Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0028754 (obesity)
 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Measurement of glomerular filtartion rate (GFR) is crucial for the detection and follow-up of an early renal impairment. Inulin clearance or radio-isotopes are the gold standard but they cannot be used routinely. Serum creatinine and creatinine clearance are the most widely used, but they lack sensibility to detect an early renal impairment and in cases of obesity, malnutrition or advanced age. Looking for a more reliable marker is necessary and cystatin C seems to be interesting. This molecule is constantly produced by nucleated cells, then freely filtrated and catabolized in the proximal tube. Clinical studies showed that cystatin C might be a more reliable marker of GFR in determined groups of patients. Moreover this molecule may have an other interest as a predictive risk factor or mortality, especially for cardiovascular events.
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PMID:[Could cystatine C replace creatinine as a market of glomerular filtration rate?]. 1656 1

The metabolic syndrome, which is characterized by obesity, serum lipid profile alterations, hypertension, and fasting hyperglycemia, is very common in developed countries, and its prevalence is likely to increase. Chronic kidney disease (CKD) also has become a significant public health problem because it affects a considerable proportion of the adult population and is a major risk factor for cardiovascular disease and premature death. Although it is widely known that the metabolic syndrome is a major risk factor for the development of type 2 diabetes and cardiovascular disease, its precise relationship with the risk for renal impairment only recently has been clarified: Patients with the metabolic syndrome are at significantly higher risk for microalbuminuria and/or CKD, and the level of risk is related to the number of components of the syndrome itself. Although it is difficult to discriminate the detrimental renal effects of the metabolic syndrome from those of hypertension and impaired glucose metabolism, its other aspects (particularly obesity) may favor independently the development of renal abnormalities and may be considered new modifiable risk factors for CKD. These observations provide a rationale for intervention studies that aim to verify whether treating the many components of the metabolic syndrome can effectively prevent the development and progression of renal damage.
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PMID:Renal manifestations in the metabolic syndrome. 1656 54

A young male presented in the Nephro-Urology Department with advanced renal failure, blindness in early childhood, polydactaly, obesity, decreased mentation and hypogonadism. With these phenotypical features and renal ultrasonographic findings, he was diagnosed as a case of Bardet-Biedl syndrome. Only one younger sister of patient had similar features. Renal impairment is frequent and an important cause of death. End stage renal disease (ESRD) is rarely seen in younger patient of Bardet-Biedl syndrome. However, ESRD in early age is associated with substantially reduced survival.
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PMID:Bardet-Biedl syndrome presenting with end stage renal failure. 1682 64

This report describes the case of a 57-year-old man who underwent a repeated renal biopsy 25 years after the first biopsy in which the diagnosis of IgA nephropathy was made. Although the patient exhibited gradually increasing proteinuria and a slowly progressive renal impairment, the histological findings of the repeat biopsy revealed no evidence of either glomerular inflammatory changes or IgA deposition. Instead, a marked decrease in the glomerular density and hypertrophy of the remnant glomeruli were noted. Almost a complete disappearance of urinary protein excretion by a calorie-restricted diet indicated that the patient's obesity and its related factors may have contributed to the present nephropathic development.
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PMID:Obesity-related nephropathy associated with a history of IgA nephropathy. 1882 22

The incidence of obesity-related nephropathy (ORG) is increasing with the growing incidence of obesity. ORG is associated with morbid obesity, proteinuria and renal biopsy findings of focal global and segmental glomerulosclerosis (FSGS), which can be associated with significant renal impairment. Weight reduction is associated with improvement of ORG, however, conservative measures aiming at long-term weight reduction are difficult to achieve. Bariatric surgery is the most effective way of achieving long-term weight reduction. We present a case of ORG with nephrotic-range proteinuria and FSGS on renal biopsy. Following bariatric surgery, patient achieved successful weight reduction with significant decrease in proteinuria and stabilization of renal function.
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PMID:Resolution of nephrotic syndrome after successful bariatric surgery in patient with biopsy-proven FSGS. 1920 53

