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)

Investigations on certain hemocoagulation indices are carried out of 52 diabetics, 32 of them with diabetic nephropathy. The following indices were determined: thrombocyte numer, thrombocyte adhesion and aggregation, recalcification and heparinrecalcification time, partial thromboplastin time (PTT) and prothrombin time, coagulation retraction and thrombelastography. Data for increased blood coagulation are established in diabetics and especially in the presence of nephropathy. Most manifested are the changes in thrombocyte adhesion, in PTT, recalcification and heparin-recalcification time. Changes in thrombelastogram and the rest of the indices are less manifested. In patients with more advanced forms of nephropathy--the increased hemocoagulation is more pronounced. The changes described are considered non diabetes specific and are associated with the accompanying atherosclerosis. Those changes might indicate inclusion of anticoagulants and antiaggregating medicines in the therapeutic program of patients with diabetic nephropathy with the respective indications.
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PMID:[Changes in blood coagulation in diabetic nephropathy]. 122 99

A reversible lysozymuria indicative of proximal tubular damage to the kidney was found in three out of five patients with diabetic ketosis, and a persistent lysozymuria was found in many patients with diabetic nephropathy. There was no relation between lysozymuria and the degree of proteinuria, and lysozymuria was not due to urinary tract infection. The degree of lysozymuria could be used to assess the severity of diabetic nephropathy.
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PMID:Lysozymuria in diabetes. 125 52

Big renin has a greater molecular weight (63,000 versus 43,000) than normal renin, but it shares the characteristic enzymatic and immunologic properties of normal renin. As it exists in the kidney or plasma of a patient, big renin is less active than normal renin, but its enzymatic activity is greatly enhanced by exposure to pH values of 3.0 to 3.6 or by brief incubation with pepsin or trypsin. Use of the terms prorenin and zymogen might be withheld until big renin is shown to exist in normal tissue or plasma and to be converted to normal renin in vivo. To date, big renin has been found in renal tumors and other abnormal kidney tissues as well as in the plasma of patients with renal disorders. The remarkable activation of big renin at pH levels of 3.3 can be used to detect its presence. If a method involving acidification is used to quantitate plasma renin activity of a patient with circulating big renin, the activated plasma renin activity greatly exceeds that measured in plasma maintained at neutral pH. Gel filtration of plasma is used to prove the presence of big renin. When large amounts of big renin are secreted by a renal tumor, hyperfusion may ensue and be cured by removal of the tumor. The secretion of small amounts of big renin does not necessarily result in any physiologic disorder. However, if there is a concomitant diminution or absence of normal renin a state of apparent hyporeninemia exists, as we have observed in diabetic nephropathy; this may be associated with hypoaldosteronism and hyperkalemia. Big renin does not appear to respond to physiologic changes that stimulate or suppress normal plasma renin activity. The finding of big renin may indicate the presence of certain renin-secreting renal tumors or other renal disorders, especially diabetic nephropathy.
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PMID:Big renin: identification, chemical properties and clinical implications. 125 3

A historical review and the present author's study on diabetic nephropathy have been presented. Three characteristic lesions in KW-lesion, namely nodular, exudative and doughnut lesion may all be regarded as to be caused by severe circulatory disturbance occurring in intraglomerular branches of the afferent artery. This circulatory disturbance is considered to be brought about by sudden spasm of the peripheral portion of the afferent branches. The diffuse form of Bell may be regarded as to be a slighter type without severe mesangiolysis. Arteriolar hyalinosis and arteriosclerosis and/or atherosclerosis may be caused by intraglomerular circulatory disturbances. The most important problem in diabetic nephropathy, including KW-lesion and Bell's diffuse form, is to elucidate the mechanism leading to the occurrence of spasm of the peripheral portion of intraglomerular afferent branches. Becker found fixation of antiactomyosin-antibody in the mesangial tissue by the immunofluorescent method. Many studies along this line have been made, but none are adequate in fully explaining the mechanism involved.
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PMID:A histopathological study on diabetic nephropathy -- light and electron microscopic observations. 127 77

