Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0011881 (diabetic nephropathy)
 10,836 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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.
 ...
PMID:Abnormalities of sodium transport in non-insulin-dependent diabetes: association with renal disease. 810 99

To clarify the development of diabetic nephropathy in Japanese insulin-dependent diabetes mellitus (IDDM), 373 patients with IDDM who had no proteinuria at the first visit to our Diabetes Center were evaluated. The incidence of persistent proteinuria increased rapidly between 10 and 19 years of diabetes duration, and only a few new cases occurred thereafter. Patients whose ages at onset of IDDM were 9-17 years (n = 167) and 18-29 years (n = 90) had rapid development of persistent proteinuria compared to the 0 to 8-year group (n = 116) (p < 0.02 and p < 0.003, respectively). Females (n = 233) developed persistent proteinuria to a greater extent until 24 years of diabetes duration than males (n = 140) (p = 0.17). Development of proteinuria did not vary according to calendar year of diagnosis of IDDM or diabetes duration at the first visit. Renal insufficiency (serum creatinine of 2.0 mg/dL or greater) followed the onset of proteinuria; 60% of the patients with the onset of IDDM between 1951 and 1969 developed renal insufficiency 10 years after the onset of proteinuria, whereas 30% of patients with the onset of IDDM after 1970 developed this condition. Development of renal insufficiency did not vary according to sex, age at onset of IDDM, or age at onset of proteinuria. Renal failure requiring dialysis therapy occurred within 4 years after renal insufficiency. In conclusion, development of diabetic nephropathy in Japanese IDDM exhibits three stages. The onset of proteinuria appears to be influenced by age at onset of IDDM and sex.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Development of diabetic nephropathy in Japanese patients with insulin-dependent diabetes mellitus: Tokyo Women's Medical College epidemiologic study. 816 91

The effect of long-term, aggressive, antihypertensive treatment on kidney function in diabetic nephropathy was studied prospectively in 11 insulin-dependent diabetic patients (mean age, 30 years). Renal function was assessed every 4 months by measurement of glomerular filtration rate (GFR) (single-bolus 51Cr-EDTA technique) and by albuminuria (radial immunodiffusion). During the median pretreatment period of 2.4 years (range, 1.9 to 5.5 years), the GFR decreased significantly and albuminuria and the arterial blood pressure increased significantly. During the 9.7-year (range, 2.8 to 10.4 year) period of antihypertensive treatment with metoprolol, hydralazine, and furosemide, the arterial blood pressure decreased from 143/96 mm Hg to 130/84 mm Hg and albuminuria decreased from 1,038 micrograms/min to 547 micrograms/min. The rate of decline in GFR decreased from 10.7 mL/min/yr (range, 5.3 to 17.5 mL/min/yr) before treatment to 2.5 mL/min/yr (range, 0.5 to 4.8 mL/min/yr) during treatment. The rate of decline in GFR is significantly smaller during the last 6 years compared with the first 3 years in patients who received long-term antihypertensive treatment (> or = 9 years). One patient died from acute myocardial infarction (GFR, 46 mL/min/1.73 m2). Effective antihypertensive treatment postpones renal insufficiency in diabetic nephropathy.
 ...
PMID:Effective antihypertensive treatment postpones renal insufficiency in diabetic nephropathy. 832 82

Diabetic nephropathy occurs in approximately 35% of all diabetic patients, both insulin and non-insulin dependent. It accounts for the largest proportion increase of all diseases as a cause for endstage renal disease in the United States. Certain populations, i.e., Pima Indians and Mexican and black Americans, have a higher propensity for developing diabetic nephropathy. The reasons for this increased incidence, however, are unclear. Pathophysiologically, numerous changes in vascular reactivity and renal physiology occur in early diabetes. These include increased sodium avidity, lower threshold for vasoconstriction secondary to angiotensin II and norepinephrine, a greater than 50% of normal increase in renal vasodilation following a protein meal, and loss of renal autoregulation. These differences are not seen in nondiabetic hypertensive subjects. The therapeutic approach to lower elevated arterial pressure in these patients should take these changes in physiology into account. Specifically, antihypertensive agents are preferred that have natriuretic properties and also blunt the effects of vasoconstrictors on both the vasculature and the cellular level, i.e., inhibit mesangial hypertrophy and matrix expansion, the hallmark of diabetes. Ideal agents, therefore, are angiotensin converting enzyme (ACE) inhibitors in the early stages of the disease, and certain calcium antagonists once renal insufficiency occurs. These choices are largely due to the hemodynamic, natriuretic, and anti-proteinuric effects of these agents. Good blood pressure control is essential for preservation of renal function, regardless of agents used. The ACE inhibitors and calcium antagonists of the verapamil and diltiazem groups have demonstrated superior efficacy for preservation of renal function over conventional therapy.
 ...
PMID:Diabetic nephropathy. 833 15

