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)

CBS domains are defined as sequence motifs that occur in several different proteins in all kingdoms of life. Although thought to be regulatory, their exact functions have been unknown. However, their importance was underlined by findings that mutations in conserved residues within them cause a variety of human hereditary diseases, including (with the gene mutated in parentheses): Wolff-Parkinson-White syndrome (gamma 2 subunit of AMP-activated protein kinase); retinitis pigmentosa (IMP dehydrogenase-1); congenital myotonia, idiopathic generalized epilepsy, hypercalciuric nephrolithiasis, and classic Bartter syndrome (CLC chloride channel family members); and homocystinuria (cystathionine beta-synthase). AMP-activated protein kinase is a sensor of cellular energy status that is activated by AMP and inhibited by ATP, but the location of the regulatory nucleotide-binding sites (which are prime targets for drugs to treat obesity and diabetes) was not characterized. We now show that tandem pairs of CBS domains from AMP-activated protein kinase, IMP dehydrogenase-2, the chloride channel CLC2, and cystathionine beta-synthase bind AMP, ATP, or S-adenosyl methionine,while mutations that cause hereditary diseases impair this binding. This shows that tandem pairs of CBS domains act, in most cases, as sensors of cellular energy status and, as such, represent a newly identified class of binding domain for adenosine derivatives.
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PMID:CBS domains form energy-sensing modules whose binding of adenosine ligands is disrupted by disease mutations. 1472 9

Morbidity and mortality rates from heart diseases are highly represented in geriatric-aged patients, but these patients also have supporting diseases. Acute coronary syndrome includes unstable angina and acute myocardial infarction with and without ST elevation. The aim of this study was to make a retrospective morbidity analysis of patients admitted to the emergency department. The study is made for a period of three years (from 1998 to 2000). It includes 588 patients divided by age (395 were 65-75 years old; 193 were older than 75 years) and sex (there were 326 men and 262 women). Comorbidity and mortality were investigated. Patients with one, two, three, and more than three supporting diseases were 6.29%, 23.13%, 68.53%, and 2.04%, respectively, of the total number. The most frequent geriatric patients had heart failure, followed by endocrinological diseases (type 2 diabetes, obesity, struma), neurological diseases (insultus, paresis), and chronic kidney diseases (pielonephritis, nephrolithiasis). The combination of hypertension, heart failure, and type 2 diabetes had the highest comorbidity frequency. The mortality rate for 1998 was 8.81%, for 1999 7.74%, and for 2000 13.41%. The mortality rate at the first 12 hours at the beginning of the acute coronary syndrome was 66.6%. Geriatric patients suffer from many diseases, and at the beginning of the onset of acute coronary syndrome they have multiorganal failure. Elderly patients are a high-risk contingent in intensive coronary care units.
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PMID:Acute coronary syndrome, comorbidity, and mortality in geriatric patients. 1524 1

High-protein (HP) weight-loss diets have existed in the United States for decades, although their popularity has recently surged as obesity has become more common. Despite their widespread use, valid concerns exist that HP diets may induce clinically important alterations in renal function and health. HP consumption has been found, under various conditions, to lead to glomerular hyperfiltration and hyperemia; acceleration of chronic kidney disease (CKD); increased proteinuria; diuresis, natriuresis, and kaliuresis with associated blood pressure changes; increased risk for nephrolithiasis; and various metabolic alterations. Unfortunately, a comprehensive understanding of the implications of HP diets is limited by the lack of a universally accepted definition for HP intake, a paucity of rigorous long-term human interventional studies that necessitate relying on short-term or fairly circumstantial evidence, and sparse data on the effects of HP consumption in obese individuals. In addition, matters are further complicated because the renal impact HP diets for limited periods is most likely different than that for more chronic consumption. Nevertheless, although there are no clear renal-related contraindications to HP diets in individuals with healthy kidney function, the theoretical risks should be reviewed carefully with the patient. In contrast, HP diets have the potential for significant harm in individuals with CKD and should be avoided if possible. Because CKD is often a silent disease, all individuals should undergo a screening serum creatinine measurement and urinary dipstick test for proteinuria before the initiation of such a diet.
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PMID:High-protein diets: potential effects on the kidney in renal health and disease. 1555 17

