Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011854 (type 1 diabetes)
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Diabetic nephropathy accounts for almost a third of all causes of ESRD. Microalbuminuria screening among diabetics can offer early detection of incipient nephropathy. Aggressive treatment with ACE inhibitors may delay the onset of overt renal failure or delay its progression. Furthermore, intensive control of blood glucose has also been proven to prevent the microvascular complications of diabetes and should be pursued in both IDDM and NIDDM. The high association of diabetes mellitus with hypertension presents another problem to the clinician. It is necessary to control blood pressure to prevent further progression of renal failure. The choice of antihypertensive medications, however, becomes a therapeutic dilemma because of the metabolic and lipid disturbances that some drugs can cause. ACE inhibitors, CCBs, alpha-agonists, and low-dose diuretics, alone or in combination, may be tried to normalize blood pressures. Although beta-blockers are widely used and effective in nondiabetics, these agents should be considered the drugs of last resort because of their adverse effects, which are particularly troublesome for diabetics. Moderate protein restriction should also be advocated as a helpful adjunct to therapy.
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PMID:Diabetic nephropathy. 916 51

Although the evolution of diabetic nephropathy is brought about mostly by persistent hyperglycemia, its progression may be influenced by various other factors such as hypertension and dietary protein intake. It has been recently suggested in the literature that the gene polymorphism of angiotensin converting enzyme (ACE) might be associated with the development of diabetic nephropathy, because the DD genotype of ACE gene is closely associated with the presence of nephropathy in diabetic subjects. However, in our present analysis the frequency of the DD genotype in patients with non-insulin dependent diabetes is not significantly related to the presence or absence of nephropathy. It remains to be clarified by multi-center analysis using large numbers of patients whether the gene polymorphism of ACE is related to the progression of diabetic nephropathy to renal failure. Furthermore, it has been postulated that the interstitial fibrosis evaluated in renal biopsy specimens is significantly correlated with the declining of renal function in diabetic patients. However, it is not possible to clinically quantitate the interstitial fibrosis without performing renal biopsy. We have recently found that the urinary excretion of type IV collagen is significantly increased in diabetic patients. Moreover, the increase in urinary type IV collagen is well correlated with the amount of urinary albumin. Since type IV collagen in the urine is probably derived from tubulointerstitial tissue, it is likely that the increased amount of type IV collagen in the urine may reflect the fibrotic change in diabetic kidneys. Whether the increase in urinary type IV collagen is able to predict for the progression of diabetic nephropathy in the future should be examined.
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PMID:Mechanism of the progression of diabetic nephropathy to renal failure. 935 Jun 77

Combined pancreas-kidney transplantation has been introduced in the treatment of patients with type 1 diabetes and renal failure 20 years ago. By 1985 374 combined pancreas-kidney transplantations had been reported to the International Pancreas Transplant Registries. Surgical drainage of the transplanted exocrine pancreas into the urinary bladder solves most of the postoperative problems encountered with the exocrine secretions. Furthermore, monitoring of pancreatic enzyme (amylase) activity in urine has been shown to be useful in diagnosis of rejection of the pancreatic graft. However, little attention has been paid to the biochemical consequences of high activities of proteolytic pancreatic enzymes on the determination of urinary proteins. The present case illustrates the difficulties in interpreting proteinuria in patients with combined pancreas-renal transplant with pancreaticocystostomia. In the propositus, interpretation of the urinary protein electrophoresis is hampered by the presence of pancreatic juice proteins and peptides originating from digestion of proteins by activated pancreatic enzymes. Results of immunochemically determined marker proteins ([micro]albumin, transferrin, beta 2-microglobulin) are unreliable due to digestion by pancreatic enzymes.
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PMID:Difficulties in evaluating urinalysis following combined pancreas-kidney transplantation. 936 5

In adult diabetic patients microalbuminuria is a marker of early vascular damage in the micro- and macrocirculation. Microalbuminuria is a powerful predictor of renal and cardiovascular disease outcome and is associated with other, potentially modifiable, risk factors of vascular damage. Studies of secondary prevention have shown that blood pressure lowering drugs effectively reduce albumin excretion rate. Angiotensin converting enzyme (ACE) inhibitors seem particularly effective in reducing the risk of progression to clinical albuminuria in both insulin dependent and non-insulin dependent diabetic patients and this beneficial effect appears to be long-lasting. Whether this postpones the onset of end-stage renal failure and/or reduces early mortality in these patients remains to be established. Recent studies of primary prevention in insulin-dependent diabetic patients predominantly with normoalbuminuria demonstrate that ACE inhibition reduces significantly the rate of progression of albumin excretion rate and, of great interest, seems to affect beneficially the progression of retinopathy. These results compare favorably with the beneficial effect of intensified insulin therapy and strict blood glucose control in this same group of patients. Thus, ACE inhibitors are a powerful tool to prevent progression of microalbuminuria in diabetes and may prove useful as an adjunct therapy to intensified insulin therapy in the prevention of development of microalbuminuria and of retinopathy progression in insulin dependent diabetes.
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PMID:Angiotensin converting enzyme inhibitors in diabetic patients with microalbuminuria or normoalbuminuria. 940 17