In the Prague register of all adult diabetics by April 1, 1992 data on 1443 patients above 18 years with type 1 DM were recorded. In 42.2% of diabetics diabetic retinopathy was observed which is manifested most frequently after 11 to 15 years' persistence of diabetes. Proteinuria, the first sign of diabetic nephropathy, was found in 13.8% of the group, 5.4% of the diabetics are in the stage of renal insufficiency. Nephropathy is 3 to 4 times more frequent in diabetics with retinopathy. Peripheral neuropathy is found in 32.8% type 1 diabetics.
 ...
PMID:[The Prague Diabetes Registry. 3. Retinopathies, nephropathies and neuropathies in type 1 diabetics. The Prague Diabetes Collective]. 840 14

Hyperlipidemia is associated with accelerated glomerular sclerosis in experimental renal insufficiency. To investigate whether the dyslipoproteinemia seen in human renal failure also influences the future course of renal insufficiency, we have correlated plasma levels of lipids and apolipoproteins at start of follow-up with the subsequent change in renal function in 34 adult patients with chronic renal disease. Nineteen patients had primary renal disease, and 15 patients had diabetic nephropathy. Except for antihypertensive therapy no specific treatment to modify the progression of the disease was given during the follow-up. The rate of progression was determined by repeated measurements of the glomerular filtration rate (GFR). The time of follow-up ranged from 12 to 91 months with an average of 39.7 +/- 16.7 months. The mean initial GFR was 34.7 +/- 13.9 ml/min x 1.73 m2 body surface area and the average decline in renal function was -0.27 +/- 0.26 ml/min/month. The entry levels of triglycerides (TG; p = 0.04), very-low-density lipoprotein cholesterol (p = 0.03), apolipoprotein-B (ApoB; p = 0.008) and systolic blood pressure (SBP; p = 0.04) were significantly correlated with the rate of progression. Among lipoprotein variables, ApoB showed the strongest correlation with the decline in GFR. Patients with a progressive course of their disease also tended to have initially higher levels of total cholesterol (TC) and low-density lipoprotein cholesterol (NS), whereas the initial plasma concentration of high-density lipoprotein cholesterol did not show an association with the progression of renal insufficiency.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Apolipoprotein-B-containing lipoproteins and the progression of renal insufficiency. 772 19

Roughly 40% of all diabetic patients, whether insulin dependent or not, develop persistent albuminuria (over 300 mg/24 hr), a decrease in the glomerular filtration rate, and elevated blood pressure, ie, diabetic nephropathy. Diabetic nephropathy is the single most important cause of end stage renal disease in the Western world, and accounts for over a quarter of all end stage renal disease. It also is a major cause of the increased morbidity and mortality seen in diabetic patients; for example, the cost of end stage renal care in the United States currently exceeds +1.8 billion per year for diabetic nephropathy alone and is rapidly rising. Increased arterial blood pressure is an early and common finding in incipient and overt diabetic nephropathy. Fluid and sodium retention with normal concentrations of active renin, angiotensin I and II, and aldosterone has been demonstrated in diabetic renal disease. An impaired nocturnal decline in blood pressure is more prevalent in patients with diabetic nephropathy and autonomic neuropathy, and may contribute to the enhanced cardiovascular morbidity found in such patients. Moreover, raised blood pressure accelerates both the development and progression of diabetic nephropathy in insulin-dependent and non-insulin-dependent diabetes. The relationship between arterial blood pressure and diabetic nephropathy thus seems to be a complex one: nephropathy increasing blood pressure and blood pressure accelerating the course of nephropathy. Effective blood pressure reduction reduces albuminuria, delays the progression of nephropathy, and postpones renal insufficiency in diabetic nephropathy. Calcium antagonists and angiotensin converting enzyme inhibitors induce an acute increase in the glomerular filtration rate, renal plasma flow, and renal sodium excretion.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Calcium antagonists and the diabetic hypertensive patient. 850 35

