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)

Proteinuria (protein excretion > 300 mg/d) is an independent risk factor for the development of cardiovascular disease and renal failure. The finding of persistent proteinuria in otherwise asymptomatic patients often precedes the development of arterial hypertension and renal failure. When proteinuria is accompanied by arterial hypertension, blood pressure control can decrease the quantity of protein excretion but not the incidence of proteinuria. In this sense, converting enzyme inhibitors seem to possess a higher capacity to reduce proteinuria. Nevertheless, the effects of reducing proteinuria on renal function and cardiovascular risk remain to be elucidated. Microalbuminuria (urine albumin excretion oscillating between 30 and 300 mg/d) seems to be a predictor of cardiovascular disease in diabetic and nondiabetic subjects and has been established as a predictor for the development of diabetic nephropathy. Blood pressure levels and urinary albumin excretion correlate positively, and antihypertensive therapy of any kind decreases the quantity of albumin present in the urine. The role of increased albumin excretion in essential hypertension and in renal failure remains to be elucidated.
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PMID:Clinical relevance of proteinuria and microalbuminuria. 792 40

Besides defining the appropriate doses of frusemide in uraemic patients, A. Heidland's contribution to the treatment of hypertension in chronic renal failure consisted in the following demonstrations: (1) In patients on chronic haemodialysis, calcium antagonists have a beneficial effect on their glucose intolerance and decreased plasma levels of 25OH vitamin D while their effect on blood lipids is neutral. (2) In 5/6 nephrectomized rats, captopril, verapamil, and metoprolol have the same protective effect on their GFR and tubular secretion of protons, at equal blood-pressure-lowering effect. (3) In rats with streptozotocin-induced diabetes, atrial natriuretic peptide does not play a role in their hyperfiltration. (4) Severe retinopathy is observed in patients with uraemic nephropathies at a much smaller elevation of their blood pressure than in patients with essential hypertension. This article reviews the following points: (1) The role of hypertension in the loss of renal function is convincingly demonstrated only in a few experimental models, and in man only in malignant hypertension and diabetic nephropathy but not in essential hypertension nor in non-diabetic nephropathy. However, preliminary results suggests that antihypertensive treatment may retard the progression of renal disease in normotensive patients (DBP <90 mmHg) with either microalbuminuric diabetes and normal renal function or non-diabetic uraemic nephropathy. (2) Only the ACE inhibitors have been proved to have a specific renal protective effect, independent of their diurnal blood-pressure-lowering effect, both in diabetic nephropathy and in non-diabetic uraemic nephropathy.
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PMID:Hypertension and progression of renal insufficiency. 807 21

We investigated both sodium-lithium countertransport (Na-Li CT) and ouabain-sensitive sodium transport (Na pump) of erythrocytes in healthy subjects (group A), patients with non-insulin-dependent diabetes (NIDDM) without nephropathy (group B), patients in the proteinuric stage (group C), and those in the renal insufficiency stage (group D). Erythrocytes from all four groups had a similar initial water and ionic content and were loaded with similar degrees of Li and Na for efflux studies. There were no significant differences in erythrocyte Na-Li CT or Na pump among the four groups. However, the maximal rate of Na-Li CT was significantly higher in a group of subjects with essential hypertension when compared with groups A, B and C, consistent with the view that there is a genetic marker for essential hypertension. Ouabain-insensitive Na efflux (Na leak) of erythrocytes was found to be significantly higher in group D than in groups A or B. Also, a significant positive correlation existed between Na leak and urine protein levels of the subjects studied. Our results thus indicate that in contrast with insulin-dependent diabetic patients (IDDM) where an elevated Na-Li CT is observed, with diabetic nephropathy, Na-Li CT in NIDDM is apparently not associated with nephropathy; rather the ouabain-insensitive Na efflux appears to be correlated with the stages of nephropathy in NIDDM. The association suggests that the rate of ouabain-insensitive Na efflux may provide an index for assessing the degree of nephropathy in NIDDM patients.
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PMID:Abnormalities of sodium transport in non-insulin-dependent diabetes: association with renal disease. 810 99

