Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011860 (type 2 diabetes)
57,723 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Recently evidence has accumulated that diabetic nephropathy clusters in families, both in insulin-dependent (IDDM) and non-insulin-dependent (NIDDM) diabetic patients. Furthermore, hypertension and cardiovascular accidents are found more frequently in families of NIDDM with diabetic nephropathy. Some observations in offspring of NIDDM patients with diabetic nephropathy point to high urinary albumin excretion and slightly greater blood pressure values, both within the normal range compared to offspring of patients without diabetic nephropathy. Further follow-up is required to assess whether these findings are indicative of a possible genetic predisposition to diabetic nephropathy.
Nephrol Dial Transplant 1997
PMID:Risk factors for development of diabetic nephropathy: a review. 926 95

Insulin-dependent diabetes mellitus (IDDM) develops predominantly in children and young adults, but may appear in all age groups. The incidence of IDDM differs greatly among populations, with Finland and Sardinia showing the greatest incidence rates (approximately 30-35% of cases annually per 100000 children up to age 14 years) and oriental populations showing the lowest rates. IDDM is diagnosed more frequently in the winter months. The major genetic susceptibility to IDDM is linked to the HLA complex on chromosome 6. These genetic backgrounds interact with environmental factors (possibly certain viruses, foods and climate) to initiate the immune-mediated process that leads to beta-cell destruction. Non-insulin dependent diabetes (NIDDM) is the most common form of diabetes. The prevalence of NIDDM varies enormously from population to population. The greatest rates have been found in Pima Indians. The major environmental factors identified as contributing to this form of diabetes are obesity and reduced physical activity. NIDDM shows strong familial aggregation in all populations and is clearly the result of an interaction between genetic susceptibility and environmental factors. Before NIDDM develops, insulin concentrations are high for the degree of glycaemia and of obesity, reflecting the presence of insulin resistance. As insulin resistance worsens, glucose levels increase, with the appearance of glucose intolerance and, finally, of NIDDM, when insulin response cannot compensate for insulin resistance.
Nephrol Dial Transplant 1998
PMID:The epidemiology of diabetes mellitus. 987 Apr 17

Type II diabetes mellitus has become the leading cause of end-stage renal failure in many countries of Western Europe. In all European countries, even in those with a relatively low prevalence of diabetic nephropathy, the number of patients with type II diabetes mellitus admitted for renal replacement therapy has recently increased continuously. Survival and medical rehabilitation of patients with type II diabetes on renal replacement therapy is significantly worse than in non-diabetic patients. It is obvious that in order to stem the tide, intense efforts are necessary (i) to inform the medical community about the renal risk of type II diabetes and the striking effectiveness of preventive measures, (ii) to provide better care for diabetic patients, and (iii) to reduce the high prevalence of diabetes in the population by modification of the Western life style.
Nephrol Dial Transplant 1998
PMID:The drama of the continuous increase in end-stage renal failure in patients with type II diabetes mellitus. 987 Apr 18

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.
Nephrol Dial Transplant 1998
PMID:Dietary treatment of diabetic nephropathy with chronic renal failure. 987 Apr 26

The 825T allele of the gene GNB3 which encodes the beta 3 subunit of heterotrimeric G proteins is associated with enhanced signal transduction via G proteins through the generation of a splice variant termed Gbeta3s. It was detected following a classical candidate gene approach using cell lines from patients with enhanced signal transduction and essential hypertension. The high frequency of the 825T allele in 'old' ethnicities, e.g. bushmen and Australian aborigines as well as in black populations, together with its strong association with obesity suggests that the 825T allele is a true 'thrifty genotype'. Development of obesity associated with the 825T allele is strongly influenced by lifestyle, e.g. physical activity, and other exogenous influences like pregnancy. In hypertension the 825T allele is associated with low renin activity and appears to strongly predict the development of left ventricular hypertrophy. In type 2 diabetes the 825T allele was reported to be predispose for end-stage renal disease, whereas this effect has not yet been confirmed for patients with type 1 diabetes.
Nephrol Dial Transplant 2000 Sep
PMID:G protein beta 3 subunit 825T allele, hypertension, obesity, and diabetic nephropathy. 1139 Jul 42

