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)

There is little data on the spectrum of renal diseases in the United Arab Emirates. A renal diseases registry has been set up in an attempt to address this issue nationwide, and we report here the first outcome of this endeavor, a retrospective histopathologic analysis of 490 native kidney biopsies performed on adult patients presenting to four hospitals in the Emirate of Abu Dhabi from 1978 to June 1996. The most common indication for a biopsy was the nephrotic syndrome (54.0%), followed by asymptomatic urinary abnormalities (29.7%), and chronic renal failure (12.7%). Primary glomerular disease accounted for 77.1% of all biopsies. Chronic proliferative glomerulonephritis as a group was the predominant pathology (36.2%), followed by idiopathic membranous glomerulopathy (20.1%), focal segmental glomerulosclerosis (18.3%), minimal change nephropathy (18.3%), and IgA nephropathy (6.3%). Of the patients with secondary kidney diseases, 33 (40.7%) had systemic lupus erythematosis, 27 (33.3%) amyloidosis, 14 interstitial nephropathy, and seven diabetic nephropathy. Kidney biopsies of 187 patients with primary glomerular disease who presented with the nephrotic syndrome were analyzed. In this group idiopathic membranous glomerulopathy, proliferative glomerulonephritis, and minimal change glomerulopathy was found in almost equal proportions (28.3%, 26.6%, 26.2%) with focal segmental glomerulosclerosis (15.4%) accounting for the bulk of the remainder. Though the overall results of this analysis do not show any major differences in the spectrum of primary glomerulopathies in the United Arab Emirates compared with other countries, a slight tendency towards a higher frequency of focal segmental glomerulosclerosis among patients indigenous to the Arabian Peninsular (20.4%) deserves further evaluation.
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PMID:Analysis of 490 kidney biopsies: data from the United Arab Emirates Renal Diseases Registry. 965 Jan 23

Diabetic nephropathy has become, one of the most frequent causes of chronic renal failure in the industrialized countries. Basic and clinical research aimed at the clarification of the pathogenesis of diabetic kidney disease is of utmost importance. The role of non-enzymatic glycosylation, the polyol cycle, oxidative stress, various hormones and cytokines in the development of diabetic nephropathy is very likely. However, there is still no unifying concept about the relative importance and interaction of these factors. This paper reviews the most important directions and results of basic research centering on diabetic kidney disease. The coming years will likely bring the elaboration of a detailed theory of the pathogenesis and an even tighter coordination of basic and clinical research.
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PMID:[Current questions concerning the pathomechanism of diabetic nephropathy]. 967 19

Nephropathy is a frequent complication of long-term diabetes. Strong evidence exists that genetic predisposition plays a major role in the development of diabetic nephropathy. The role of the angiotensin I-converting enzyme gene (ACE) in the susceptibility to nephropathy in diabetes, especially in non-insulin dependent diabetes mellitus (NIDDM), remains unclear. This study examines the association of two ACE polymorphisms: a 287-bp insertion/deletion (I/D) in intron 16 and PstI (A/G substitution in intron 7; alleles P/M) with renal complications in 941 NIDDM patients. From this group, for further analysis 127 patients were selected with overt proteinuria or chronic renal failure, 335 patients with microalbuminuria, and a control group of 254 normoalbuminuric patients with a diabetes duration of at least 10 yr. No significant differences in the distribution of ACE I/D and PstI genotypes or allele frequencies were observed between the examined groups. The results of this study strongly suggest that there is no association between the ACE gene I/D and PstI polymorphisms and nephropathy in NIDDM.
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PMID:Angiotensin I-converting enzyme gene polymorphisms: relationship to nephropathy in patients with non-insulin dependent diabetes mellitus. 972 75

Blockade of the renin-angiotensin system with angiotensin-converting enzyme (ACE) inhibitors is now recognized as an effective approach for the treatment of hypertension and congestive heart failure. In addition, ACE inhibitors are very effective for the prevention of chronic renal failure. Today, it is possible to antagonize the effects of angiotensin II more specifically using AT1 receptor antagonists. Several non-peptide, orally active angiotensin II receptor antagonists have recently been developed clinically. These new molecules are as effective as ACE inhibitors, calcium antagonists and beta-blockers at reducing blood pressure in hypertensive patients. Furthermore, they appear to have similar systemic and renal hemodynamic properties in patients with congestive heart failure and renal diseases. Now, several large clinical trials such as the LIFE, the RENAAL and the ELITE II studies are under way to investigate the long-term benefits of one of these compounds in hypertension, heart failure and type II diabetic nephropathy.
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PMID:[Angiotensin II AT1 receptor antagonists: clinical development and future perspectives]. 977 27