Despite the availability of multiple nonpharmacological and pharmacological antihypertensive regimens large scale control of BP on a population basis is still unsatisfactory. To achieve a better quality in hypertension care we have developed and evaluated a structured outpatient hypertension treatment and teaching programme. This programme aims at improving of patients' compliance to antihypertensive therapy and is based on four groups sessions mainly conducted by paramedical personnel. This programme was evaluated in three different settings: in patients with hypertension, diabetes mellitus and poor compliance to antihypertensive drug therapy; in blind patients with diabetic nephropathy and severe hypertension; and in patients with essential hypertension as treated by primary healthcare physicians in general practice. In all three studies a significant improvement in compliance to antihypertensive therapy and, hence, in BP control was demonstrated leading to preservation of renal function in diabetic nephropathy and fewer drug prescriptions in essential hypertension. In conclusion, studies evaluating the effect of large scale implementation of such structured treatment and teaching programmes on the quality of hypertension care in the community should be carried out.
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PMID:Improvement of hypertension care by a structured treatment and teaching programme. 811 50

Previous studies of erythrocyte sodium-lithium countertransport activity, a putative genetic marker of essential hypertension, in Type I and Type II diabetic patients with nephropathy have given conflicting results. We have found changes in the maximum velocity (Vmax) and sodium-affinity constant (Km) of sodium-lithium countertransport in Type I diabetic patients with diabetic nephropathy. In this study, sodium-lithium countertransport kinetics were measured in Type II diabetic patients with established diabetic nephropathy, matched uncomplicated Type II diabetic patients, non-diabetic patients with nephropathy and healthy control subjects. Mean standard sodium-lithium countertransport activity was not significantly increased in either of the groups of diabetic patients compared with the non-diabetic control groups. The Type II diabetic patients with nephropathy had a significantly reduced km and Vmax compared with the uncomplicated diabetic patients and non-diabetic control group. These kinetic changes are identical to those observed in Type I diabetic nephropathy patients. There are similar underlying changes in the erythrocyte plasma membrane with the development of nephropathy in both Type I and Type II diabetes.
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PMID:Nephropathy and changes in sodium-lithium countertransport kinetics in type 2 (non-insulin-dependent) diabetes mellitus. 815 3

Proteinuric diabetic patients have an increased risk of cardiovascular disease and almost always have hypertension. In the early stages of diabetic renal disease (microalbuminuria) when renal function is well preserved, systemic arterial blood pressure is already elevated compared to insulin-dependent diabetic patients without microalbuminuria. Prospective studies have shown that normoalbuminuric patients who progress to microalbuminuria have higher blood pressures (albeit within the normal range) than those who persistently remain normoalbuminuric. Parents of insulin-dependent diabetic patients with nephropathy have a higher prevalence of hypertension and cardiovascular disease compared to those of patients without nephropathy. Moreover, diabetic nephropathy clusters within families. Erythrocyte sodium-lithium countertransport activity, the most consistent marker for essential hypertension and its cardiorenal complications, is elevated in diabetic patients with nephropathy and in their non-diabetic parents. These data suggest that a familial predisposition to arterial hypertension and cardiovascular disease increases the risk for the development of nephropathy and its associated cardiovascular complications in insulin-dependent diabetes. Arterial hypertension is a state of insulin resistance and diabetic patients susceptible to nephropathy have been found to be less insulin sensitive. Preventive strategies of diabetic kidney disease in the future will have to take into account its metabolic hemodynamic and familial basis.
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PMID:Familial, hemodynamic and metabolic factors in the predisposition to diabetic kidney disease. 816 30

Cellular Na+/H+ exchanger (NHE) activity is elevated in type 1 diabetic patients with nephropathy and patients with essential hypertension. The characteristics of this NHE phenotype in hypertension (raised Vmax and a lowered Hill coefficient) are preserved in Epstein-Barr virus-transformed lymphoblasts from hypertensive patients. In this study, we have determined NHE kinetics in cultured lymphoblasts from diabetic patients with and without nephropathy, with nondiabetic controls, using fluorometry with the pH indicator 2,7'-bis-(carboxyethyl)-5,6-carboxyfluorescein and estimation of NHE isoform 1 (NHE-1) density with specific polyclonal antibodies. The Vmax of NHE was elevated significantly, and the Hill coefficient for internal H+ binding was lowered in cells from patients with diabetic nephropathy compared with both normal controls and normoalbuminuric diabetic patients. NHE-1 density as measured by Western blotting was similar in all groups. The turnover number of NHE-1 was thus elevated in cells from nephropathy patients. This phenotype in cells from diabetic nephropathy patients resembles that in essential hypertension and suggests that such patients may have a predisposition to hypertension. Moreover, as these changes persist in cultured lymphoblasts in vitro, these cells should provide a cell culture model to further define the basic mechanisms leading to NHE activation in diabetic nephropathy.
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PMID:Abnormal Na+/H+ antiporter phenotype and turnover of immortalized lymphoblasts from type 1 diabetic patients with nephropathy. 820 Oct 13