We are carried out to determine the detection of glycosylated protein of renal tissues using nitroblue tetrazolium (NBT) reaction in streptozotocin (STZ)-induced diabetic rats. The levels of glomerular non-enzymatic glycosylation were measured by thiobarbituric acid (TBA) method. There was no significant difference in the intensity of NBT in renal tissues between the 4-week diabetic rats and the same age control rats. The intensity of NBT in the glomerular mesangial areas and capillary walls was marked in 12-week diabetic rats. The staining of NBT was also observed in the tubular epithelial cells in 4- and 12-week diabetic rats. The levels of glomerular non-enzymatic glycosylated protein in 4- or 12-week diabetic rats were significantly greater than those in the same age control rats. It appears that the non-enzymatic glycosylation of renal tissues increased in the early stage of diabetic nephropathy, i.e. 4- or 12-week diabetic rats. It is concluded that the non-enzymatic glycosylation may play an important role in the initiation of renal injuries in diabetic nephropathy.
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PMID:[Detection of glycosylated protein of renal tissues using NBT reaction in STZ-induced diabetic rats]. 128 36

The kidney is a site of insulin-like growth factor I (IGF-I) production and IGF-I mediates effects on kidney growth and function. Diabetes is associated with kidney growth in man and the rat and, in the latter, commences within 48 h of induction of diabetes. Levels of kidney IGF-I are increased during the first 2-3 days of diabetes and this is at least partially due to increased production. Additionally, IGF-I binding is increased in diabetic rat kidney, due to increased binding to the IGF-I receptor and induction of proximal tubular binding protein expression. These changes are attenuated in prepubertal rats suggesting hormonal regulation. Further studies suggest that the changes are partly GH-dependent but independent of direct sex steroid effects. As kidney growth has been implicated in the subsequent development of diabetic nephropathy, further exploration of the close association between diabetes-related kidney growth and IGF-I accumulation may lead to an improved understanding of this complication.
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PMID:IGF-I and IGF binding proteins in diabetes-related kidney growth. 128 98

The course and prognosis of chronic renal failure are much worse in hypertensive patients than in normotensive patients with otherwise similar basic disease. Therefore, antihypertensive measures with a combination of diuretics, beta-blockers, and vasodilators have clearly been shown to improve the progression of diabetic nephropathy. Treatment of hypertension with angiotensin-converting enzyme (ACE) inhibitors has also been shown to have a favorable effect on the prognosis of chronic renal failure. In the past few years, more knowledge about the pathogenesis of hypertension and the development of hypertension-induced organ damage has been followed by changing attitudes to antihypertensive therapy and the introduction of calcium antagonists for the treatment of hypertension, even in chronic renal failure. ACE inhibitors and calcium antagonists seem to be advantageous in the prognosis of chronic renal failure as they act on the humoral and trophogenic factors now known to be important in antihypertensive therapy.
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PMID:The effect of antihypertensive therapy on the course of renal failure. 128 93

Diabetes mellitus can lead, along the years of its course, to chronic renal failure in a high proportion of cases. An early risk-indicator of later diabetic nephropathy is the presence of microalbuminuria, but it usually takes about fifteen to twenty years to appear. Before that, no clinical signs can disclose the underlying alterations of glomerular basement membrane that will eventually bring forth overt nephropathy. The usefulness of the altered excretion of isoenzymes of amylase as an early marker of the glomerular charge selectivity was tested in 202 juvenile onset insulin-dependent diabetics, compared with 51 normal subjects matched for age and sex. The diabetic patients studied showed increased excretion of salivary amylase into urine. The salivary to pancreatic amylase ratio of concentrations in urine was always below 1 in normal subjects, and was increased over 1 in 33.2% of diabetics, although microalbuminuria was present only in 26.2% of patients. The excretion of other proteins was within reference values in the majority of cases, indicating that the kidney was not seriously affected in those patients. Moreover, the altered salivary to pancreatic amylase ratio in urine was more prevalent than microalbuminuria (36.6% vs 18%) in the first decade of the evolution of the diabetes. These results indicate that the ratio of excretions of both isoamylases into urine is a more sensible and earlier marker of altered glomerular charge barrier for anionic proteins.
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PMID:Utility of filtration markers to monitor the quality of glomerular function. 128 36