A total of 684 patients who had not been diagnosed with renal cyst but had undergone abdominal ultrasonography for various reasons were evaluated. Patients with and without renal cyst were classified into two groups and were compared in terms of hypertension (HT), hyperlipidemia (HL), diabetes mellitus (DM) and obesity (body mass index: > or = 30 kg/m2) prevalence. Although 94 patients (13.7%) were established with a renal cyst, 590 patients (86.3%) did not have a renal cyst. The mean age of the patients established with a simple renal cyst was 67.3 +/- 12.1 years (range: 28-82 years); 54 (57.4%) of them were women and 40 (42.6%) were men. Of the patients established with a simple renal cyst, 64 (68.1%) had HT, 40 (42.6%) had DM, 20 (21.3%) had HL, 42 (44.7%) were obese, 18 (19.1%) had nephrolithiasis, and 6 (6.4%) had urinary tract infection. Of the patients without a cyst, 272 (46.1%) had DM, 212 (35.9%) had HT, 122 (20.7%) had HL, and 96 (16.3%) were obese. HT and obesity were significantly higher in patients with a renal cyst when compared with those without a cyst. However, although HL incidence was higher in patients with a cyst, the difference was not significant statistically. HT, HL, and obesity are more prevalent in patients with a renal cyst when compared with patients without. Consequently, patients with a simple renal cyst should be evaluated and followed up in terms of atherosclerotic risk factors.
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PMID:Simple renal cyst prevalence in internal medicine department and concomitant diseases. 1653 73

Excess body weight may be associated with various functional/structural lesions of the kidney. The spectrum ranges from glomerulomegaly with or without focal or segmental glomerulosclerosis, to diabetic nephropathy, to carcinoma of the kidney and nephrolithiasis. The first sign of renal injury is microalbuminuria or frank proteinuria, in particular in the presence of hypertension. The occurrence of microalbuminuria and/or chronic kidney insufficiency (glomerular filtration rate < 60 mL/min/1.73 m2) is related to the increasing number of components of the metabolic syndrome, ie, central obesity, elevated fasting blood glucose level, hypertriglycerides, low high-density lipoprotein cholesterol, and hypertension. In the long run, end-stage renal failure may develop. An increased body mass index is particularly harmful in patients with reduced renal functional mass (unilateral renal agenesis or nephrectomy) and other renal diseases (immunoglobulin A nephritis and chronic graft dysfunction after kidney transplantation). In the pathogenesis of obesity-associated glomerulopathy, hyperfiltration is of fundamental importance. The factors involved are energy intake (high protein and salt), hyperinsulinemia, and enhanced tubuloglomerular feedback because of increased sodium reabsorption. The adrenergic and renin-angiotensin-aldosterone systems as well as glucocorticoids are stimulated. In addition, several active proteins generated in the central adipose tissue, such as leptin, proinflammatory cytokines, plasminogen activator inhibitor-1, angiotensinogen, and growth factors (transforming growth factor-beta1), as well as low levels of the protective adiponectin, may contribute to renal injury. Of greatest importance is the development of hypertension and of diabetes, which are directly related to the severity of central obesity. Obesity-associated renal disease should be prevented or retarded by weight reduction following lifestyle modification (salt restriction, hypocaloric diet, aerobic exercise), or eventually by antiobesity medication or bariatric surgery. In the presence of glomerulopathy and/or hypertension, angiotensin converting enzyme inhibitors or angiotensin II type I receptor blockers are the drugs of choice to improve glomerular hyperfiltration.
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PMID:Renal disease in obesity: the need for greater attention. 1682 23

Obesity and being overweight are risk factors for kidney diseases. The spectrum ranges from glomerulomegaly with or without focal or segmental glomerulosclerosis, to diabetic nephropathy, to carcinoma of the kidney and nephrolithiasis. The first sign of renal injury is microalbuminuria or frank proteinuria, in particular in the presence of hypertension. The occurrence of microalbuminuria and/or chronic kidney insufficiency (glomerular filtration rate < 60 ml/min/1.73 m(2)) is related to the increasing number of components of the metabolic syndrome; that is, central obesity, elevated fasting blood glucose level, hypertriglycerides, low high-density lipoprotein cholesterol level and hypertension. Obesity-associated renal disease should be prevented or retarded by weight reduction following lifestyle modification (salt restriction, hypocaloric diet, aerobic exercise) or eventually by antiobesity medication or bariatric surgery. Rimonabant, a new antiobesity medication, showed beneficial potential effect in treating clusters of metabolic syndrome, which may ultimately suggest potential benefit in treating obesity-related glomerulopathy.
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PMID:Rimonabant as a potential new treatment for an emerging epidemic of obesity-related glomerulopathy? 1706 18

Roux-en-Y bypass surgery is the most common bariatric procedure currently performed in the United States for medically complicated obesity. Although this leads to a marked and sustained weight loss, we have identified an increasing number of patients with episodes of nephrolithiasis afterwards. We describe a case series of 60 patients seen at Mayo Clinic-Rochester that developed nephrolithiasis after Roux-en-Y gastric bypass (RYGB), including a subset of 31 patients who had undergone metabolic evaluation in the Mayo Stone Clinic. The mean body mass index of the patients before procedure was 57 kg/m(2) with a mean decrease of 20 kg/m(2) at the time of the stone event, which averaged 2.2 years post-procedure. When analyzed, calcium oxalate stones were found in 19 and mixed calcium oxalate/uric acid stones in two patients. Hyperoxaluria was a prevalent factor even in patients without a prior history of nephrolithiasis, and usually presented more than 6 months after the procedure. Calcium oxalate supersaturation, however, was equally high in patients less than 6 months post-procedure due to lower urine volumes. In a small random sampling of patients undergoing this bypass procedure, hyperoxaluria was rare preoperatively but common 12 months after surgery. We conclude that hyperoxaluria is a potential complicating factor of RYGB surgery manifested as a risk for calcium oxalate stones.
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PMID:Hyperoxaluric nephrolithiasis is a complication of Roux-en-Y gastric bypass surgery. 1759 87

