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Biomedical subjects

G Bakris

Publications and source records attributed to G Bakris.

At least 19 recordsLinked to original sources
PubMed2003

Rosiglitazone reduces urinary albumin excretion in type II diabetes.

This study examines the effect of rosiglitazone on urinary albumin excretion (UAE) in patients with type II diabetes. Urinary albumin: creatinine ratio (ACR) was measured in a 52-week, open-label, cardiac safety study comparing rosiglitazone and glyburide. Patients were randomised to treatment with rosiglitazone 4 mg b.i.d. or glyburide. ACR was measured at baseline and after 28 and 52 weeks of treatment. Statistically significant reductions from baseline in ACR were observed in both treatment groups at week 28. By week 52, only the rosiglitazone group showed a significant reduction from baseline. Similar results were observed for the overall study population and for the subset of patients with baseline microalbuminuria. For patients with microalbuminuria at baseline, reductions in ACR did not correlate strongly with reductions in glycosylated haemoglobin, or fasting plasma glucose, but showed strong correlation with changes in mean 24-h systolic and diastolic blood pressure for rosiglitazone-treated patients (deltaACR vs deltamean 24-h systolic blood pressure, r=0.875; deltaACR vs deltamean 24-h diastolic blood pressure, r=0.755; P < 0.05 for both). No such correlation was observed for glyburide-treated patients. In conclusion, rosiglitazone treatment was associated with a decrease in urinary albumin excretion. These findings suggest a potential beneficial effect of rosiglitazone in the treatment or prevention of renal and vascular complications of type II diabetes.

Administration, Oral↗
PubMed2001

Choices and goals in the treatment of the diabetic hypertensive patient.

The number of people living in the United States who have diabetes and high blood pressure is over 11 million and rising. Together, these two diseases are devastating to the whole body if not aggressively controlled. The tight recommendations put forth by the Joint National Committee VI for better control of blood pressure and control of proteinuria have helped diminish further organ failure in patients with hypertension and diabetes. Combination therapy has been found to be very effective, and one arm should be an angiotensin converting enzyme inhibitor.

Cardiovascular Diseases↗
PubMed2000

Lack of evidence of blood pressure-independent protection by renin-angiotensin system blockade after renal ablation.

BACKGROUND: The superiority of renin-angiotensin system (RAS) blockade in providing renoprotection has been attributed to class-specific blood pressure "(BP)-independent" mechanisms. However, the conventional BP measurement methodology on which such conclusions are based is inherently limited for an accurate assessment of the fluctuating ambient BP profiles. The present studies were undertaken to rigorously examine the relationship of renoprotection to the antihypertensive effects of RAS blockade using chronic BP radiotelemetry in the 5/6 renal ablation model. METHODS: Rats with 5/6 renal ablation received either no treatment, the angiotensin-converting enzyme inhibitor benazepril at a dose of 25, 50, and 100 mg/L; or the angiotensin receptor antagonist losartan at a dose of 50, 120, and 180 mg/L of drinking H2O; and were followed for seven weeks. RESULTS: Glomerulosclerosis (GS) at sacrifice (approximately 7 weeks) demonstrated a close correlation with the average systolic BP in untreated (r = 0.76, N = 20), benazepril-treated (r = 0.80, N = 33), losartan-treated (r = 0.83, N = 32), or all animals combined (r = 0.81, N = 85, P < 0.0001 for all correlations). The slope of the relationship between GS and BP (percentage of increase in GS/mm Hg increase in BP) in untreated rats (0.7 +/- 0.14) was not significantly altered by either benazepril (0.96 +/- 0.13) or losartan (0.60 +/- 0.08), indicating that RAS blockade, by either agent, resulted in renoprotection that was proportionate to the achieved BP reductions. CONCLUSIONS: These data demonstrate that RAS blockade provides renoprotection in the rat remnant kidney model of progressive GS, primarily through "BP-dependent" and not "BP-independent" mechanisms.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed2000

Hypertension in patients with diabetes. Why is aggressive treatment essential?