As outcomes after liver transplant surgery continue to improve, management of the long-term consequences of the procedure and the associated immunosuppression become increasingly important. Liver allograft recipients have, compared with age and sex-matched controls, increased risk for cardiovascular and cerebrovascular events and death, for bone disease, and for some cancers. Early recognition and treatment of modifiable risk factors, especially of hypertension (present in up to 77% recipients), diabetes (in up to 22%), obesity (up to 40%), renal impairment (in up to 50%), and hyperlipidemia (in up to 66%) are necessary to maintain prolonged and healthy survival. Early recognition of de novo cancers (which occur in up to 26% recipients) indicates the need for additional monitoring for skin cancer and lymphoproliferative disorders, as well as cancers of the lung, colon, and upper gastrointestinal track. Early recognition of bone disease and appropriate intervention will allow introduction of strategies to reduce bone fracture. In this article, we review the evidence for the extent and treatment of these modifiable conditions in the allograft recipient.
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PMID:Long-term care of the liver allograft recipient. 1923 63

Bardet-Biedl Syndrome (BBS) is an autosomal recessive, multisystem, genetically heterogeneous, ciliopathic condition caused by mutations in multiple genes. Here we sought to determine if inheritance of a single BBS mutation increased the risks of frequent disorders of this syndrome such as obesity, hypertension, and diabetes. Various metabolic and renal diseases in a cohort of 46 patients with BBS, prospectively followed for up to 28 years, were compared to recent assessments of these factors in 96 relatives with a heterozygote mutation (carriers) and 37 relatives without a contributing mutation (non-carriers). Ten mutations in 6 genes causing this syndrome were identified in 21 families from whom DNA was obtained. The body mass index or the incidences of hypertension, diabetes, or stage 3 chronic kidney diseases were found to be similar between carriers and non-carriers but were all significantly less than those of family members with BBS. Similarly, the median age of onset of hypertension or diagnosis of stage 3 kidney disease, or the diagnosis of diabetes by age 70 were all significantly lower in those with BBS than in gene carriers or non-carriers. While our study shows that metabolic and renal events occurred frequently and at an early age in BBS, the heterozygous inheritance of any of the 10 described BBS mutations did not predispose family members to obesity, diabetes, hypertension, or renal impairment.
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PMID:Autosomal recessive Bardet-Biedl syndrome: first-degree relatives have no predisposition to metabolic and renal disorders. 1936 29

Telavancin is a lipoglycopeptide derivative of vancomycin. Similar to vancomycin, it demonstrates activity in vitro against a variety of Gram-positive pathogens, including but not limited to methicillin-resistant Staphylococccus aureus (MRSA) and penicillin-resistant Streptococcus pneumoniae (PRSP). Modifications to vancomycin's structure expanded telavancin's spectrum of activity in vitro to include organisms such as glycopeptide-intermediate S. aureus (GISA), vancomycin-resistant S. aureus (VRSA) and vancomycin-resistant enterococci (VRE). However, the clinical implications of this are currently unknown. Similar to other glycopeptides, televancin binds to the D-alanyl-D-alanine (D-Ala-D-Ala) terminus in Gram-positive organisms, resulting in inhibition of bacterial cell wall synthesis. In addition, telavancin causes depolarization of the bacterial cell membrane and increased membrane permeability. The resulting activity in vitro is rapidly bactericidal and concentration dependent, with the ratio of area under the time concentration curve to minimum inhibitory concentration (AUC/MIC) as the best predictor of activity in animal models to date. In humans, telavancin exhibits a pharmacokinetic profile that permits once-daily intravenous administration. Doses of 7.5 and 10 mg/kg/day have been studied in clinical trials. The need for dosage adjustments based on age, gender and obesity appear unnecessary. In addition, moderate hepatic impairment does not appreciably alter the pharmacokinetics of the drug. Because telavancin is extensively cleared by the kidneys, dosage adjustments will be required in patients with moderate to severe renal impairment. Published phase II and III clinical trials have shown telavancin to be comparable to standard therapy for the treatment of complicated skin and soft tissue infections. Clinical trials in the treatment of S. aureus bacteremia and hospital-acquired pneumonia are under way. Adverse effects overall appear to be mild and reversible, with taste disturbance, foamy urine, headache, procedural site pain, nausea and vomiting being the most commonly reported. However, renal toxicity was reported more frequently with telavancin than with vancomycin in two phase III clinical trials (3% versus 1%). Prolongation of the corrected QT (QTc) interval has been more common with telavancin than comparator agents, but no clinically significant electrocardiogram (ECG) changes or cardiac abnormalities have been observed to date. Although human pregnancy data is not currently available, animal data revealed limb malformations that were possibly related to telavancin therapy. Therefore, the potential teratogenicity of this agent must be considered in women who are pregnant or may become pregnant.
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PMID:Telavancin: a new lipoglycopeptide for gram-positive infections. 1943 39

