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)

A strong familial clustering of ESRD has been reported among African Americans, suggesting that factors predisposing to renal failure, whether genetic, environmental, or both, may disproportionately affect certain families. A case-control study was undertaken to determine if a familial risk of ESRD was present among white Americans, if this risk differed among causes of ESRD, and if variability in age at onset was attributed to familial factors. Data were obtained from 103 white American patients (cases) with ESRD receiving dialysis treatments at the Bowman Gray School of Medicine's affiliated dialysis facility in Winston-Salem, NC. One hundred three age-, sex- and race-matched non-ESRD controls were consecutively selected from the Wake Forest University Physicians internal medicine clinic. Odds ratios (OR) and associated 95% confidence intervals (CI) were calculated to signify the prevalence of a relative with ESRD among cases versus controls. The presence of either a first- or second-degree relative increased a white American's risk for developing ESRD nearly threefold (OR = 2.7, 95% CI 1.1 to 7.2; P = 0.038), whereas the presence of either a first-, second- or third-degree relative with ESRD increased the risk nearly fourfold (OR = 3.5, 95% CI 1.5 to 8.4; P = 0.004). Cases with chronic glomerulonephritis and Type II diabetic nephropathy as the cause of ESRD had relatives with ESRD more often than cases with Type I diabetic nephropathy, interstitial nephritis, or renal artery stenosis. The average correlation (f) of ages at onset of ESRD among individuals in a single family (cases and their relatives) was 55%.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Familial risk, age at onset, and cause of end-stage renal disease in white Americans. 778 48

A semiquantitative light microscopic study of 274 renal biopsy and 12 nephrectomy specimens was carried out to assess the frequency and severity of tubulitis (mononuclear leukocytes in the renal tubular wall) in all common glomerular diseases, diabetic nephropathy, renal amyloidosis and renal artery stenosis. The extent of interstitial inflammatory infiltrates and severity of interstitial fibrosis were also graded. Tubulitis was 1) frequent in crescentic glomerulonephritis (GN) with pauci-immune, linear and granular immune deposits, renal artery stenosis, diabetic nephropathy, lupus GN of WHO type IV, and IgA GN; 2) rare in minimal change and idiopathic membranous nephropathy; 3) usually severe in crescentic GN and renal artery stenosis; and 4) predominantly located in atrophic tubules in renal artery stenosis, diabetic nephropathy and IgA GN. The most important parameter for the grading of tubulitis was interstitial infiltration. However, no correlation was found between the grades of tubulitis, interstitial infiltrates and interstitial fibrosis in crescentic and lupus GN. It is suggested that renal ischemic injury, by eliciting expression of proinflammatory cytokines and neo-antigens in the tubulointerstitial space, might play a role in the development of tubulitis in vascular and glomerular renal diseases.
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PMID:Tubulitis in primary vascular and glomerular renal disease. 892 73

The renin-angiotensin system is central to the pathophysiology of a number of cardiovascular disorders. Most obviously this is so with renin secreting tumours, but the system is of central importance in other disorders such as scleroderma renal crisis and most cases of malignant hypertension. Activation of the renin-angiotensin system in unilateral renal artery stenosis is pivotal to the development of hypertension and the disturbances in electrolyte and volume balance -- most particularly in the hyponatraemic-hypertensive syndrome. Likewise, stimulation of the renin-angiotensin system is an important contributor, amongst many other systems, to the pathophysiology of cardiac failure. In diabetic nephropathy, the renin-angiotensin system is often suppressed as gauged by circulating levels of renin, yet it appears to make an important contribution to the progressive decline in renal function. Much less clear is the role of the renin-angiotensin system in essential hypertension insofar as it contributes to the level of blood pressure, to the development of left ventricular hypertrophy, and in the evolution of complications such as stroke and myocardial infarction. Blockade of the renin-angiotensin system with angiotensin-converting enzyme inhibitors has contributed to our understanding of the role of this system in cardiovascular disease. The advent of selective angiotensin II type-1 receptor blockers will further increase knowledge in this area.
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PMID:The importance of the renin-angiotensin system in cardiovascular disease. 965 50