Divergent findings in recent clinical and experimental studies have caused considerable controversy as to whether or how elevated plasma levels of human atrial natriuretic peptide (hANP) may contribute to the pathogenesis of diabetic nephropathy in type I diabetic patients. Therefore, we decided to examine potential changes of urinary albumin excretion (UAE), urinary excretion of alpha-1-microglobulin (A-1-M), mean arterial blood pressure (MAP), hANP levels, creatinine clearance and HbA1 in the course of a prospective one-year study in 19 patients (13 females, six males, age 29 +/- 2 years). All patients had intensified insulin treatment. Seven patients at increased risk for eventually developing nephropathy (group 1) were identified by repeatedly showing elevated UAE ( > 30 mg/24 h). The other patients served as controls (group 2). Patients in group 1 differed from those in group 2 in increased A-1-M (maximal difference, 10.1 +/- 1.5 vs. 5.5 +/- 1.0 mg/l, p < 0.01). In the second half of the study, 43% of the MAP measurements in group 1 exceeded 100 mmHg in comparison to 19% in group 2 (p < 0.01). Simultaneously, 38% of the hANP levels in plasma in group 1 were higher than 25 pg/ml (upper limit of normal range) in comparison to 15% in group 2 (p < 0.05). There were no differences in creatinine clearance between both groups. 58% of the HbA1 concentrations measured in group 1 in the course of the study exceeded 8.5% in comparison to 47% in group 2 (p < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[The role of human atrial natriuretic peptide on pathogenesis of nephropathy in patients with type I diabetes mellitus]. 128 23

Diabetes mellitus (DM)-linked metabolic alterations and hypertension concomitantly accelerate or precipitate cerebrovascular and coronary heart disease, nephropathy, retinopathy and widespread macroangiopathy, thereby conferring to diabetic patients a very high risk of morbidity, disability and early death. Therefore, the long-term care for diabetic patients should be aimed at concomitant metabolic and blood pressure (BP) control. Dietary measures are indispensable; a high fibre, low fat, low salt diet is recommended, complemented with caloric restriction and physical exercise when body weight is above the ideal. Antidiabetic pharmacotherapy involves an unresolved dilemma. The desired achievement of euglycemia necessitates effective levels of insulin, but hyperinsulinemia (due to parenteral [over]treatment in insulin-dependent DM) is suspected to promote atherogenesis and represents a coronary risk factor and perhaps even facilitates hypertension. Considering antihypertensive pharmacotherapy, thiazide-type or loop diuretics are problematic drugs in DM because they can aggravate metabolic alterations. These agents also seem to exert only a limited preventive or regressive effect on left ventricular hypertrophy (LVH); beta-blockers are also not considered ideal, since they decrease the awareness of hypoglycemia and tend to promote glucose intolerance. Unselective beta-blockers in particular promote peripheral ischemia and insulin-induced hypoglycemia, while beta-blockers without intrinsic sympathomimetic activity lower serum HDL-cholesterol. Calcium antagonists and ACE inhibitors have equivalent antihypertensive efficacy, do not impair carbohydrate and lipid homeostasis or peripheral perfusion and can effectively improve LVH. Certain ACE inhibitors may even slightly ameliorate abnormal insulin sensitivity and plasma glucose levels. While alpha-blockers share most of these desirable properties, these agents are more prone to precipitate orthostatic hypotension in the diabetic patient. The non-thiazide diuretic indapamide and the serotonin2-antagonist ketanserin also combine antihypertensive efficacy with metabolic neutrality. The ultimate goal of therapy is to improve life prognosis. In essential hypertension, conventional drug treatment based on diuretics in high dosage satisfactorily reduced cerebrovascular but not coronary complications or sudden death. In diabetic patients, the influence of antihypertensive therapy on prognosis has not been assessed prospectively. Based on retrospective analyses, Warram et al reported a 3.8 times higher mortality in diabetics treated with diuretics alone, than in diabetics with untreated hypertension (Arch Intern Med. 1991;151:1350). H. H. Parving calculated that effective BP control in patients with diabetic nephropathy might reduce 10 year-mortality from about 65 to 20 percent (J Hypertension. 1990; 8[Suppl 7]:187).(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Antihypertensive therapy in diabetic patients. 128 10


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