Biomedical subjects

Rubin Zhang

Publications and source records attributed to Rubin Zhang.

7 recordsLinked to original sources

PubMed2005

Hypertension and the metabolic syndrome.

The cause of hypertension in the metabolic syndrome is complex and multifactorial and all of the elements of the metabolic syndrome, including obesity, insulin resistance, and the characteristic dyslipidemia probably are involved in mediating changes ultimately resulting in hypertension and modifying its course. Of these elements, obesity may play the most important and pivotal role in creating the conditions that lead to hypertension in the metabolic syndrome. This is not to say that the other elements of the syndrome are less important, and, as we gain more insight into the processes involved, we should be able to better manage the disease and tailor our therapeutic interventions appropriately.

Dyslipidemias↗

PubMed2005

Kidney disease and the metabolic syndrome.

The epidemic of metabolic syndrome contributes to the rapid growth of cardiovascular and renal diseases. Hyper-hemodynamics, impaired pressure natriuresis, excess excretory load, insulin resistance, endothelial dysfunction, chronic inflammation, and prothrombotic status individually and interdependently initiate renal injury in metabolic syndrome. The prevention and treatment of kidney disease require a multifactorial approach. Weight loss through diet control and exercise can reverse many pathophysiologic processes. Pharmacologic intervention includes insulin sensitizers, tight glycemic and lipid control, blockage of renin angiotensin aldosterone system, and anti-inflammatory and antithrombotic therapies. Each peroxisome proliferator-activated receptor isoform plays a distinct role in metabolic syndrome, and their agonists may prevent or reverse the early renal injuries.

Cardiovascular Diseases↗

PubMed2004

Kidney transplantation: the evolving challenges.

Kidney transplantation is the treatment of choice for patients with end stage renal disease. Kidney transplantation not only improves the quality of life but also prolongs life. Over the last decade, the short-term allograft survival rate has been improved dramatically. Chronic allograft nephropathy and death from cardiovascular diseases become predominant causes of later graft loss. Prevention and treatment of these disease processes require a comprehensive approach. The ever-increasing shortage of organ supply becomes the greatest challenge for the transplant community and modern medicine. More and more patients are waiting for organs; many of them are dying while waiting. Xenotransplantation and organ engineering and cloning are promising techniques and can potentially provide organs for transplantation in the future.

Animals↗

PubMed2003

Regression of left ventricular hypertrophy is a key goal of hypertension management.

Left ventricular hypertrophy (LVH) in patients with hypertension is associated with an increased risk for many cardiovascular events and predicts a higher mortality rate. The pathogenesis of LVH is complicated. In addition to the hemodynamic burden (pressure or volume overload) and demographic factors, several trophic humoral factors, such as angiotensin II, aldosterone, endothelin, leptin, and catecholamines, may also contribute to the development and progression of LVH. Effective antihypertensive therapy can reverse LVH as well as prevent its development. Regression of LVH decreases subsequent cardiovascular morbidity and mortality. The commonly used drugs have various effects on LVH. Angiotensin receptor blockers and angiotensin-converting enzyme inhibitors seem most effective. Several new agents, including direct antifibrotic drugs, aldosterone blockade, vasopeptidase inhibitors, and endothelin receptor antagonists that more specifically target the underlying pathogenesis of LVH may provide us with innovative approaches to treat LVH.

Angiotensin II Type 1 Receptor Blockers↗

PubMed2003

Hypertension in chronic dialysis patients: pathophysiology, monitoring, and treatment.

The prevalence of hypertension in the population with ESRD is very high, approaching 100% in some populations, and may account for the fact that cardiovascular disease continues to be the leading cause of morbidity and mortality in ESRD. The pathophysiology of hypertension in ESRD is reviewed, suggesting multifactorial causes; a dominant cause is that of volume expansion and an inappropriate increase in systemic vascular resistance because of activation of the renin-angiotensin system. The primary goal in the treatment of hypertension should be to attain a dry-weight and maintain volume control through limiting salt and fluid intake and ultrafiltration of excess fluids. If this approach is unsuccessful, an array of antihypertensive medications are available to help control blood pressure in patients with ESRD.

Antihypertensive Agents↗

PubMed2003

Hypertension after kidney transplantation: impact, pathogenesis and therapy.

Hypertension (HTN) contributes to the high incidence of cardiovascular disease mortality as well as chronic allograft nephropathy (CAN) and late graft failure in renal transplant recipients. The mechanisms are complex and may involve pathogenic factors attributable to the host, allograft, and immunosuppressive drugs. Calcium channel blockers should be used to ameliorate the nephrotoxicity of calcineurin inhibitors in the early years after transplantation. Angiotensin-converting enzyme inhibitors and angiotensin-2 type-1 receptor blockers are safe and effective, have antiproteinuric effects, slow the progression of CAN, and may provide survival benefits. Diuretics and/or beta-adrenergic receptor blockers are frequently added in combination regimen. Appropriate adjustment of the immunosuppressive drugs should also be considered for the long-term care of kidney recipients with HTN.

Antihypertensive Agents↗

PubMed2002

Endocarditis and hemorrhagic stroke caused by Cunninghamella bertholletiae infection after kidney transplantation.

Cunninghamella bertholletiae is a saprophytic fungus found in soil. Infection with this organism is extremely rare, occurring almost exclusively in immunosuppressed hosts. There have been only three previous cases of infection with this fungus reported in solid-organ recipients. We report an unusual case of disseminated Cunninghamella infection in a woman who had received a renal transplant. A 48-year-old woman received a living-related kidney transplant for focal segmental glomerulonephritis. She was treated with plasmapheresis and muromonab-CD3 (OKT3) for two episodes of rejection. Because of recurrent focal segmental glomerulonephritis with diuretic-resistant edema, she underwent transplant nephrectomy, was restarted on hemodialysis, and had her immunosuppression stopped. Shortly thereafter, the patient presented with pulmonary infiltrates and hemorrhagic stroke with a rapidly fatal course. Autopsy revealed widely disseminated C bertholletiae involving the central nervous system, lungs, and heart. This is the first reported case of endocarditis caused by this organism. Diagnosis of this fungal infection is often difficult. Because the few patients who have survived this infection seemed to have been diagnosed early, it is important for clinicians caring for transplant patients to be aware of this invasive infection. Successful treatment requires prompt diagnosis and high-dose amphotericin B.

Cerebral Hemorrhage↗