Diabetic nephropathy is the most common cause of end-stage renal disease (ESRD) in the United States, and accounts for 35% of all the patients with ESRD entering a dialysis program; 63% of patients with diabetic nephropathy have type II diabetes mellitus. Hypertension is a major risk factor for renal disease and is common in people with diabetes mellitus. Strategies for preventing the progression of renal failure in patients with diabetes mellitus include glycemic control, and control of blood pressure. Blocking the renin-angiotensin system (RAS) slows the progression of established diabetic nephropathy in type I diabetes mellitus, and inhibiting angiotensin II formation retards or impedes the progression from microalbuminuria to established diabetic nephropathy (macroproteinuria) in people with type I diabetes mellitus. The situation could be the same for people with type II diabetes mellitus. The ability of RAS blockade using irbesartan, an AT1 angiotensin II receptor antagonist, to slow the progression in renal failure has been compared with that of the calcium channel blocker amlodipine and placebo in a pilot study. The results suggest that blockade of the RAS, in this case with irbesartan, is at least equivalent to calcium channel blockers with respect to antihypertensive efficacy, but provides better renoprotective benefits.
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PMID:Renoprotection and renin-angiotensin system blockade in diabetes mellitus. 943 77

The related homeodomain-containing transcription factors HNF1 (HNF1 alpha) and vHNF1 (HNF1 beta) recognise common target DNA sequences in the regulatory regions of many genes and are expressed in several parenchymal cell types, predominantly in liver, kidney, intestine and pancreas. HNF1-null mutant mice, with a wild-type vHNF1 gene, develop normally, but die within a few weeks of birth with severe liver and kidney failure. Humans with a mutation in the HNF1 alpha gene develop non-insulin dependent diabetes on maturity (MODY 3). To determine distinctive roles for each of these proteins we produced a set of polyclonal sera and monoclonal antibodies, directed against different parts of the rat HNF1 and vHNF1 proteins. These antibodies reveal that HNF1 is present in vivo as a heterogeneous mixture of 92-98 kDa molecular mass polypeptides, a mass higher than that expected from its amino acid sequence. vHNF1 is present in the form of two isoforms of roughly the expected molecular masses, 65 and 68 kDa. In addition, some antibodies prepared against bacterially-produced HNF1 recognise vHNF1 but not HNF1, in liver and kidney extracts. Hence, we present the first evidence for differential post-translational modification of HNF1 and vHNF1 proteins.
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PMID:A set of polyclonal and monoclonal antibodies reveals major differences in post-translational modification of the rat HNF1 and vHNF1 homeoproteins. 952 12

The objective of this study was to test the relationship between neurologic and microvascular complications of type 1 diabetes mellitus. It was hypothesized that the mechanisms operative in autonomic dysfunction seen in diabetic patients with microangiopathy play a role in the rapidity of progression to renal failure. Twenty-six type 1 diabetic patients with proteinuria were studied with computerized monitoring of heart rate variation during timed ventilation, assumption of upright posture, and Valsalva maneuver and with 24-h ambulatory blood pressure monitoring at baseline. Renal function was evaluated over the ensuing 12 months of intensive insulin therapy. Blood pressure was treated so as to achieve consistent 24-h readings < 140/90 mm Hg. Angiotensin converting enzyme inhibitors were the preferred antihypertensive agents. Serial serum creatinine concentrations were compared using repeated measures analysis of variance. Over 12 months there were no significant serum creatinine changes for any autonomic test group with normal results at baseline. Groups with abnormal autonomic results at baseline demonstrated statistically significant increases in serum creatinine over 12 months compared to their baseline. Of the tests, Valsalva separated groups of patients with similar degrees of baseline renal impairment. Each of the sympathetic plus Valsalva combinations demonstrated a significant difference in progression of serum creatinine increase over 12 months. In each instance, if both sympathetic and Valsalva results were abnormal, there was a statistically significant increase in serum creatinine over 12 months when compared to groups in which one or both test results were normal. There is a relationship between autonomic function and the progression of renal dysfunction. The inability to vary the heart rate to a Valsalva maneuver identifies a degree of parasympathetic dysfunction that permits unopposed sympathetic tone, heralding more rapid renal destruction. A simple inexpensive bedside laboratory test discerned a relatively low-risk group of diabetic patients with proteinuria that demonstrated no deterioration in renal function over 12 months. When the Valsalva maneuver was markedly abnormal the presence of a mean arterial pressure > 100 mm Hg was associated with a greater likelihood of rapid renal deterioration. This group at higher risk of renal deterioration should undergo aggressive lowering of mean arterial blood pressure to < 95 mm Hg.
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PMID:Relationship between autonomic function and progression of renal disease in diabetic proteinuria: clinical correlations and implications for blood pressure control. 954 70

