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

The clinical course of diabetic nephropathy was evaluated in 150 patients and the effect of hemodialysis in 68 of them. Proteinuria was the first sign of renal disease. Once renal dysfunction becomes evident, there is a rapid deterioration leading to dialysis within 3.0 +/- 0.2 years. Hypertension and circulatory congestion are common complications. The hypertension is probably volume dependent. Retinopathy was not invariably present at the onset of renal insufficiency but appeared with progression of renal failure. The course during hemodialysis was complicated by continued progression of diabetic vascular disease manifested by vascular access difficulties, worsening of retinopathy and blindness, and cardio- and cerebrovascular deaths. Mortality was higher than in nondiabetic dialysis patients.
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PMID:Diabetic nephropathy: clinical course and effect of hemodialysis. 64 44

Proteinuria has been analysed in 334 maturity-onset diabetics and 80 matched controls. Proteinuria measured in the recumbent position exceeded 100 mug/min in 53% of the diabetic population. The percentage of excessive proteinuria increased with duration of the disease. Sex and age had no influence. Out of 55 first year diabetics, 49% had abnormal quantitative proteinuria; this is in contrast to 76 longterm diabetics (over 12 years) of whom 38% had proteinuria under 100 mug/min. Electrophoresis and immuno-electrophoresis showed a glomerular pattern in 40%, a tubular pattern in 15% and a mixed pattern in 8% of all the diabetics. 32% of the diabetics with quantitatively normal proteinuria were abnormal qualitatively, and this may be the first manifestation of diabetic nephropathy. Thirty-eight other patients had a normal electrophoretic pattern in spite of increased proteinuria. Proteinuria levels were significantly associated with hematuria, bacteriuria and reduced GFR, but not with leukocyturia, insulin dependence and hypertension. Upright position increased the proteinuria to a greater degree amongst the patients with normal proteinuria. We discuss the role of increased filtration pressure and glomerular permeability in modifying proteinuria in diabetes. Sensitive quantitative and qualitative proteinuria determinations are important tools both in early diagnosis of diabetic nephropathy in clinical practice and in epidemiological studies.
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PMID:[Proteinuria in mature diabetic patients. Quantitative and qualitative analysis]. 121 95

Our study compared the effects of an angiotensin-converting enzyme inhibitor (captopril) versus a calcium antagonist (nifedipine) on proteinuria and renal function in patients with diabetic nephropathy. A randomized follow-up study was designed. Type 2 diabetic patients, with established diabetic nephropathy (proteinuria greater than 0.5 g/24 h), were treated with nifedipine (10 patients, group A) or captopril (10 patients, group B) for 6 months. Arterial blood pressure, metabolic parameters, proteinuria and renal function were measured and compared. Mean percentage differences for glomerular filtration rate, renal plasma flow and filtration fraction between the two groups were calculated. No significant differences were observed in serum glucose, glycosylated hemoglobin (hemoglobin A1c), Na+, K+ or albumin in either group or between groups. Blood pressure decreased significantly with both treatments and mean blood pressure was significantly lower in group A compared with group B at 6 months (Mann-Whitney U-test, P = 0.03). Proteinuria was similar in both groups at randomization, but after 3 and 6 months of treatment significant reductions were observed only in the group treated with captopril (P less than 0.01). A significant decrease in filtration fraction was observed in group B with an increase in group A (Mann-Whitney U-test, P = 0.03). Multiple regression analysis identified the therapeutic agent administered as an independent variable for decrease in proteinuria. It is concluded that antihypertensive treatment with captopril, but not with nifedipine, reduced proteinuria in patients with diabetic nephropathy, although a better mean blood pressure was obtained with nifedipine.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Comparative effects of captopril versus nifedipine on proteinuria and renal function of type 2 diabetic patients. 142 58

Diabetic nephropathy leading to kidney failure is a major complication of type I (insulin-dependent) diabetes mellitus and is associated with progressive proteinuria. In the present 6-month study, effects of two structurally dissimilar aldose reductase inhibitors (sorbinil and ponalrestat or Statil) were examined on prevention of proteinuria in insulin-dependent spontaneously diabetic BB rats and compared with age-matched BB resistant controls. Prior to aldose reductase inhibitor treatment, all diabetic BB rats exhibited hyperglycemia (> 300 mg/dl), glycosuria (> 2,000 mg/dl) and 24-hour urinary protein excretion ranging from 5.01 to 11.23 mg/day. After daily administration of ponalrestat (20 mg/kg) for 3 months, 24-hour urinary protein excretion was 11.53 +/- 1.76 mg/day in ponalrestat-treated rats, despite persistence of hyperglycemia (444 +/- 31 mg/dl) and glycosuria (> 2,000 mg/dl); by contrast, urinary protein excretion was 17.76 +/- 2.59 mg/day in the control group of untreated BB diabetic rats. Ponalrestat initially protected against excretion of an array of urinary proteins having molecular weights between 30,000 and 100,000 daltons. These effects sustained throughout the 4th month of treatment, tended to change toward valves in control rats by the 5th month. At the end of 6 months, ponalrestat-treated diabetic rats excreted 18.73 +/- 3.20 mg/day of protein, similar to valves in untreated BB diabetic rats; both demonstrated a 4-fold increase in urinary protein excretion when compared to age-matched BB resistant controls. Proteinuria was attributed to an increase in albumin and an array of proteins having molecular weights between 30,000 and 100,000 daltons.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Comparison of sorbinil and ponalrestat (Statil) diminution of proteinuria in the BB rat. 146 75