Approximately 150 million people worldwide have diabetes mellitus, of whom 90% are type II diabetics. It is therefore of no surprise that diabetic nephropathy has become the leading cause of end-stage renal disease. Opposite to what has been known previously, kidney disease is at least as common in type II as in type I diabetes. However, because the majority of type II diabetics has hypertension for many years before diabetes mellitus becomes clinically relevant, renal lesions are often heterogeneous with frequent exclusive presence of ischemic changes. For the treatment of hypertension in diabetics without nephropathy (no microalbuminuria), drugs that exert beneficial effects or are at least neutral with respect to lipid and glucose metabolism, such as ACE inhibitors, angiotensin II-receptor antagonists, non-dihydropyridine-calcium channel blockers and the thiazide-like indapamide, are to be preferred. Although metabolically neutral, dihydropyridine calcium channel blockers should be used with caution, since an increase in cardiovascular morbidity and mortality in type II diabetics treated with these compounds has most recently been described. Once that diabetic nephropathy is established, blood pressure should be lowered to 120/80 mmHg (measured in seated position). Antihypertensive treatment should primarily be based on ACE inhibitors; angiotensin II-receptor antagonists are a valuable alternative if ACE inhibitors are not tolerated. Both ACE inhibitors and angiotensin II-receptor antagonists should be used with high caution in elderly patients with severe atherosclerosis in whom acute renal failure could occur due to the presence of bilateral renal artery stenosis. Newer studies indicate that non-dihydropyridine calcium channel blockers such as verapamil and diltiazem may be as effective as ACE inhibitors in preserving renal function in diabetic nephropathy. A fix-dose combination of the ACE inhibitor trandolapril with verapamil is now available; it should be reserved for patients whose blood pressure and/or proteinuria can not be adequately controlled with ACE inhibitors. Finally, indapamide is the only antihypertensive diuretic with nephroprotective properties.
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PMID:[Antihypertensive therapy in diabetes mellitus]. 1006 31

This retrospective study aimed to use captopril renography (CR) for predicting the benefits of captopril treatment in hypertensive patients with diabetic nephropathy. CR was utilized in 60 hypertensive patients with diabetic nephropathy for detecting the probability of renovascular hypertension (RVH) and predicting the benefits of renal artery revascularization or captopril treatment. Ten of the 60 patients showed a high probability of RVH with marked changes of the renogram curve after an oral intake of 50-mg captopril compared to baseline findings. All of the 10 patients confirmed significant main renal artery stenosis in all of them, bilaterally in four patients and unilaterally in the remaining six patients by renal angiographic findings. After successful revascularization, blood pressure was well controlled and renal function was preserved in all of the 10 patients. The other 50 patients showed a low or intermediate probability of RVH with normal findings or unchanged on CR after 50-mg captopril. Then, captopril alone or combination treatment started and continued on 50 patients. After monitoring for at least 6 months, blood pressure was well controlled and renal function was preserved in all the 50 patients on captopril treatment. We conclude that CR should be considered as the standard diagnostic criteria of RVH and may be helpful in predicting the beneficial impact of captopril treatment in hypertensive patients with diabetic nephropathy.
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PMID:Usefulness of captopril renography to predict the benefits of renal artery revascularization or captopril treatment in hypertensive patients with diabetic nephropathy. 1220 78

The renin-angiotensin-aldosterone system (RAAS) exerts a principal influence in maintaining vascular tone, optimal salt and water homeostasis, and forward cardiac output in human beings. Overactivity of the RAAS can lead to pathologic consequences in states of diabetic nephropathy, hypertension, renal artery stenosis, left ventricular hypertrophy, coronary atherosclerosis, myocardial infarction, and congestive heart failure. In addition to fluid and hemodynamic effects, the RAAS may have a critical role in the activation of the sympathetic nervous system, the progression of atherosclerosis, the dysregulation of endothelial function, and the inhibition of the fibrinolytic system. Accumulated basic and clinical evidence supports the use of inhibitors of the RAAS, including aldosterone antagonists, angiotensin-converting enzyme inhibitors, and angiotensin receptor blockers, in treating hypertension, improving diabetic nephropathy, preventing or ameliorating congestive heart failure, and optimizing the prognosis after myocardial infarction.
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PMID:Renin-angiotensin-aldosterone system: fundamental aspects and clinical implications in renal and cardiovascular disorders. 1267 84