Hypertension and diabetes are interrelated diseases. Alone, each condition is a risk factor for cardiovascular disease and, together, they strongly predispose to end-stage renal disease, coronary artery disease, and peripheral vascular and cerebrovascular disease. Pharmacologic treatment of hypertension can substantially reduce morbidity and mortality in diabetic patients with hypertension, but adequate control of blood pressure is seldom achieved in a clinical setting. More aggressive treatment is needed to improve the prognosis for this over-expanding patient population.

Antihypertensive Agents↗
PubMed2000

Hypertension in patients with diabetes. Overcoming barriers to effective control.

The management of diabetic hypertension poses special problems for the medical community. Although patient adherence is often a major barrier to successful management, physicians' beliefs and prejudices also negatively impact treatment. In addition, healthcare organizations need to provide better support to physicians who feel isolated in their efforts to manage diabetic hypertension. Reductions of morbidity and mortality are achievable goals but require aggressive treatment and improved adherence if they are to be reached.

Antihypertensive Agents↗
PubMed2000

Hypertension in patients with diabetes. Strategies for drug therapy to reduce complications.

Hypertension in diabetic patients must be treated aggressively if patients are to benefit from reduced risk of morbidity and mortality. Diabetes itself must be diagnosed promptly, particularly in at-risk patients, so appropriate lifestyle modifications can be made at the earliest opportunity. Although this may reduce or delay onset of hypertension, antihypertensive drug treatment should be initiated in the diabetic patient with even high-normal blood pressure. Traditional approaches to management of hypertension are inappropriate for most patients with diabetes. While ACE inhibitors, calcium antagonists, angiotensin II receptor blockers, beta blockers, and low-dose diuretics, alone or in combination, all currently have roles in hypertension management, the outcomes of studies now under way may clarify some still unanswered questions about the dangerous combination of high blood pressure and diabetes.

Diabetes Complications↗
PubMed1998

Diabetic hypertensive patients: improving their prognosis.

Diabetes is a devastating disease with multiple adverse effects on the vasculature. Moreover, hypertension is a prerequisite for patients with diabetes to progress to end-stage renal disease and to develop cardiovascular complications. Adequate control of blood glucose and blood pressure are the two most important factors that predict a favorable renal outcome. Recent studies have also shown that some classes of antihypertensive medications, such as the angiotensin-converting enzyme (ACE) inhibitors, may be ideal initial agents to control blood pressure in the hypertensive diabetic patient and thus to preserve renal function. In addition, nondihydropyridine calcium-channel blockers have been shown to retard the decline in renal function in patients with non-insulin-dependent diabetes mellitus (NIDDM) nephropathy who have lost at least 50% of their renal function. Retrospective analyses demonstrate that a reduction in blood pressure, especially to levels of <130/85 mg Hg in diabetic patients, retards the progression of renal disease. Reduction in arterial pressure to these low levels is probably more important than the agents used to achieve this goal. Because many of these patients require more than one medication to achieve these lower levels of arterial pressure, it is clear that fixed-dose combinations of such agents will both improve the likelihood of achieving a given blood pressure goal as well as medication compliance.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1997

Effects of an ACE inhibitor combined with a calcium channel blocker on progression of diabetic nephropathy.