Metabolism of proteins which compose capillary basement membrane is altered in diabetic patients. In the kidney, this leads to an impaired permselectivity of glomerular basement membrane and consequently to onset of proteinuria. Proteinuria which is often increased by hemodynamic factors, initiates and promotes the development of diabetic glomerusclerosis. Aside from near-normal metabolic control, special antihypertensive treatment can reduce proteinuria and retard loss of kidney function in proteinuric diabetic patients. The beneficial effect of ACE-inhibitors on course of diabetic nephropathy is generally thought to be a consequence of decreased systemic and intraglomerular pressure. However, recent longterm studies in Type I and Type II diabetic patients with nephropathy showed that ACE-inhibition can reduce proteinuria independent from their hemodynamic effects and, thus, improves the filtration properties of glomerular basement membrane. This may be due to an influence of ACE-inhibition on metabolism of basement membrane proteins.
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PMID:[ACE inhibitor effects on structure and function of the glomerular basement membrane]. 161 91

Until recently Type 1 diabetes has been characterized by a considerable degree of mortality, mainly associated with the development of diabetic nephropathy. Diabetic nephropathy is characterized by persistent proteinuria, decreasing glomerular filtration rate (GFR), increasing blood pressure, and morphological changes. Proteinuria represents a late stage in a prolonged process, which begins at the onset of Type 1 diabetes, when urinary albumin excretion is at the lower end of its normal range (less than 10 mg 24-h-1). However, in those patients who will later develop persistent proteinuria, urinary albumin excretion increases exponentially at about 20% per year. These patients also tend to have rising blood pressure and falling GFR, higher rates of proliferative retinopathy and coronary heart disease, and elevated levels of cardiovascular risk factors. As intervention is possible in all these areas, identification of such patients is required and especially as the imposition of strict metabolic control may postpone or arrest progression to overt nephropathy. Where patients deteriorate despite such control the institution of early antihypertensive therapy and the effective management of end stage renal disease will bring further improvements in the prognosis of diabetic nephropathy.
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PMID:Natural history of diabetic complications: early detection and progression. 182 54

A personal series of 6780 patients with diabetes mellitus is reported. Of these 1410 were thought to have insulin-dependent (Type 1) diabetes and 4926 non-insulin-dependent (Type 2) diabetes. Among the former, 128 patients were only diagnosed when in severe ketoacidosis or coma. In 116 patients the diabetes was diagnosed in pregnancy. Chronic alcoholism was an aetiological factor in 75 patients; in 52 it led to the diagnosis being made, and it complicated treatment in 129 additional patients. In the patients with Type 2 diabetes whose treatment was stabilized 23.5% were having insulin injections, 44.5% tablets, and 32.0% diet only. Sight-threatening retinopathy developed in 21.3% of patients with Type 1 and 7.9% of those with Type 2 diabetes. The rate of developing sight-threatening retinopathy was 1.1% of patients per year. Blindness occurred in 0.28% of patients with Type 1 diabetes per year and 0.097% per year in Type 2 diabetes. If the mean survival of patients with retinopathy going blind is 7.5 years, this would mean 7500 people in the UK blind from diabetic retinopathy. There was a striking drop in the annual incidence of blindness after 1970 coinciding with the introduction of specific treatment for diabetic retinopathy. Juvenile cataract developed in 1.7% of patients who developed Type 1 diabetes before 30 years of age. Clinically important diabetic neuropathy developed in 17.4% of patients with Type 1 and 11.6% of those with Type 2 diabetes. The main features were paraesthesiae and numbness (49%), neuropathic ulceration (37%), pain (5%), autonomic symptoms (5%), and amyotrophy (4%). Oculomotor palsies and mononeuropathies were noted. Foot ulceration occurred in 81 patients with Type 1 and 279 of those with Type 2 diabetes. Charcot changes in the feet were noted in 21 patients. Major amputations were needed in 18 patients with Type 1 and 60 with Type 2 diabetes. Proteinuria believed to be due to diabetic nephropathy developed in 12.8% of patients with Type 1 and 4.7% of those with Type 2 diabetes. The prevalence of early renal failure was 4.6% and 1.4%, respectively. Coronary artery disease was noted in 9% of patients with Type 1 diabetes, and was more common in those who developed diabetes after 20 years of age. Myocardial infarction was as common in women as in men. In Type 2 diabetes coronary artery disease gave rise to symptoms in 19.1%, and myocardial infarction was more common in men.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Diabetes in the United Kingdom: a personal series. 182 47