OBJECTIVE Most diabetic patients with impaired renal function have a urinary albumin excretion rate in the normal range. In these patients, the etiology of renal impairment is unclear, and it is also unclear whether this nonalbumunuric renal impairment is unique to diabetes. RESEARCH DESIGN AND METHODS In this study, we examined the frequency and predictors of nonalbumunuric renal impairment (estimated glomerular filtration rate [eGFR] <60 ml/min per 1.73 m(2)) in a nationally representative cohort of 3,893 patients with type 2 diabetes and compared our findings with rates observed in the general population from the Australian Diabetes, Obesity and Lifestyle Study (AusDiab) survey (n = 11,247). RESULTS Of the 23.1% of individuals with type 2 diabetes who had eGFR <60 ml/min per 1.73 m(2) (95% CI 21.8-24.5%), more than half (55%) had a urinary albumin excretion rate that was persistently in the normal range. This rate of renal impairment was predictably higher than that observed in the general population (adjusted odds ratio 1.3, 95% CI 1.1-1.5, P < 0.01) but was solely due to chronic kidney disease associated with albuminuria. In contrast, renal impairment in the absence of albuminuria was less common in those with diabetes than in the general population, independent of sex, ethnicity, and duration of diabetes (0.6, 0.5-0.7, P < 0.001). CONCLUSIONS Nonalbuminuric renal impairment is not more common in those with diabetes. However, its impact may be more significant. New studies are required to address the pathogenesis, prevention, and treatment of nonalbuminuric renal disease.
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PMID:Nonalbuminuric renal impairment in type 2 diabetic patients and in the general population (national evaluation of the frequency of renal impairment cO-existing with NIDDM [NEFRON] 11). 1947 Aug 39

We studied the effects of exercise training in treating renal impairment due to hypertension and obesity in rats. Diet-induced obese and non-obese Wistar rats were assigned to four groups: Sed-Ob, Ex-Ob, Sed-C, and Ex-C (motor treadmill for 13 weeks; Ex=exercise-trained, C=control, Ob=obese, Sed=sedentary). Creatinine, proteinuria, and kidney structure were evaluated. Sed-C rats had normal and stable blood pressure (BP), while Sed-Ob rats developed hypertension. After 4 weeks of exercise, BP decreased in exercise-trained groups (less than 25% at the end of the experiment in obese rats, and less than 10% in non-obese rats). Both the body mass and retroperitoneal fat mass were lower in the exercise-trained groups than in the sedentary ones. Serum creatinine was not different among the groups, but the urinary protein excretion was significantly higher in the Sed-Ob group than in the matched non-obese group. Compared to the non-obese animals the mean glomerular volume increased by 45% in Sed-Ob rats and by 30% in Ex-Ob rats. Obese animals also showed increased mesangial volume density compared to non-obese animals. The present findings allow us to conclude that the exercise training could be an auxiliary practice to attenuate renal alterations seen in diet-induced obesity.
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PMID:Exercise counters diet-induced obesity, proteinuria, and structural kidney alterations in rat. 2009 56


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