It is clear that angiotensin-converting enzyme (ACE) inhibitors slow progression of diabetic nephropathy to a greater extent than other antihypertensive agents when blood pressure (BP) is reduced to levels below 140/90 mm Hg. Recent studies also demonstrate that nondihydropyridine calcium channel blockers (NDCCBs) slow progression of diabetic nephropathy in people with pre-existing renal insufficiency secondary to non-insulin dependent diabetes mellitus. The combined effects of both a CCB and ACE inhibitor have recently been examined in both animal models of diabetes as well as patients with established diabetic nephropathy. These studies demonstrate the following points: (a) at comparable BP levels, a combination of an ACE inhibitor with a NDCCB result in a greater reduction in proteinuria when compared to either components alone; and (b) conversely, addition of an ACE inhibitor to a dihydropyridine CCB (DCCB) yields effects on proteinuria similar to the ACE inhibitor alone. Therefore, addition of an ACE inhibitor to a DCCB demonstrates protection against the effects of DCCB alone. Addition of an ACE inhibitor to a NDCCB does not potentiate the preservation of renal morphology associated with progression of diabetic nephropathy when compared to either of its components alone. Conversely, a DCCB/ACE inhibitor combination yields morphologic results similar to the ACE inhibitor alone. Taken together these results suggest that ACE inhibitors when combined with a NDCCB result in greater reductions in proteinuria, and similar preservation of renal morphology when compared to either of its components alone.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1997

Role of vasopressin in essential hypertension: racial differences.

BACKGROUND: Arginine vasopressin (AVP), in addition to being an antidiuretic hormone, might also have pressor effects relevant to the maintenance of hypertension. Results from several experimental and clinical studies suggested that the pressor function of AVP is more important in low-renin hypertension and in the salt-loaded state and that it might be further maximized under sympathetic suppression. OBJECTIVE: To assess whether selective vasopressin receptor inhibition lowers the blood pressure in a racially diverse group of low-renin hypertensive subjects. METHODS: Thirty-nine hypertensive subjects (16 Caucasian, 23 African-American) eating a 200 mmol/day sodium diet were administered a single intravenous dose of a selective vasopressin receptor antagonist and their blood pressure was monitored constantly for the ensuing 3 h. The protocol was repeated 3 days later after treatment with a single oral dose of 0.4 mg clonidine. RESULTS: Of these patients, 54% had their blood sampled for determination of hormone profiles. African-Americans with hypertension had higher baseline plasma AVP levels than did Caucasians (1.13 +/- 0.05 versus 0.37 +/- 0.06 pg/ml, respectively, P < 0.05), and lower plasma renin activity (0.34 +/- 0.07 versus 1.03 +/- 0.08 ng/ml per h, respectively, P < 0.05). Selective vasopressin receptor inhibition lowered the mean arterial pressure in African-Americans but not that in Caucasians (lowering by 28 +/- 4 mmHg in African-Americans versus lowering by 5 +/- 3 mmHg in Caucasians, P < 0.05). Moreover, vasopressin receptor blockade further reduced the arterial pressure in African-Americans but not that in Caucasians after pretreatment with clonidine. CONCLUSION: AVP seems to play a more important role as a pressor hormone in maintaining the elevation of arterial pressure in African-American hypertensives than it does in Caucasian hypertensives.

Antidiuretic Hormone Receptor Antagonists↗
PubMed1996

Newer approaches to antihypertensive therapy. Use of fixed-dose combination therapy.

Despite the availability of many newer antihypertensive agents, hypertensive patients remain at higher risk of premature death than the general population. This persistence of morbidity and mortality may be accounted for by the frequent failure to achieve adequate blood pressure reduction despite an extensive array of available antihypertensive agents. Such considerations have led to reassessment of the potential role of fixed-dose combination agents in the antihypertensive armamentarium. The rationale for combination therapy relates to the concept that antihypertensive efficacy may be enhanced when 2 classes of agents are combined. In addition, combination therapy enhances tolerability-1 drug of a fixed combination can antagonize some of the adverse effects of the second drug. Fixed-dose combination therapy simplifies the treatment regimen, preventing treatment failures that might result from missed doses. An additional novel concept is the possibility of enhancing salutary effects on target organs, including regressing left ventricular hypertension and retarding progression of renal disease, by combination therapy over and above the effects expected from the fall in arterial pressure alone. The recent approval by the Food and Drug Administration of 2 fixed-dose angiotensin-converting enzyme inhibitor/calcium antagonist combinations has focused attention on and prompted reexamination of this issue.

