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)

Renal diseases as glomerulonephritis, diabetic nephropathy, interstitial nephritis (e.g. analgetic nephropathy) or systemic disease with renal involvement are responsible for renal hypertension. High blood pressure remains the most important factor for progression of chronic renal failure. On the other hand, effective anti-hypertensive therapy results in inhibition of progression. Clinical and experimental studies show a renoprotective effect of ACE inhibitors due to lowering of systemic blood pressure, reduction of glomerular capillary pressure, reduction of proteinuria and antiproliferative effects.
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PMID:[ACE inhibitors and the kidney]. 892 21

The factors that initiate chronic renal failure in patients with hypertension, diabetes mellitus, and chronic glomerular disease are largely unknown. The likely genetic contribution to ESRD, particularly in African Americans, suggests that linkage analysis may be useful to evaluate the role of candidate genes in the pathogenesis of chronic renal failure. The renin-angiotensin-aldosterone (RAA) axis has been intensively evaluated for its contribution to cardiovascular disease and nephropathy. This study tested for linkage between candidate genes in the RAA axis and chronic renal failure, using 85 African-American sibling pairs (from 65 families) concordant for ESRD. Angiotensinogen was selected because of the putative link between it and mild to moderate essential hypertension and nephrosclerosis; angiotensin-converting enzyme because of its possible contribution to diabetic nephropathy; and renin, the angiotensin II receptor, and kallikrein because of their roles in hypertension and renal perfusion. These candidate loci did not demonstrate linkage to either diabetic or nondiabetic renal disease in this study's collection of sibling pairs. These results suggest that polymorphisms at these RAA axis loci do not make major contributions to the pathogenesis of renal disease in African Americans.
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PMID:Linkage analysis between loci in the renin-angiotensin axis and end-stage renal disease in African Americans. 898 34

Angiotensin converting enzyme (ACE) inhibitors are used widely in the treatment of hypertension and congestive heart failure. An increasing number of patients with chronic renal failure is treated with ACE inhibitors because of their antiproteinuric effect. In patients with diabetic nephropathy ACE inhibitors also slow the progression of renal failure. Direct drug related nephrotoxic effects, like the induction of proteinuria, glucosuria or an interstitial nephritis are rare events. The often observed reduction of the glomerular filtration rate after the induction of an ACE inhibitor therapy is due to the specific intrarenal action of these agents and therefore not an adverse drug reaction.
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PMID:[Renal side effects of angiotensin converting enzyme inhibitors]. 903 83

Mannitol is widely used because of its osmotic diuretic action and its presumed antioxidant properties. In pre-existent renal dysfunction, however, mannitol may accumulate leading to potentially deleterious effects. We describe a 71-year-old woman with moderate chronic renal failure due to diabetic nephropathy who developed acute anuric renal failure after mannitol administration for post-traumatic reflex sympathetic dystrophy. After haemodialysis symptoms of acute renal failure rapidly disappeared with recovery of pre-existent renal function. Daily measurement of the osmolal gap as a simple and accurate way of monitoring patients receiving mannitol infusion is emphasized. A rapid increase in the osmolar gap should prompt adjustment of the dose or even discontinuation of mannitol, especially in the case of pre-existent risk factors.
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PMID:Mannitol-induced acute renal failure. 903 39