The purpose of the present study was to compare the clinical characteristics of "pure" uric acid (UA) stone formers with that of "pure" calcium oxalate (CaOx) stone formers and to determine whether renal handling of UA, urinary pH, and urinary excretion of promoters and inhibitors of stone formation were different between the two groups. Study subjects comprised 59 patients identified by records of stone analysis: 30 of them had "pure" UA stones and 29 had "pure" CaOx nephrolithiasis. Both groups underwent full outpatient evaluation of stone risk analysis that included renal handling of UA and urinary pH. Compared to CaOx stone formers, UA stone formers were older (53.3 +/- 11.8 years vs. 44.5 +/- 10.0 years; P = 0.003); they had higher mean weight (88.6 +/- 12.5 kg vs. 78.0 +/- 11.0 kg; P = 0.001) and body mass index (29.5 +/- 4.2 kg/m(2) vs. 26.3 +/- 3.5 kg/m(2); P = 0.002) with a greater proportion of obese subjects (43.3% vs. 16.1%; P = 0.01). Patients with "pure" UA lithiasis had significantly lower UA clearance, UA fractional excretion, and UA/creatinine ratio, with significantly higher serum UA. The mean urinary pH was significantly lower in UA stone formers compared to CaOx stone formers (5.17 +/- 0.20 vs. 5.93 +/- 0.42; P < 0.0001). Patients with CaOx stones were a decade younger, having higher 24-h urinary calcium excretion (218.5 +/- 56.3 mg/24 h vs. 181.3 +/- 57.1 mg/24 h; P = 0.01) and a higher activity product index for CaOx [AP (CaOx) index]. Overweight/obesity and older age associated with low urine pH were the principal characteristic of "pure" UA stone formers. Impairment in urate excretion associated with increased serum UA was also another characteristic of UA stone formers that resembles patients with primary gout. Patients with pure CaOx stones were younger; they had a low proportion of obese subjects, a higher urinary calcium excretion, and a higher AP index for CaOx.
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PMID:Clinical and biochemical profile of patients with "pure" uric acid nephrolithiasis compared with "pure" calcium oxalate stone formers. 1778 20

Arthritis caused by gout (i.e., gouty arthritis) accounts for millions of outpatient visits annually, and the prevalence is increasing. Gout is caused by monosodium urate crystal deposition in tissues leading to arthritis, soft tissue masses (i.e., tophi), nephrolithiasis, and urate nephropathy. The biologic precursor to gout is elevated serum uric acid levels (i.e., hyperuricemia). Asymptomatic hyperuricemia is common and usually does not progress to clinical gout. Acute gout most often presents as attacks of pain, erythema, and swelling of one or a few joints in the lower extremities. The diagnosis is confirmed if monosodium urate crystals are present in synovial fluid. First-line therapy for acute gout is nonsteroidal anti-inflammatory drugs or corticosteroids, depending on comorbidities; colchicine is second-line therapy. After the first gout attack, modifiable risk factors (e.g., high-purine diet, alcohol use, obesity, diuretic therapy) should be addressed. Urate-lowering therapy for gout is initiated after multiple attacks or after the development of tophi or urate nephrolithiasis. Allopurinol is the most common therapy for chronic gout. Uricosuric agents are alternative therapies in patients with preserved renal function and no history of nephrolithiasis. During urate-lowering therapy, the dose should be titrated upward until the serum uric acid level is less than 6 mg per dL (355 micromol per L). When initiating urate-lowering therapy, concurrent prophylactic therapy with low-dose colchicine for three to six months may reduce flare-ups.
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PMID:Gout: an update. 1869

Obesity represents an increasing burden to health care resources. Nephrolithiasis is associated with obesity and type 2 diabetes and the consumption of diets rich in protein, fat and carbohydrates; this article addresses some of the pathophysiological mechanisms associated with stone formation in these patients. Management of stone disease can be more difficult in obese patients; even diagnosis can be problematic because imaging techniques are less sensitive in these patients. Treatment with extracorporeal shockwave lithotripsy and surgery in obese patients can be challenging, and outcome data for the different treatments are discussed in this Review.
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PMID:Management of renal stone disease in obese patients. 1805 47


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