Late rearrangement products that accumulate by glycation of proteins, known as advanced glycation end products (AGEs), have been implicated in the pathogenesis of complications related to diabetes. Circulating AGEs, especially in the form of a small peptide (AGE-peptide) of less than 10 kd, increase in the blood of diabetic patients with end-stage renal disease (ESRD). The aim of the study was to evaluate AGE-peptide levels by measuring AGE-specific fluorescence (excitation at 370 nm and emission at 440 nm) and to examine the relationship between AGE-peptide and diabetic nephropathy. AGE-specific fluorescence in serum and urine were examined in diabetic subjects with various levels of renal complications of varying severity: normoalbuminuria (N), microalbuminuria (Mi), macroalbuminuria (Ma), chronic renal failure (C), and hemodialysis (HD). We also assessed correlations among the AGE-peptide level and age, duration of diabetes, hemoglobin A1c (HbA1c), serum creatinine, and creatinine clearance. Serum and urine AGE-peptide levels in C and HD were significantly higher than in N, Mi, and Ma. Serum AGE-peptide levels were significantly correlated with serum creatinine (r=.866, P < .0001) and creatinine clearance (r=-.720, P < .0001) but not with duration of diabetes or age. There was a significant correlation between AGE-peptide levels measured by enzyme-linked immunosorbent assay (ELISA) and levels determined from the specific fluorescence intensity (r=.688, P < .0001). These findings suggest that renal function may play a greater role in the accumulation of AGEs than persistent hyperglycemia in diabetic patients. Measurement of AGE-specific fluorescence (ie, AGE-peptide) may serve as a simple and useful test to assess circulating AGE levels and monitor AGE excretion.
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PMID:Specific fluorescence assay for advanced glycation end products in blood and urine of diabetic patients. 982 11

Since the discovery at the end of the seventies of angiotensin converting enzyme inhibitors (ACEI), numerous clinical data became available in the indications for which these agents were initialy developed, taking into account the putative role of renin angiotensin system: first in severe hypertension, secondly in moderate hypertension and then in heart failure. At the same time, an increasing interest was raised for "evidence based medicine" leading to a change in clinical study design: from clinical documentation of effects based on intermediate end points such as blood pressure, serum lipids, serum electrolytes or physical training capabilities to clear demonstrations through double blind placebo controlled trial with a positive effect on morbi-mortality. This evolution was furthermore stimulated by advances of knowledge on physiopathological mechanisms as well as the emergence of new drugs within this therapeutic class both stimulating clinical research. In that prospective, three examples are obvious: treatment of myocardial infarction, slowing down of the progression of diabetic nephropathy and of chronic renal failure. All these new indications for ACEI were obtained though large morbi-mortality clinical studies which are reviewed in this article. Finally, clinical studies are running with ACEI in order to demonstrate a possible effect on primary or secondary prevention of cardiovascular morbi-mortality in high risk populations results which should be available at the beginning of the next century.
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PMID:[Conversion enzyme inhibitors against the progression of renal and vascular diseases: yes but again]. 985 84

We examined serum and urinary cytokeratin 19 fragment (CYFRA 21-1) levels in patients with diabetic nephropathy as a model of chronic renal failure, to investigate the mechanism of increased serum CYFRA 21-1 levels in chronic renal failure. Serum and urinary CYFRA 21-1 levels in non-insulin-dependent diabetes mellitus (NIDDM) patients with abnormal urinary immunoglobulin G (IgG) levels (>1.1 mg/g x Cr, n=126) were higher than those with normal urinary IgG levels. In NIDDM patients with normal urinary IgG levels (n=81); the urinary albumin or transferrin levels were not related to serum or urinary CYFRA 21-1 levels. We speculate that the increased serum CYFRA 21-1 levels contribute to metabolic abnormality in the kidney itself rather than the decreased urinary excretion per se, and that increased urinary CYFRA 21-1 levels are found in advanced cases of diabetic nephropathy with destruction of the size barrier.
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PMID:Mechanism of increased serum cytokeratin 19 fragment levels in patients with diabetic nephropathy as a model of chronic renal failure. 986 51