Hypertension, diabetes mellitus and chronic glomerular diseases reportedly cause in excess of 80% of the incident cases of end-stage renal disease (ESRD) in the U.S. The factors that initiate progressive renal failure in patients with these disorders remain unknown. Several investigators have reported enhanced synthesis and activity of cytokines in the kidneys of patients with renal failure. The ensuing inflammation and fibrosis have been postulated to contribute to the development of progressive renal failure. There is also abundant evidence supporting the contribution of genetic factors in ESRD susceptibility based upon the strong familial clustering of ESRD, particularly in African Americans. Therefore, genetic linkage analysis may be useful to evaluate the role of candidate genes in several cytokine cascades that could contribute to the pathogenesis of chronic renal failure. We tested for genetic linkage between eight cytokine candidate genes and chronic renal failure in a collection of African American sibling pairs concordant for ESRD. Epidermal growth factor (EGF), platelet-derived growth factor (PDGF), transforming growth factor (TGF) beta 1, TGF-beta 2 and TGF-beta 3, and tumor necrosis factor (TNF)-alpha and TNF-beta candidate genes were selected for analysis due to their putative roles in diabetic renal disease and chronic glomerulonephritis. The interleukin-1 receptor antagonist gene (IL1RN) was also genotyped due to its reported association with diabetic nephropathy. Non-parametric (genetic model independent) affected sib pair linkage analysis was used to evaluate evidence for linkage. In order to genotype TGF-beta 3, we identified four closely linked, previously unidentified, highly polymorphic microsatellite loci near the TGF-beta 3 gene. Linkage of ESRD and transforming growth factor beta 2 polymorphisms on human chromosome 1 approached significance for non-diabetic nephropathy (predominantly chronic glomerular disease, hypertensive nephrosclerosis and unknown etiology) (P = 0.08), but showed no linkage to diabetic nephropathy. The other candidate loci did not demonstrate linkage to ESRD in the total population or in the subgroups with diabetic or non-diabetic etiologies of ESRD. The IL1RN gene did not show significant evidence for linkage to ESRD; however, we did confirm an association between allele 2 of IL1RN and ESRD (as reported in diabetic nephropathy). Overall, these results suggest that these growth factor loci do not make major contributions to the pathogenesis of ESRD in African Americans.
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PMID:Genetic linkage analysis of growth factor loci and end-stage renal disease in African Americans. 906 16

Diabetic nephropathy is one of the most frequent causes of chronic renal failure worldwide. Altogether, 35% of patients with insulin-dependent diabetes mellitus and a somewhat smaller percentage of patients with non-insulin-dependent diabetes mellitus ultimately develop diabetic kidney disease. Early diagnosis is of utmost importance since the development of diabetic nephropathy affects the general health, the carbohydrate metabolism of the patient, moreover it aggravates hypertension and accelerates atherosclerosis. Microalbuminuria is a sensitive but relatively late marker of diabetic kidney disease. Still, screening of diabetic patients for microalbuminuria is of great importance since there is no other screening test capable of diagnosing diabetic nephropathy at an earlier stage. The description of the genetic substrate of susceptibility to diabetic kidney disease would revolutionize the diagnosis and prevention of diabetic nephropathy. Until then, compliance with therapeutic guidelines outlined in milestone clinical studies of the last years may significantly decrease morbidity, the progression of, and the mortality associated with diabetic kidney disease.
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PMID:[Current issues in the diagnosis and therapy of diabetic nephropathy]. 907 51

Patients with any of four different types of chronic renal failure (CRF) (glomerular disease, interstitial nephritis, diabetic nephropathy, or polycystic disease) were observed using sequential determinations of glomerular filtration rate (GFR). Those whose GFR showed progression were either given ketoconazole 200 to 600 mg/d (to suppress cortisol production) plus prednisone 2.5 mg/d (to prevent anterior pituitary escape) and observed with the use of more GFRs, or were observed while four additional GFRs were determined before starting these drugs; some patients were subsequently withdrawn from these drugs and were observed using more GFRs. The effect of these drugs on rate of progression was estimated by a linear spline technique, using observations before, during, and (when available) after treatment. In 20 patients, sufficient data were obtained to estimate the magnitude of this effect. In seven patients with chronic glomerular disease, progressing at -0.62 +/- 0.12 mL/min/mo, progression slowed by 66% +/- 12% (P < 0.01). In five patients with interstitial nephritis of various etiologies, progressing at -1.19 +/- 0.34 mL/min/mo, progression slowed by 55% +/- 27% (P < 0.05). In five diabetic patients progressing at -1.22 +/- 0.14 mL/min/mo, progression slowed by an average of 77% +/- 14% (P < 0.01). In contrast, in four patients with polycystic kidney disease, progression accelerated by 99% +/- 63%. Mean urinary steroid excretion decreased significantly; plasma corticotropin did not increase. Neither proteinuria nor serum lipid levels changed. Urinary nitrate excretion decreased significantly, but serum nitrate did not change. Blood pressure decreased slightly (4.3 mm Hg). Three patients developed transiently elevated serum transaminase levels; two others withdrew because of side effects. We conclude that in chronic glomerular disease, diabetic nephropathy, and interstitial nephritis, this combination of drugs is as safe as ketoconazole in the absence of renal disease and shows promise of slowing progression. In polycystic kidney disease, it is apparently ineffective or harmful.
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PMID:Effect of ketoconazole plus low-dose prednisone on progression of chronic renal failure. 910 38