Recent data suggest genetic contributions to the microvascular complications of Type 1 (insulin-dependent) diabetes mellitus. Most research has focused on the HLA region, and the potential role of other genetic loci has not been adequately explored. We examined the possible relationship between DNA polymorphisms in the region 5' to the insulin gene on chromosome 11 and diabetic nephropathy. This was done by comparison of those diabetic patients homozygous for class 1 alleles at the 5' insulin gene polymorphism locus to 1/3 heterozygotes in a well-characterized series of 324 insulin-requiring diabetic patients from the Wisconsin Epidemiologic Study of Diabetic Retinopathy. Proteinuria (defined as greater than or equal to 0.3 g protein/l urine), was used as suggestive evidence for diabetic nephropathy. Hypertension, a frequent associated finding in diabetic patients with nephropathy, was defined as a blood pressure greater than 140/90 or a history of previous treatment of hypertension. The two genotypically defined groups did not differ from each other in regard to sex ratio, age at diagnosis, age at examination, duration of diabetes, body mass, HbAlc or C-peptide. The 1+1 group had a higher prevalence of proteinuria, 29% as compared to 16.2% in other genotypes (p less than 0.05). There was no significant difference in the frequency of hypertension between the two genotypic groups. This finding suggests that the 5' insulin gene polymorphism may be associated with risk for nephropathy, but the pathophysiologic mechanism remains unclear.
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PMID:The 5' insulin gene polymorphism and the genetics of vascular complications in type 1 (insulin-dependent) diabetes mellitus. 195 2

Haemostatic activation was measured in patients with either non-diabetic chronic renal failure (CRF) or diabetic nephropathy. We have investigated the relationship between these haemostatic markers and the rate of progression of renal failure. When compared with age- and sex-matched healthy controls, both patient groups showed significantly elevated plasma concentrations of D dimer, von Willebrand factor antigen (vWFAg), and C-reactive protein (CRP) (all P less than 0.001), as well as an increase in spontaneous platelet aggregation (P less than 0.01). Plasma concentration of platelet factor 4 was slightly but not significantly increased. Serum thromboxane was subnormal (P less than 0.01). Multiple regression analysis showed that in non-diabetic CRF proteinuria and serum TxB2 were independently related to the rate of progression of renal failure; in diabetic nephropathy proteinuria and vWFAg were independently related to the rate of progression. In both groups the relationship was stronger with proteinuria (standardised regression coefficients 0.56 and 0.45 respectively) than with serum TxB2 (0.29) or with vWFAg (0.37). We have found haemostatic activation in both non-diabetic and diabetic progressive renal failure. Proteinuria, and also in this study serum TxB2 and vWFAg, appear to be determining factors in the progression of renal failure, and their measurement may have prognostic value.
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PMID:Haemostatic activation and proteinuria as factors in the progression of chronic renal failure. 205 12

In patients with diabetic nephropathy, near-normalization of blood pressure (BP) and blood sugar may have a beneficial impact on changes in kidney function, but visually impaired patients may face difficulties when striving for optimal control of hypertension and hyperglycemia. In a prospective feasibility study, we followed a group of nine blind Type I (insulin-dependent) diabetic patients (mean age 30 +/- 4 years) with overt diabetic nephropathy and uncontrolled hypertension. All patients received intensified insulin therapy after a structured diabetes treatment and teaching program, and adapted their antihypertensive drug treatment to self-monitored BP values. At recruitment, HbA1c values were 5.8 +/- 0.6%, and remained stable at 6.3 +/- 1.7% after a mean observation period of 27 months. BP pressure decreased from 150 +/- 14/99 +/- 14 mmHg to 130 +/- 17/86 +/- 10 mmHg after 1 year, and to 140 +/- 14/92 +/- 9 mmHg at the last examination, (p less than 0.05). Serum creatinine and creatinine clearance remained stable over the observation period at 165 +/- 56 mumol/L and 0.8 +/- 0.4 ml/s/1.72m2 at recruitment, and 152 +/- 47 mumol/L and 1.0 +/- 0.5 ml/s/1.72m2 at the final examination. Proteinuria decreased from 3.2 to 1.4 g/24 h (p less than 0.05). No patient needed renal replacement therapy.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Near-normotension and near-normoglycemia in blind type I diabetic patients with overt diabetic nephropathy. 215 Dec 31


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