Thirty-two patients with diabetes mellitus (22 IDDM and 10 NIDDM, 21 males and 11 females, age 44+/-11.8 years) were followed for 5.2+/-3.8 years after the onset of chronic renal failure, with the aim of evaluating the effect of low protein diets on the rate of decline of the residual renal function. During the 1.8+/-1.6 year follow-up period on free or uncontrolled low protein diet the mean rate of decline of creatinine clearance was 0.9+/-0.6 ml/min/month, significantly greater than that observed during 3.7+/-3.1 years on low or very low protein diets. The reduction of protein intake was followed by a significant decrease in daily urinary protein loss. A better glycaemic control was obtained on the low protein diet, and the daily insulin requirement decreased. The anthropometry, as well as the serum concentrations of rapid turnover proteins, did not change, in spite of the low or very low protein dietary supply for a long duration. The values of mean arterial pressure were quite similar during the follow-up period on free or uncontrolled low protein diet and during the study period on the low protein diet. A good compliance with reduced dietary intake (as demonstrated by the measurement of the daily urea excretion) was obtained in a large number of patients. In conclusion, our study confirms the protective effect on the residual renal function of low protein diets in IDDM and NIDDM patients with chronic renal failure due to diabetic nephropathy, in the absence of any sign of protein malnutrition.
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PMID:Dietary treatment of diabetic nephropathy with chronic renal failure. 987 Apr 26

The course of chronic renal failure is generally progressive and mediated by several factors that operate in combination. Several extrarenal events which may cause transient or permanent deterioration of renal function, are important, because their correction may slow the progression of renal disease e.g. volume disorders, infection, nephrotoxic agents. In progression of chronic renal disease leading factors are hypertension, proteinuria and high protein/phosphorus intake. Number of evidence suggests that ameliorating hypertension, reducing proteinuria slow the progression of chronic renal failure. Clinical studies in diabetic nephropathy demonstrated that the renoprotective effect of ACE inhibitors was independent of their effect of systemic blood pressure. In ESRD patients access for renal replacement therapy should be obtained as early as possible. An A-V fistula may take several weeks to mature especially in diabetic or elderly patients. Early dialysis has been advocated in diabetic patients. In general, patients can start ESRD therapy when residual kidney function drops to 5-10% of normal value. High quality of dialysis should be provided to the uremic patient with respect of successful renal transplantation.
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PMID:[Current therapy of chronic renal failure]. 987 58

One of the most important characteristics of chronic renal failure (CRF) is its progression to end stage renal disease. CRF progression depends of many factors indicated in numerous experimental and clinical studies. The present study was undertaken with the aim to examine the role of sex, etiology of CRF, renal function at the beginning of the study, hypertension and protein intake on CRF progression. Ninety-two patients (47 female and 45 male) aged between 17 and 70, with various underlying kidney diseases and various degrees of CRF were followed for 8 years. CRF progression was expressed as Creatinine clearance (CCr) and reciprocal values of serum Creatinine (SCr) against time. CRF progression was slower in women than in men, but not significantly. Patients with diabetic nephropathy (b = 0.00006) and glomerulonephritis (b = 0.00005) had faster progression of CRF than patients with nephrosclerosis (b = 0.00002), tubulointerstitial nephritis (b = 0.00003) and polycystic kidney disease (b = 0.00003). The fastest progression of CRF was in patients with the lowest SCr values at the beginning of the study. Proper regulation of blood pressure was the most important factor in slowing down CRF progression, independently of kind of antihypertensive drugs. Neither angiotensin converting enzyme inhibitors (b = -0.00001) nor calcium channel blockers (b = -0.00002) showed better effects on CRF progression slowing down in comparison with other antihypertensive drugs (b = -0.00001). Low protein diet slowed down CRF progression, but not significantly. In conclusion, our retrospective study confirms that CRF progression depends on sex, underlying renal diseases and serum Creatinine levels at the beginning of the study. Good regulation of blood pressure and low protein diet can slow down CRF progression.
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PMID:Analysis of factors influencing chronic renal failure progression. 1008 78


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