialyzation treatment or transplantation must not be delayed.
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PMID:[Controlling the progression of diabetic nephropathy]. 974 81

The purpose of the current study is to report the effect of diabetic nephropathy on pregnancy outcomes based on a review of the world's literature from 1981 to 1996. In addition, the effects of pregnancy on renal function in a select subpopulation of patients is also presented. The Medline Computer System was used to survey the English language literature on diabetic nephropathy complicating pregnancy between 1981 and 1996, which yielded a total patient population of 315. The database was analyzed according to patient population, clinical management, maternal complications and outcomes, and fetal complications and outcomes. The frequency of chronic hypertension was 42% with 60% of women manifesting hypertension by the third trimester. Pre-eclampsia developed in 41% of patients; proliferative retinopathy was observed in 63% of patients prior to pregnancy, and cesarean section delivery was performed in 74% of the patients. Among the fetal outcomes, intrauterine growth restriction (IUGR) was observed in 15%, preterm delivery in 22%, and major congenital malformations in 8% of the patients included in the database. The observed overall perinatal morality rate was 5%. Gestational age at delivery was significantly correlated with first-trimester Cr/Cl (p < 0.01), third-trimester Cr/Cl (p < 0.05), third trimester proteinuria (p < 0.01), and third-trimester blood pressure (p < 0.001). Birth weight was significantly correlated with first-trimester Cr/Cl (p < 0.01), third-trimester Cr/Cl (p < 0.001), third-trimester proteinuria (p < 0.01), and third-trimester blood pressure (p < 0.001). Of the 185 patients available for long-term follow-up (mean 35 months), 17% developed end-stage renal disease, and 5% died as a result of renal insufficiency. Among the renovascular parameters, proteinuria and mean arterial pressure significantly increased from the first to the third trimester (p < 0.05). When these parameters were evaluated at follow-up, blood pressure did not show a significant increase from first trimester values, however, proteinuria did show a weak, but significant, increase postpartum. These data suggest that with contemporary methods of perinatal care, fetal survival rates of 95% are achievable in diabetic women with nephropathy. Furthermore, although many women experienced a temporary decline in renal function during gestation, pregnancy per se, does not appear to worsen the natural progression to end-stage renal disease for most women with renal insufficiency.
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PMID:Pregnancy performance and outcomes associated with diabetic nephropathy. 975 8

There is now increasing evidence that essential hypertension is a serious risk factor for renal insufficiency. It has been known for many years that malignant essential hypertension rapidly causes deterioration of kidney function. This can be prevented by treatment with anti-hypertensive drugs. Mild-to-moderate essential hypertension causes significant renal function impairment only after a number of years. There are now data suggesting that the decline of renal function caused by mild-to-moderate essential hypertension can be prevented by anti-hypertensive treatment. In recent years, it has been demonstrated that anti-hypertensive drugs have a beneficial effect on the progression of renal insufficiency in patients with diabetic nephropathy and in chronic glomerulonephritis. In these situations, ACE inhibitors appear to be superior to other classes of anti-hypertensive drugs.
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PMID:Renal function in treated and untreated hypertension. 978 87

The importance of the level to which blood pressure is reduced becomes increasingly important when one considers preservation of renal function. It is clear that three major subsets of patients emerge as requiring levels of blood pressure control of < 130/85 mm Hg to preserve renal function. Such individuals include black Americans, those with diabetic nephropathy, and those with renal insufficiency or > or = 1 g of proteinuria. It is clearly important to achieve such levels of blood pressure control in these high-risk individuals. It is also clear that single-agent therapy will never achieve these levels of blood pressure control. Therefore, multiple antihypertensive agents will be required to achieve such a goal. With increasing numbers of medications, however, there is also, unfortunately, a decrease in compliance. Therefore, fixed-dose combinations emerge as playing a major part both in achieving a level of blood pressure control as well as maintaining levels of compliance. Certain types of angiotensin-converting enzyme inhibitors, as well as calcium channel antagonist combinations, however, appear to have better overall effects than others do. These and related data are reviewed in this paper.
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PMID:The role of combination antihypertensive therapy and the progression of renal disease hypertension: looking toward the next millennium. 979 50

Diabetic nephropathy (DN) appears in about 30% of patients with type 1 diabetes (D1) and 15 to 60% of patients with type 2 diabetes (D2). It is preceded by microalbuminuria. Microalbuminuria is defined as an albumin excretion rate between 30 and 300 mg/24 h (on a 24-hour urine collection) or between 20 and 200 micrograms/min (on an overnight collection) in at least two out of three consecutive collections made within a 6-month period. Alternative screening techniques use either dipstick (Micral-Test II) or the albumin to creatinine ratio on an early morning urine sample (30-300 mg/g creatinine). Once persistent microalbuminuria is confirmed, 80% of type 1 diabetic patients and 20 to 50% of type 2 diabetic patients will progress to DN. In D2, microalbuminuria also represents a powerful predictor of early mortality from cardiovascular disease. Macroalbuminuria (AER > 300 mg/24 h, corresponding to a total protein excretion > 500 mg/24 h) will eventually lead to a end-stage renal insufficiency within 10 to 20 years. In D2, numerous patients will die from cardiovascular disease before reaching end-stage renal failure. Angiotensin-converting enzyme inhibitors can slow down the evolution toward DN when prescribed when microalbuminuria appears. Screening for microalbuminuria should therefore be a part of the annual clinical assessment in every diabetic patient.
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PMID:[How I evaluate...diabetic nephropathy. First part: micro- and macroalbuminuria]. 981 Feb 12

