Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0033687 (proteinuria)
 24,015 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Diabetic late complications are characterized by morphological and biochemical alterations of the extracellular matrix. In particular, longstanding diabetes causes quantitative and qualitative changes in basement membrane structure of retinal and renal capillaries. Immunohistochemical investigations of diabetic kidneys with diffuse glomerulosclerosis show increased collagen type IV deposition in the mesangial matrix and decreased heparan sulfate proteoglycan content in the mesangial matrix and glomerular basement membrane as well. In nodular glomerulosclerosis normal basement membrane components are decreased or absent while the occurrence of collagen type III in this stage has been interpreted as an irreversible alteration of the glomerular structure. These changes seem to be the underlying cause for the alterations in renal functions like persistent albuminuria and proteinuria. Increased intra- and extracellular levels of glucose and its derivatives are thought to be responsible for diabetic tissue dysfunction although there are reports on possible genetic defects causing increased susceptibility to develop diabetic nephropathy. Recent results, however, focus on the role of glucose-induced cytokine secretion as mediator for altered metabolism of glomerular matrix proteins. In vitro studies with cultured kidney cells have shown that the glucose-induced dysregulation of the basement membrane synthesis may be mediated by a glucose dependent activation of protein kinase C. Alternatively or synergistically, the formation of AGE products formed after prolonged exposure of matrix proteins to elevated glucose may also lead to cytokine secretion subsequently inducing synthesis of extracellular matrix proteins. Studies in experimental animals confirm the diabetes induced dysregulation of the synthesis of extracellular matrix components on the molecular level.
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PMID:Alterations of glomerular matrix proteins in the pathogenesis of diabetic nephropathy. 851 35

The pathophysiology and natural history of diabetic nephropathy are described, and recent developments in its prevention and treatment are discussed. Diabetic nephropathy can occur in both insulin-dependent and non-insulin-dependent diabetics. It is characterized by arterial hypertension, proteinuria, and progressive loss of renal function. Although the exact mechanism has not been fully elucidated, hyperglycemia with altered intraglomerular hemodynamics is an important contributor to the initiation and progression of the disease. Concurrent hypertension aggravates progression of the disease. Currently accepted strategies to slow the progression of diabetic renal disease have focused on antihypertensive therapy, strict glucose control, and restriction of dietary proteins. Recent publications support the hypothesis that angiotensin-converting-enzyme inhibitors have a unique ability, independent of their antihypertensive effect, to slow the progression of diabetic nephropathy. Investigational agents (e.g., aminoguanidine) may prove helpful in the management of the condition. Information about the prevention of diabetic nephropathy has grown significantly in the past few years.
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PMID:Prevention and treatment of diabetic nephropathy. 852 34

Diabetes mellitus (or type 1) is a long-lasting disease (even twenty years or more) which causes kidney disease and, in the event of pregnancy, it can make differential diagnostic difficult even fort the most expert clinician. Metabolic changes caused by this type of diabetes (e.g., hypoglycemia, hyperglycemia, ketoacidosis) and their difficult compensation can often lead to the onset of eclampsia or convulsion. The diagnostic suspicion of diabetes is supported by the finding of proteinuria, edema and hypertension that are strictly correlated with the evolution of diabetic disease and sometimes exist prior to pregnancy. This cas report focuses on the diagnostic importance of clotting tests, especially in clarifying diagnostic doubts.
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PMID:[Diabetic nephropathy and pregnancy]. 854 41

This study examined factors contributing to the development of microalbuminuria in diabetic patients. A total of 236 patients with Type 2 diabetes were studied: 143 were normoalbuminuric and 86 were also normotensive. Multiple regression analysis was used to identify factors influencing the urinary albumin index (UAI), an index of proteinuria based on urinary albumin adjusted for urinary creatinine. Significant factors (retinopathy, systolic blood pressure, and glycosylated haemoglobin) were used to generate a formula for estimating the log(e) UAI. Target values for systolic blood pressure and glycosylated haemoglobin to maintain the urinary albumin index at or below 22 were determined for different degrees of retinopathy. Normoalbuminuric patients were followed for 3 years to evaluate their progression to microalbuminuria. Each month, blood pressure, urinary albumin and creatinine, and glycosylated haemoglobin were measured. In normotensive, normoalbuminuric patients, initial urinary albumin index and log(e) UAI were significantly higher in patients who subsequently developed microalbuminuria. Patients with initial log(e) UAI > 3.09 or initial glycosylated haemoglobin > 6.0% also showed greater progression to microalbuminuria. Hyperglycaemia was an independent factor for the development of microalbuminuria in Type 2 diabetes. The urinary albumin index was most significantly affected by retinopathy, systolic blood pressure, and glycosylated haemoglobin. The estimated loge UAI calculated from these factors is a useful predictor of progression to microalbuminuria.
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PMID:Estimated urinary albumin index: a predictor of microalbuminuria in type 2 diabetes. 867