Hypertension and the kidney are closely linked in several ways. The kidney normally responds rapidly to changes in blood pressure by alteration of renal haemodynamics and sodium excretion. These functions of the kidney are reset in established hypertension. However, several subtle abnormalities of renal function are demonstrable in normotensive offspring of hypertensive parents, suggesting that the kidney may play a central role in the pathogenesis of essential hypertension--a possibility supported by a number of cross-transplantation studies in different animal models of hypertension. Hypertension itself commonly causes severe renal failure when the malignant phase develops, but the question of whether benign hypertension causes renal impairment remains controversial. Firm data that this is so are in general lacking, although in black subjects hypertensive nephropathy appears to be up to 18-fold more frequent than in whites, and is reported as a common cause of end-stage renal failure. The reasons for this racial difference in susceptibility to hypertensive renal injury remain unknown. Secondary hypertension also commonly develops in patients with underlying renal disease, and the co-existence of hypertension with renal impairment greatly worsens the rate of the deterioration of renal function. Effective treatment of hypertension in renal disease, particularly with converting enzyme inhibitors, is capable of slowing the rate of loss of function, both in animal models and in human disease, though in the latter case this benefit has so far been demonstrated unequivocally only in patients with diabetic nephropathy.
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PMID:Hypertension and the kidney. 820 61

The US Renal Data System Annual Report reveals that 57% of new cases and of end-stage renal disease are attributed to hypertensive nephropathy and diabetic nephropathy. Analyses of the data on serum creatinine from the Multiple Risk Factor Intervention Trial confirms that one in 20 of the hypertensive men exhibits a rate of decline in renal function that equals or exceeds 3% per year, the rate of loss being greater in older men, black men, and men with higher baseline blood pressure. Effective blood pressure treatment with maintenance of diastolic blood pressure below 95 mm Hg protected renal function in non-blacks but not in blacks, despite comparable blood pressure reduction in blacks. A longitudinal study of a diabetic cohort (n = 131) revealed that hypertension, plasma angiotensin II, and aldosterone are independent predictors of accelerated loss of renal function in diabetic nephropathy, possibly aggravated by diuretic usage as part of the antihypertensive regimen in diabetic nephropathy. No significant loss of renal function could be documented in those individuals whose blood pressure was adequately controlled (systolic blood pressure, < 140 mm Hg). These findings provide emphasis for the importance of adequate blood pressure control in both essential hypertension and hypertension associated with diabetes mellitus. They also provide support for the proposal that careful blood pressure control offers promise for reducing the incidence of end-stage renal disease in both hypertensive nephropathy and diabetic nephropathy.
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PMID:Hypertension-related renal injury: a major contributor to end-stage renal disease. 832 80

Elevated erythrocyte sodium-lithium countertransport (SLC) activity is an intermediate phenotype of essential hypertension among Caucasians, and is controversially associated with nephropathy in Type 1 (insulin-dependent) diabetes. Hypertriglyceridemia is a frequent concomitant of elevated SLC in the general population, and may be found in diabetic nephropathy. The present study was designed to investigate the influence of kidney disease, serum triglycerides and blood pressure on the interindividual variability of SLC in Type 1 diabetes. SLC and fasting major serum lipids were studied in 35 Type 1 diabetic patients with persistently elevated urinary albumin excretion and in a group of patients matched for age, sex and duration of diabetes, but with normoalbuminuria. SLC was elevated in patients with clinical nephropathy (N = 10; median: 420 mumol.1RBC-1.hr-1) and in patients with microalbuminuria (N = 25; median: 405 mumol.1RBC-1.hr-1) compared with normoalbuminuric patients (median: 296 mumol.1RBC-1.hr-1; P < 0.01 vs. both groups). Hypertriglyceridemia and hypercholesterolemia were found only among patients with macroalbuminuria. Analysis of covariance indicated that the association of elevated SLC with kidney disease (P < 0.006 in all models) was largely independent of serum triglycerides, but also of total cholesterol, insulin dose and measures of glycemic control. Only diastolic blood pressure was positively associated with SLC (P < 0.02) independently from nephropathy (P < 0.005) also after restricting analysis to the normoalbuminuric patients. Kidney disease and raised blood pressure remain major concomitants of elevated SLC in Type 1 diabetics.
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PMID:Sodium-lithium countertransport and triglycerides in diabetic nephropathy. 835 53


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