Chronic renal failure is an unusual complication of hereditary clotting disorders (HCDs), but this situation could change in the near future. The modality of dialysis for end-stage renal disease (ESRD) in patients with an HCD is a difficult choice. Hemodialysis (HD) may be considered, but intensive treatment with coagulation factors is required for vascular access execution and for each HD procedure. Peritoneal dialysis (PD) has been infrequently proposed. However, PD requires coagulation replacement therapy only during peritoneal catheter placement. The aim of this paper is to describe our experience of three patients with ESRD and HCD, successfully treated with chronic PD in the medium term. Case 1 was a 58-year-old man with moderate hemophilia A, type 2 diabetes mellitus, and hepatitis C virus (HCV) infection. His ESRD was secondary to glomerulonephritis. A double-cuff peritoneal catheter was surgically placed with pre-emptive factor VIII administration. He began treatment with continuous ambulatory peritoneal dialysis (CAPD). An inguinal hernia was repaired without complications. After eleven months of follow-up, no hemorrhage episodes have been observed and clinical outcome is optimal. Case 2 was a 46-year-old man with severe hemophilia A, type 2 diabetes mellitus, and HCV and human immunodeficiency virus (HIV) infections. He developed a diabetic nephropathy that required renal replacement therapy. A permanent silicone catheter was inserted in the left internal jugular vein, and the patient started HD treatment. Later on, PD therapy was proposed. A peritoneal catheter was implanted with simultaneous factor VIII infusion. Minimal bleeding was observed at the subcutaneous tunnel over the following 48 hours. The patient started PD treatment without complications, and two months later, remaining asymptomatic, transferred to another center. Case 3 was a 41-year-old woman diagnosed with von Willebrand disease type 2A, HCV infection, and polycystic kidney disease, who presented with ESRD. An internal arteriovenous fistula was performed under coagulation factor cover. During a fistulography, and despite coagulation factor substitutive treatment, the patient showed an important hematoma. Afterwards, PD was considered. A peritoneal catheter was implanted under coagulation factor cover. The postoperative course was uncomplicated, and the patient started CAPD treatment. During follow up, she suffered two hemoperitoneum episodes that were resolved with cold dialysate. After nine months, she uneventfully continued on PD. In conclusion, PD is the therapy of choice for patients with hereditary clotting disorders and ESRD requiring dialysis. Peritoneal dialysis therapy avoids many of the complications related to HD therapy.
Adv Perit Dial 2000
PMID:Peritoneal dialysis is the therapy of choice for end-stage renal disease patients with hereditary clotting disorders. 1104 86

The prevalence of type 2 diabetes is rising in all Westernized societies. Presumably as a consequence of diminishing cardiovascular mortality, end-stage renal failure (ESRF) in patients with diabetes (mostly type 2) as a co-morbid condition has risen dramatically in the past decade. This constellation has become the single most common cause of ESRF in most countries. Such an epidemiological trend is particularly regrettable, since in uraemic diabetic patients, medical rehabilitation and survival are remarkably poor. Recent studies indicate that an interplay between genetic predisposition and factors, some of them susceptible to intervention, such as hyperglycaemia, blood pressure, smoking, age, gender and ethnicity, predispose to the development and progression of nephropathy. It has also become clear that trace albuminuria ('microalbuminuria') provides unique opportunities to recognize incipient renal involvement early on, although it is less specific in type 2 as compared with type 1 diabetes. Factors that promote progression include hypertension, proteinuria, smoking, glycaemic control and, less certainly, dietary protein intake and hyperlipidaemia. Cumulating evidence indicates that early intervention delays progression of nephropathy. The most important strategies to combat the medical catastrophe of increasing numbers of diabetic patients with ESRF include: (i) prevention of diabetes (mainly type 2); (ii) glycaemic control to prevent onset of renal involvement; and (iii) meticulous antihypertensive treatment to avoid progression of nephropathy.
Nephrol Dial Transplant 2001
PMID:Renal disease in type 2 diabetes. 1150 79