A 13-year-old, neutered female domestic shorthair was referred for evaluation of chronic, intermittent vomiting of approximately two years' duration. On physical examination, a fluctuant mass was palpated in the left cranial abdominal quadrant. Significant laboratory findings included neutrophilia, hyperglycemia, hyperlipasemia, and proteinuria. A distinct mass within the left cranial quadrant was noted on abdominal radiographs. Ultrasonographically, the pancreas appeared slightly hyperechoic with a hypoechoic mass arising from its left lobe. A cystic mass in the left lobe of the pancreas was identified during an exploratory celiotomy. The mass and affected areas of the pancreas and a portion of the spleen were resected. The cat recovered completely. Cytological, histological, and laboratory evaluations of the mass were consistent with pancreatic pseudocyst formation, which has been reported in dogs and humans but has not yet been reported in cats.
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PMID:Pancreatic pseudocyst associated with chronic-active necrotizing pancreatitis in a cat. 868 Sep 21

Triamcinolone or triiodothyronine (T3) was administered to rats with nephrosis induced by aminonucleoside of puromycin and to control nontreated rats. Triamcinolone produced hyperglycemia, hyperinsulinemia and liver glycogen deposition in control rats and to a lesser extent in nephrotic rats. Triamcinolone treatment did not affect plasma protein and albumin levels but increased the level of plasma triglycerides and cholesterol in the very low density lipoprotein (VLDL) and LDL but not high density lipoprotein fractions. The exacerbation of hyperlipoproteinemia was attributed both to increase hepatic lipid synthesis and delayed removal, since it was associated with the induction of hepatic acetyl-CoA carboxylase, the regulatory enzyme of lipogenesis, as well as with marked suppression of adipose tissue lipoprotein lipase (LPL). The hepatic lipase activity was found to be elevated in nephrotic rats but was suppressed by triamcinolone treatment, indicating a reduced capacity of VLDL to LDL conversion. T3 treatment resulted in serum glucose and insulin increases similar to triamcinolone, but more moderate in nephrotic vs. control rats, and in marked reduction in liver glycogen content. Plasma protein levels were not affected, but contrary to control rats, T3 treatment produced an elevation in serum triglycerides and cholesterol in nephrotic rats. The activity of several hepatic lipogenic enzymes, including acetyl-CoA carboxylase, was markedly elevated, as was the activity of gluconeogenic enzymes. Thus, the hyperlipoproteinemia on T3 treatment appeared to be mainly due to predomination of lipid synthesis over removal, since the activities of enzymes responsible for plasma lipid disposal, adipose tissue LPL and hepatic lipase were enhanced both in control and nephrotic rats. It is remarkable that both T3 and triamcinolone induce the lipogenic enzymes and apolipoproteins in the liver of nephrotic rats, already pronouncedly stimulated to replace the excreted plasma proteins. Thus, the nephrotic liver is able to respond to hormonal stimulation with further specific protein and lipid synthesis. It is also pertinent that the recovery from immunosuppressive treatment of human nephrosis, developing on an immune background, may result in more impressive amelioration of proteinuria and hypoproteinemia than of hyperlipoproteinemia because of the lipidemic effect of glucocorticoids.
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PMID:Hyperlipoproteinemia of aminonucleoside-induced nephrotic syndrome--modulation by glucocorticoids and triiodothyronine. 868 44