Antihypertensive Agents↗
PubMed1994

Effects of different antihypertensive treatments on morphologic progression of diabetic nephropathy in uninephrectomized dogs.

We previously reported the renal hemodynamic effects of different antihypertensive regimens in uninephrectomized, alloxan-induced, diabetic (DM) beagle dogs following one year of treatment. Dogs were prospectively randomized to one of five groups (N = 26): nondiabetic controls, Group I; dogs with DM on no antihypertensive drugs, Group II; dogs on a converting enzyme inhibitor, lisinopril (L), Group III; dogs on a calcium antagonist, TA3090 (diltiazem-like), Group IV; and dogs on a combination of each drug, in reduced doses, Group V. The current paper extends our previous studies by describing the morphologic changes that occurred within each group of dogs studied. More than 100 glomeruli from the renal cortex of each dog were evaluated for increases in mesangial volume fraction (Vv), glomerulosclerosis (GS) and ateriolar hyalinosis. The interstitium was also evaluated for associated changes. Increases in Vv were attenuated in all treated groups (0.28 +/- 0.04, DM alone versus 0.16 +/- 0.05 L; 0.21 +/- 0.07, TA-3090; 0.19 +/- 0.06 micron 2/micron 2, L+TA 3090; P < 0.05) compared to untreated DM. An attenuated increase in Vv also correlated with a blunted rise in proteinuria in Groups III (r = 0.79) and V (r = 0.81) but not Group IV (r = 0.29). Development of focal GS was blunted in all treated groups; however, global GS was fourfold greater in Group IV compared to untreated DM. The degree of interstitial fibrosis also correlated with the degree of global GS. These data support the concept that both a converting enzyme inhibitor and heart rate lowering calcium antagonist attenuate morphologic progression of diabetic renal disease.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1994

Antihypertensive therapy and progression of diabetic renal disease.

A number of changes in intrarenal hemodynamics and morphology are characteristic of diabetic nephropathy. These changes include: increases in intraglomerular pressure and volume, glomerular capillary permeability to macromolecules, and mesangial matrix expansion. Most antihypertensive drugs attenuate some of the increases in these parameters. Certain antihypertensive agents, however, have effects on all these parameters. Studies in animal models of diabetes demonstrate that the angiotensin-converting enzyme (ACE) inhibitors reduce both intraglomerular volume and pressure, mesangial matrix expansion, and albuminuria. The calcium antagonists TA-3090 (diltiazem-like) and verapamil recently have been shown to have most of these effects. Conversely, the dihydropyridine calcium antagonists (nifedipine, felodipine, nitrendipine) do not attenuate increases in most of these parameters. In several clinical studies, nifedipine either did not affect or increased urinary albumin excretion in diabetic patients with renal insufficiency. Moreover, in animal models of diabetes, most dihydropyridine compounds do not prevent progression of glomerulosclerosis in spite of blood pressure control. Although the majority of clinical studies support the concept that reduction of arterial pressure preserves renal function, recent long-term clinical studies show that ACE inhibitors and heart-rate-lowering calcium antagonists (diltiazem, verapamil) attenuate progression of diabetes to a greater extent than most other agents do.

Albuminuria↗
PubMed1993

Renal effects of antihypertensive medications: an overview.

A variety of antihypertensive agents are available for management of elevated arterial pressure. Although these agents all effectively lower arterial pressure, they have somewhat diverse renal hemodynamic profiles. This report reviews the various similarities and differences in renal hemodynamic profiles among the different antihypertensive agents.

Adrenergic alpha-Antagonists↗
PubMed1991

Exfoliative dermatitis secondary to tobramycin sulfate.

We report a case of exfoliative dermatitis clearly linked to intravenous and intraperitoneal administration of tobramycin. Despite the complicated drug regimen with which the patient was treated, tobramycin was implicated by rechallenge with the drug once before its role was understood and again at an outside hospital.

Drug Eruptions↗