Exit-site infections (ESIs) are frequently due to gram-positive organisms and occasionally to gram-negative organisms. Initial empiric antibiotic therapy is therefore directed against these organisms until culture reports are available. Two cases of ESI associated with Mycobacterium are here reported. The first patient, a 63-year-old man with type 2 diabetes, recently treated for Staphylococcus epidermidis peritonitis, presented with acute purulent drainage at the catheter exit site, accompanied by pain and erythema. No tunnel abscess was identified by ultrasound. Empiric antibiotic therapy was initiated with ofloxacin and vancomycin. A rapid-growing acid-fast bacillus (AFB) noted four days after culture was eventually identified as Mycobacterium fortuitum. Ofloxacin was continued, vancomycin was discontinued, and clarithromycin was added. The ESI initially showed improvement; therapy was therefore continued for several months. However, cultures remained positive for M. fortuitum, and the catheter was removed 5 months after therapy was initiated. The second patient, a 28-year-old woman, presented with severe pain and tenderness at the exit site without erythema or drainage. Empiric therapy with cefazolin, gentamicin, and cephalexin was initiated. Gram-positive cocci and an AFB were identified from the exit-site culture, and antibiotics were initially changed to clarithromycin, trimethoprim/sulfamethoxazole, and ofloxacin. The organisms were subsequently identified as M. chelonae-M. abscessus complex and coagulase-negative Staphylococcus. The patient continued to improve after 3 weeks of antibiotic therapy. However, despite the initial improvement in the ESI, the M. chelonae-M. abscessus complex continued to grow, and amikacin was added intravenously. Despite continued treatment, the ESI did not resolve, and the catheter was removed after 4 months of therapy. Despite unusual exist-site infections with rapidly growing AFBs, both patients continued continuous ambulatory peritoneal dialysis (CAPD) while undergoing treatment for ESI. Catheters were left intact, as improvement was initially seen with no evidence of tunnel infection or peritonitis. Rapid-growing AFB should be considered another possible causative agent for ESI. Two cases of atypical mycobacterial exit-site infection are presented to illustrate the difficulties in managing this complication of peritoneal dialysis. Ofloxacin--or other quinolones--may provide a better spectrum of coverage when choosing empiric therapy in patients presenting with ESI.
Adv Perit Dial 2001
PMID:Treatment of mycobacterial exit-site infections in patients on continuous ambulatory peritoneal dialysis. 1151 Feb 69

The introduction of recombinant erythropoietin (Epo, epoetin) has resulted in a shift in focus from the treatment to the prevention of anaemia. This shift in treatment goals has provided nephrologists with the challenge of implementing preventative strategies in clinical practice. While this area of nephrology is still developing, a lot can be learned from the methods applied by clinicians involved in the prevention of other diseases, particularly non-insulin-dependent (type 2) diabetes mellitus. The prevention of type 2 diabetes has become a major aim of healthcare providers globally due to the epidemic proportions of the disease. In order to reverse this worrying trend, diabetologists have had to develop effective management strategies based upon their current knowledge. Nephrologists must now adopt a similar approach if the increasing threat from diabetic nephropathy is to be reversed. This should include strict normotension, the prescribing of angiotensin-converting enzyme (ACE) inhibitors, administration of lipid-lowering agents, and the near-normalization of anaemia with epoetin. However, the implementation of treatment strategies alone is unlikely to be sufficient. Indeed, an effective programme of education is required to ensure that patients understand the seriousness of their condition and remain compliant with treatment. Similarly, educating the general public may help to reduce the burden of type 2 diabetes and the subsequent problems associated with the disease, including renal disease.
Nephrol Dial Transplant 2001
PMID:Advances in nephrology: successes and lessons learnt from diabetes mellitus. 1159 Feb 57

Several strategies are available to delay progression of renal disease and the development of associated co-morbidities. Hypertension is a strong independent risk factor for end-stage renal disease (ESRD) and there is consensus that blood pressure (BP) management is an important aspect of care in patients with chronic renal insufficiency (CRI). Clinical studies have shown that angiotensin-converting enzyme (ACE) inhibitors have renoprotective properties, independent of their antihypertensive effects, which can delay the onset of ESRD. Studies have also shown that intensive therapy of both type 1 and type 2 diabetes patients, to give near normal blood glucose concentrations, can reduce the incidence of progressive clinical proteinuria and may, therefore, protect against ESRD. Additionally, data are emerging that treatment of renal anaemia with epoetin can reduce mortality and delay the onset of dialysis in CRI patients, but these encouraging results need to be confirmed in large prospective studies. In conclusion, control of BP and hyperglycaemia, as well as use of ACE inhibitors and anaemia treatment, all have potential in delaying the progression of CRI or improving patient outcomes. If benefit is proven in future studies, these strategies will be most effective if implemented early in the course of CRI.
Nephrol Dial Transplant 2001
PMID:The rationale for early management of chronic renal insufficiency. 1159 Feb 58


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