The activity of gamma-glutamyl transferase (GGT), alkaline phosphatase (AP), lactate dehydrogenase (LDG), N-acetyl-beta-D-glucosaminidase (NAG) was assessed in 53 patients with psoriasis (PS), 24 PS patients with affected kidneys, 50 patients with type 1 diabetes mellitus(DM). Enhanced activity of the enzymes occurred not only in nephropathy patients but also in those without proteinuria. AP and NAG were more active in PS, while LDG and NAG in DM. Both in PS and DM, NAG activity rose 3-4-fold compared to control. A direct correlation was found between enzymuria and uremia, glycemia (in hyperglycemia only) and cholesterolemia. An inverse relationship existed between enzymuria and uricosuria. The above changes in enzymic activity are attributed to impairment of tubules of the kidney induced by PS and DM. Diagnostic significance of enzymuria as a marker of early tubular involvement is confirmed by investigations of renal biopsies.
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PMID:[Urinary enzymes in the assessment of the early stage of kidney involvement in psoriasis and diabetes mellitus]. 877 18

Hyperglycemia can result in key biochemical reactions that may contribute to thickening of basement membranes, dysfunction of pericytes and endothelial cells, and closure of retinal vessels. The Diabetes Control and Complications Trial has proved the value of good glycemic control in preventing retinopathy and/or delaying its progression. The primary care physician has a crucial role in translating these results into practice. Recognition and management of other risk factors, such as proteinuria, smoking, and hypertension, are easily done in the primary care setting. Also, appropriate referral to an ophthalmologist for retinal evaluation and treatment is both necessary and cost effective in reducing the burden of this devastating complication of diabetes.
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PMID:Diabetic retinopathy: a review for the primary care physician. 879 Mar 5

The renal kallikrein-kinin system (KKS) was studied in pair-fed streptozotocin (STZ)-induced diabetic rats and compared with age-matched controls. Twelve weeks after STZ injection, rats were normotensive, showed hyperglycemia, proteinuria, polydipsia and reduced glomerular filtration rate (GFR) and body weight. The activities of urinary prekallikrein (PKLK) and kallikrein (KLK) were reduced accompanied by an up to 3-fold increase of bradykinin (BK) excretion compared to controls. The increased BK excretion suggests that the renal KKS in STZ-diabetes is activated and that the reduction in urinary PKLK and KLK activity may be due to an increased consumption of these enzymes or to a negative feedback mechanism. The stimulation of the renal KKS in STZ-diabetes could reflect an attempt of the organism to balance glomerular hypertension.
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PMID:Bradykinin excretion is increased in severely hyperglycemic streptozotocin-diabetic rats. 885 82

Streptozotocin (STZ) has been extensively used to produce type I diabetes in animals. This experimental disease is characterized by a mild inflammatory reaction in the Langerhans islets. Because kinins have been proposed as prominent inflammatory mediators in the pathogenesis of several diseases, we decided to evaluate the role of kinins and their receptors in the evolution of insulitis. Male C57BL/Ks mdb mice were injected with STZ (40 mg/kg) for 5 consecutive days. The kinin B1 receptor antagonist [Leu8]des-Arg9-bradykinin or the B2 antagonist d-Arg[Hyp3,Thi5,D-Tic7, Oic8]bradykinin (HOE-140) was injected subcutaneously into STZ mice at 300 micrograms/kg body weight twice a day and 500 micrograms/kg per day, respectively. Treatment with antagonists was started 3 days after STZ and lasted for 10 days. Plasma glucose was determined by the glucose oxidase method, and urine samples collected on day 13 were assayed for proteins, nitrites, and kallikreins. Diabetic mice showed hyperglycemia and increased diuresis, marked proteinuria, and increased excretion of nitrites and kallikreins. The treatment with the B2 receptor antagonist did not show any effect on glycemia, but it significantly reduced water and protein excretion, compared with the STZ group. STZ mice treated with the B1 receptor antagonist showed normal glycemia and complete normalization of diuresis and protein, nitrite, and kallikrein excretion. The results obtained in the present investigation support the assumption that the kallikrein-kinin system intervenes in the maintenance of diabetic lesions, and they also indicate that B1 kinin receptors play a significant role in this experimental disease.
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PMID:Effects of B1 and B2 kinin receptor antagonists in diabetic mice. 888 24


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