France occupies second position among industrial countries for the number of patients with chronic renal failure. The incidence of chronic renal failure is 61 per million of inhabitants, and increases by 10 to 20% each year. One third of patients with CRF are renal transplant recipients, while 6% of the remaining patients are treated by chronic ambulatory peritoneal dialysis, 6% by domiciliary haemodialysis and 57% by haemodialysis in a dialysis centre or autodialysis. The mean age of management of patients with end-stage chronic renal failure is 59 years. The role of glomerulonephritis and chronic pyelonephritis appears to be decreasing, but the incidence of diabetic nephropathy has doubled over the last decade. The mean age of transplant recipients is 45 years. The number of transplantations has regularly decreased over several years due to the lack of organs. Chronic renal failure patients essentially die from cardiovascular causes, and the frequency of malignant disease responsible for death is estimated to be 10%.
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PMID:[Epidemiologic aspects of terminal chronic kidney failure and its therapeutic modalities]. 910 13

The aim of the study was to answer the questions: 1) does the prolactin secretion in the TRH test (0.4 mg i.v.) differ in haemodialyzed patients with diabetes nephropathy in the end stage renal failure in comparison to haemodialyzed chronic renal failure patients with non-diabetic nephropathy and healthy subjects; 2) does the opiate receptors blockade with naloxone (2 mg i.v.) modify the prolactin secretion during the TRH test in those patients. 39 subjects were studied. The patients were divided into three groups: group I: 12 haemodialyzed patients with IDDM and diabetic nephropathy in the end stage renal failure, group II: 15 haemodialyzed chronic renal patients with non-diabetic nephropathy and the control group: 12 healthy persons. The basic prolactin secretion and area over basic value (AOBV) of the prolactin were estimated. Prolactin concentration was measured by LIA. 1) The basic prolactin secretion was significantly higher in the patients with chronic renal failure. 2) The basic prolactin secretion in IDDM patients with diabetic nephropathy in the end stage renal failure treated with haemodialysis was significantly lower than in haemodialyzed patients with chronic renal failure of non-diabetic etiology. 3) TRH and TRH with naloxone caused significant increase of prolactin secretion in all investigated groups, but the increase is significantly lower in chronic renal failure patients than in healthy subjects. 4) Naloxone decreases significantly the prolactin secretion during TRH test only in haemodialyzed patients with chronic renal failure of non-diabetic etiology.
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PMID:[Effects of opiate receptor blockade with naloxone on prolactin (PRL) secretion in patients with diabetes type I (IDDM) with chronic renal failure treated with hemodialysis (HD)]. 912 1

Erythropoietin (EPO) is reported to be mainly produced by renal peritubular interstitial cells. Serum levels of EPO may provide new information on the tubulointerstitial lesions in patients with diabetic nephropathy. We determined EPO, hemoglobin (Hb), and Hb x EPO in 63 diabetic patients who showed normo-, micro- or macroalbuminuria with normal or reduced renal function (creatinine clearance, Ccr, > or = 60 ml/min or < 60 ml/min). In addition, we followed up Ccr during a mean of 26 months in 13 patients with overt nephropathy and normal renal function. The following results were obtained: (1) Hb, EPO, and Hb x EPO values gradually decreased along with advancing stages of nephropathy, and (2) 6 patients with rapidly decreasing renal function showed significantly lower initial EPO and Hb x EPO values than 7 patients without it (p < 0.01). We conclude that EPO and Hb x EPO values may be a new marker predicting future chronic renal failure in diabetic overt nephropathy.
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PMID:Serum levels of erythropoietin as a novel marker reflecting the severity of diabetic nephropathy. 912 29


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