We would like to present 23 calcaneal fractures in 22 patients of whom 21 had type I diabetes mellitus. There appear to be three basic fracture types: (1) a superiorly displaced extra-articular avulsion fracture of the posterior calcaneus (or Iowa fracture), which occurred in 12 patients (five men, seven women); (2) a mid-calcaneal compression fracture in six patients (four men, two women), and (3) a cleavage or "wedge" type fracture in four patients extending from the calcaneal tubercle (one man, 3 women). All four of this last group of patients had a history of a chronic penetrating ulcer, and this is noteworthy since only one other patient out of the remaining 18 in groups 1 and 2 had a similar history. Most patients had decreased bone mineralization: 15 patients were on long-term, high-dose steroids, and 18 patients had either poor renal function or complete renal failure (11 of 12). Fourteen patients had received either renal or pancreas transplants. Eight patients were on restricted weight bearing prior to their fractures. We believe that diabetic patients are more prone to calcaneal fractures than the general population, and early diagnosis is imperative, followed by early treatment to prevent significant bony deformity.
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PMID:Calcaneal fractures in diabetic patients. 955 85

The number of Americans with diabetes mellitus has increased 50% since 1983 to 16 million. An interesting and startling factor is that only half of these diabetics are aware they have the disease. Diabetes mellitus can lead to blindness, heart disease, stroke, nerve damage, kidney failure, and periodontal disease. It is the fourth leading cause of death in the United States. A metabolic disorder affecting insulin metabolism and associated blood glucose intolerance regulation, diabetes may be classified by the following categories: type I-insulin dependent diabetes mellitus which is commonly found in children and adolescents and type II-non-insulin-dependent or adult-onset diabetes which occurs in patients over forty and is associated with obesity. The dental hygienist's role in education, prevention, and therapeutics has expanded to detection and recognition of oral manifestations of diabetes. The dental hygienist may be the first to recognize the presence of the disease. This article aims to acquaint the dental hygienist with the clinical picture of a dental patient with diabetes mellitus.
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PMID:A dental hygiene perspective in the detection of diabetes mellitus. 959 74

The prevalence of abnormally elevated albumin excretion rate (> 30 mg/24 h) is approximately 40% in insulin-dependent (IDDM) and non-insulin-dependent (NIDDM) diabetic patients. Diabetes has become the leading cause of end-stage renal failure in the US, Japan and Europe. Approximately 90% of the direct and indirect cost of caring for diabetic patients are spent on the complications of diabetes. Identification of patients at high risk of developing diabetic nephropathy is possible by screening for microalbuminuria (30-300 mg/24 h). Elevated urinary albumin excretion rate indicates a substantially increased mortality risk in diabetic patients. Randomised controlled trials in normotensive IDDM and NIDDM patients with persistent microalbuminuria indicate that ACE inhibitors diminish urinary albumin excretion rate, postpone it and may even prevent progression to clinical overt nephropathy. These findings indicate that screening and intervention programs are likely to have life saving effects and lead to considerable economic savings. Systemic blood pressure elevation to a hypertensive level is an early and frequent phenomenon in diabetic nephropathy. Furthermore, nocturnal blood pressure elevation (non-dippers) occurs more frequently in patients with nephropathy. Systemic blood pressure elevation and to a lesser degree albuminuria accelerate the progression of diabetic nephropathy. Effective blood pressure reduction with non-ACE-inhibitors and/or ACE-inhibitors frequently in combination with diuretics: (a) reduces albuminuria; (b) delays the progression of nephropathy; (c) postpones renal insufficiency; and (d) improves survival in IDDM and NIDDM patients with diabetic nephropathy. A specific renal protective effect of ACE-inhibitors in diabetic nephropathy has been demonstrated in IDDM patients with moderately reduced kidney function (s-creatinine > 133 mumol/l) while the data conflict with NIDDM patients. Antihypertensive treatment for diabetic nephropathy simultaneously extends life and saves money. Finally, reduced risk of fatal and non-fatal cardiovascular events have been demonstrated when diabetic patients with isolated systolic hypertension are treated with blood pressure lowering agents. Absolute risk reduction with active treatment compared to placebo was twice as great for the diabetic versus non-diabetic patients (101/1000 versus 51/1000 randomised participants at the 5-year follow-up), reflecting the higher risk of diabetic patients. In conclusion, early detection and aggressive treatment of arterial hypertension with ACE-inhibitors, long acting calcium antagonist and low dose diuretics as first line drugs are highly warranted in diabetic patients with or without diabetic renal disease.
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PMID:Is antihypertensive treatment the same for NIDDM and IDDM patients? 964 59


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