Intravenous immune globulin (IVIg) is advocated as a safe treatment for immune-mediated neurologic disease. We reviewed the medical records of 88 patients who were given IVIg for a neurologic illness. Major complications in four patients (4.5%) included congestive heart failure in a patient with polymyositis, hypotension after a recent myocardial infarction, deep venous thrombosis in a bed-bound patient, and acute renal failure with diabetic nephropathy. Other adverse effects included vasomotor symptoms 26, headache 23, rash 5, leukopenia 4, fever 3, neutropenia 1, proteinuria (1.9 g/day) 1, viral syndrome 1, dyspnea 1, and pruritus 1. Fifty-two patients (59%) had some adverse effect of IVIg infusion, most commonly vasomotor symptoms, headaches, fever, or shortness of breath in 40 (45%), which improved with reduced infusion rate or symptomatic medications. Five (6%) had asymptomatic laboratory abnormalities and seven (8%) had other minor adverse effects. Adverse effects led to discontinuation of therapy in 16% and permanent termination of therapy in 10% of patients. There was no mortality or long-term morbidity. Although adverse effects were frequent, serious complications were rare except in patients with heart disease, renal insufficiency, and bed-bound state.
 ...
PMID:Complications of intravenous immune globulin treatment in neurologic disease. 930 72

An increase of renal ammoniagenesis has been implicated in renal hypertrophy associated with various clinical disorders such as metabolic acidosis, diabetic nephropathy, and renal insufficiency. In vivo and in vitro studies have shown that ammonia promotes hypertrophy in tubular epithelial cells. To elucidate its role on protein turnover, the effects of NH4Cl on the activities of cathepsins B, H, and L+B, as well as on protein synthesis and degradation in LLC-PK1 cells, were investigated. The results show that NH4Cl (20 mM) induced cell hypertrophy, as defined by an increase in both cell protein content and cell volume (+25.5 +/- 1.3 and +10.4 +/- 0.1% after 48 h). This hypertrophy was associated with the suppression of the activities of cathepsins B and L+B (-57.0 +/- 0.9 and -54.5 +/- 1.5% after 48 h) and a reduction of protein degradation rate (-59.7 +/- 4.1% after 48 h), but without enhanced protein synthesis. The findings were further supported with an additional experiment, showing that the protein synthesis inhibitor cycloheximide (10 microM) did not blunt NH4Cl-induced cell hypertrophy. Moreover, NH4Cl (20 mM) resulted in a persistent elevation of the lysosomal pH, whereas the rise in the cytosolic pH was only transient. This alkalinization in lysosomes may be causatively involved in the impairment of the activities of cathepsins B and L+B. In conclusion, the suppression of the activities of cathepsins B and L+B and the subsequent reduction of protein breakdown due to intralysosomal alkalinization contribute to NH4Cl-induced hypertrophy in LLC-PK1 cells.
 ...
PMID:Role of lysosomal cathepsin activities in cell hypertrophy induced by NH4Cl in cultured renal proximal tubule cells. 880 12

Treatment of hypertension with ACE inhibitors in diabetic patients reduces proteinuria and slows progression of nephropathy compared with agents that do not maintain declines in proteinuria. Calcium channel blockers (CCBs) have variable effects on proteinuria; their long-term effects on progression of diabetic nephropathy are not known. The current study examines the hypothesis that CCBs that maintain reductions in proteinuria slow progression of nephropathy associated with non-insulin dependent diabetes mellitus (NIDDM) by a degree comparable to ACE inhibitors, given similar levels of blood pressure control. To test this hypothesis we randomized 52 patients with NIDDM associated nephropathy and hypertension, mean age of 63 +/- 8 years, to either the ACE inhibitor, lisinopril (N = 18), nondihydropyridine CCBs (NDCCBs), verapamil SR (N = 8) or diltiazem SR (N = 10), or the beta blocker, atenolol (N = 16). Goal blood pressure was < or = 140/90 mm Hg. Patients were followed for a mean period of 63 +/- 7 months. The primary end point was change in creatinine clearance (CCr) slope in each group. There was no significant difference in mean arterial pressure reduction among the groups over the study period (P = 0.14). The mean rate of decline in CCr was greatest in the atenolol group (-3.48 ml/min/year/1.73 m2; P < 0.0001). There was no difference in the CCr slopes between lisinopril and NDCCBs groups (P = 0.36). Proteinuria was reduced to a similar extent in the lisinopril and NDCCBs groups (P > 0.99). Therefore, in persons with renal insufficiency secondary to NIDDM, similar levels of blood pressure control with either lisinopril or NDCCBs slowed progression of renal disease to a greater extent than atenolol. Moreover, this enhanced slowing of renal disease progression correlated with sustained and significant reductions in proteinuria, findings not observed in the atenolol group.
 ...
PMID:Calcium channel blockers versus other antihypertensive therapies on progression of NIDDM associated nephropathy. 891 31


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>