Diabetic nephropathy is a serious microangiopathic complication of diabetes type I and II, which accounts for a marked proportion of the high morbidity and invalidity of diabetics. Although when the disease is fully developed, progression is inevitable, ther are ways how to prevent its development and retard its course. Because reliable prediction of diabetic nephropathy is not possible, primary prevention is essential in all diabetics. It involves, as soon as the diagnosis of diabetes is established, systematic checks of the blood sugar level and permanent satisfactory compensation of diabetes (HbA1c less than 6.5%) which is the main principle during the whole subsequent course of the disease. The principle of secondary prevention the purpose of which is to prevent the development of manifest nephropathy with permanent proteinuria is monitoring of microalbuminuria and maintenance of a normal blood pressure. With regard to pathophysiological associations, in the treatment angiotensin-converting enzymes inhibitors are preferred. The objective of tertiary prevention is to delay renal insufficiency by fortified hypotensive therapy, correction of hyperlipoproteinaemia, dietary protein restriction and satisfactory compensation of diabetes. In case of renal failure dialyzation treatment or transplantation must not be delayed.
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PMID:[Controlling the progression of diabetic nephropathy]. 982 Jan 10

Protein alteration resulting from a nonenzymatic reaction between ambient glucose and primary amino groups on proteins to form glycated residues called Amadori products is termed the Maillard reaction. By dehydration and fragmentation reactions, Amadori products are transformed to stable covalent adducts called advanced glycosylation end products (AGEs). In diabetes, accelerated synthesis and tissue deposition of AGEs is proposed as a contributing mechanism in the pathogenesis of clinical complications. Uremia in diabetes is associated with both a high serum level of AGEs and accelerated macro- and microvasculopathy. Diabetic uremic patients accumulate advanced glycosylated end products in "toxic" amounts that are not decreased to normal by hemodialysis or peritoneal dialysis but fall sharply to within the normal range within 8 h of restoration of half-normal glomerular filtration by renal transplantation. It follows that the higher mortality of hemodialysis-treated diabetic patients compared with those given a renal transplant may relate, in part, to persistent AGE toxicity. Pharmacologic prevention of AGE formation is an attractive means of preempting diabetic microvascular complications because it bypasses the necessity of having to attain euglycemia, an often unattainable goal. Pimagidine (aminoguanidine) interferes with nonenzymatic glycosylation and reduces measured AGE levels leading to its investigation as a potential treatment. The mechanism by which pimagidine prevents renal, eye, nerve, and other microvascular complications in animal models of diabetes is under investigation. Separate multicenter clinical trials of pimagidine in type 1 and type 2 diabetes, where proteinuria is attributable to diabetic nephropathy, are in progress. The effect of treatment on the amount of proteinuria, progression of renal insufficiency, and the course of retinopathy will be monitored.
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PMID:Advanced glycosylated end products and hyperglycemia in the pathogenesis of diabetic complications. 1009 2

Nephropathy in patients with type I and II diabetes mellitus is a rapidly increasing problem worldwide. Studies using both glomerular and tubular cells have delineated some of the consequences induced by acute hyperglycemia. In vitro studies have clearly demonstrated that exposure of cultured renal cells, such as glomerular mesangial cells and proximal tubular epithelial cells, to elevated glucose concentrations, may alter cell proliferation and/or extracellular matrix turnover. The latter is effected both directly and indirectly by the alteration of cytokine generation. Furthermore, these in vitro studies have allowed detailed examination of the mechanisms by which exposure of these cells to high ambient glucose concentrations may alter cell function. Extension of these studies to the experimental in vivo situation has confirmed most of the in vitro findings. Important insights gained from models of type I diabetes (i.e. streptocotocin-induced diabetes) as well as type II diabetes (i.e. Goto-Kakizaki (GK) rats and obese Zucker rats) include: (1) The demonstration that increased glomerular cell proliferation and renal matrix accumulation, driven by TGF-beta and/or PDGF, occur in streptocotocin-induced diabetes, yet that nephropathy in these rats does not progress to renal failure. (2) The demonstration that prolonged mild type II diabetes does induce morphological changes characteristic of pre-clinical diabetic nephropathy in GK-rats but does not result in albuminuria or progressive renal disease. (3) The demonstration that the association of type II diabetes with hyperlipidemia in obese Zucker rats results in early podocyte damage and subsequent progression to glomerulosclerosis, tubulointerstitial damage, and renal insufficiency. Identification of the mediators involved in the above processes and in particular of the conditions that will determine progression of subclinical morphological changes to overt nephropathy and renal failure will likely result in future novel therapeutic approaches to diabetic nephropathy.
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PMID:Progression of diabetic nephropathy. Insights from cell culture studies and animal models. 1035 11


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