The renin-angiotensin-aldosterone system (RAAS) plays an integral role in maintaining vascular tone, optimal salt and water homeostasis, and cardiac function in humans. However, it has been recognized in recent years that pathologic consequences may also result from overactivity of the RAAS. Clinical disease states such as renal artery stenosis, hypertension, diabetic and nondiabetic nephropathies, left ventricular hypertrophy, coronary atherosclerosis, myocardial infarction, and congestive heart failure (CHF) are examples. Part of the adverse cardiorenal effects of the RAAS may be related to the prominent role that this system plays in the activation of the sympathetic nervous system, the dysregulation of endothelial function and progression of atherosclerosis, as well as inhibition of the fibrinolytic system. Also, direct profibrotic actions of angiotensin II and aldosterone in the kidney and heart promote end organ injury. Current basic science and clinical research supports the use of inhibitors of the RAAS, including angiotensin converting enzyme inhibitors, angiotensin receptor blockers, and aldosterone antagonists in treating hypertension, improving diabetic nephropathy and other forms of chronic kidney disease, preventing or ameliorating CHF, and optimizing prognosis after myocardial infarction.
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PMID:The renin-angiotensin-aldosterone system: cardiorenal effects and implications for renal and cardiovascular disease states. 1286 Nov 21

Early renal insufficiency (ERI), defined as a calculated or measured glomerular filtration rate (GFR) between 30 and 60 mL/min per 1.73 m2, is present in more than 10% of the adult Australian population. This pernicious condition is frequently unrecognised, progressive and accompanied by multiple associated comorbidities, including hypertension, renal osteodystrophy, anaemia, sleep apnoea, cardiovascular disease, hyperparathyroidism and malnutrition. Several treatments have been suggested to retard GFR decline in ERI, including blood pressure reduction, angiotensin-converting enzyme inhibition, angiotensin receptor antagonism, calcium channel blockade, cholesterol reduction, smoking cessation, erythropoietin therapy, dietary protein restriction, intensive glycaemic control and early intensive multidisciplinary patient education within a renal unit. In addition, specific interventions have been reported to be renoprotective in atherosclerotic renal artery stenosis, diabetic nephropathy, lupus nephritis and certain forms of primary glomerulonephritis. The present paper reviews the available published randomised controlled clinical trials and meta-analyses supporting (or refuting) a role for each of these therapeutic manoeuvres.
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PMID:Evidence-based guide to slowing the progression of early renal insufficiency. 1474 14

Renal ultrasonography has become the standard imaging modality in the investigation of kidneys because it displays excellent anatomic detail, requires no special preparation of the patient and does not expose the patient to radiation or contrast agents. Ultrasonography is used to determine the site and size of the kidney and to detect focal lesions like tumors, cysts and renal stones. Furthermore the presence and urodynamic relevance of hydronephrosis can reliably be revealed. Also renoparenchymatous diseases are discernible to the experienced investigator, however most glomerular diseases cannot be further subclassified. Exceptions are primarily renovascular disorders like hypertensive nephrosclerosis, diabetic nephropathy or renal vasculitis. Color Doppler sonography allows the detection and quantification of renal artery stenosis, increased resistance index values may indicate irreversible disease. Ultrasonography has also been found of value in the evaluation of renal transplant kidneys. Especially in the early transplant course potentially fatal but reversible diseases like renal vein thrombosis or urinomas are detected with high sensitivity. In the long term, an increased resistance index value may also predict allograft failure.
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PMID:[Ultrasound of the kidney and renal vessels. I: Normal findings, congenital diseases, diseases of the kidney parenchyma]. 1475 29

Patients with end-stage renal disease have a high mortality, with the majority of deaths due to vascular disease. The prevalence of vascular risk factors and vascular disease in predialysis chronic renal failure (CRF) is poorly characterized. The aim of the present study was to determine the prevalence of vascular risk factors and clinically overt vascular disease in an Australian cohort of patients with predialysis CRF. We performed a retrospective chart review of outpatients with CRF and noted demographic data, the cause of renal failure, the presence or otherwise of vascular risk factors and vascular disease and calculated glomerular filtration rate. The prevalence of overt vascular disease and modifiable vascular risk factors was calculated. One hundred and eighty patients completed the study. Eighty-nine per cent of patients had hypertension, 68% had dyslipidaemia, 32% were diabetic and 38% were previous smokers. The subgroup with diabetic nephropathy had significantly more risk factors (P < 0.001) than other groups. Twenty-seven per cent of the group had cardiovascular disease, 22% had cerebrovascular disease, 23% had peripheral vascular disease and 9% had renal artery stenosis. Patients with ischaemic nephropathy had significantly more vascular disease than other groups (P < 0.001). Patients with overt vascular disease were older, had a higher number of risk factors and a higher calcium phosphate product than those without vascular disease. In conclusion, the present study suggests a high prevalence of vascular risk factors and vascular disease in predialysis CRF. Early detection provides an opportunity for early intervention and may help reduce the development of vascular disease, and the associated mortality, once these patients progress to dialysis.
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PMID:Prevalence of vascular risk factors and vascular disease in predialysis chronic renal failure. 1501 97


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