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Anton C Schoolwerth

Publications and source records attributed to Anton C Schoolwerth.

12 recordsLinked to original sources
PubMed2006

Chronic kidney disease: a public health problem that needs a public health action plan.

For a health problem or condition to be considered a public health issue, four criteria must be met: 1) the health condition must place a large burden on society, a burden that is getting larger despite existing control efforts; 2) the burden must be distributed unfairly (i.e., certain segments of the population are unequally affected); 3) there must be evidence that upstream preventive strategies could substantially reduce the burden of the condition; and 4) such preventive strategies are not yet in place. Chronic kidney disease meets these criteria for a public health issue. Therefore, as a complement to clinical approaches to controlling it, a broad and coordinated public health approach will be necessary to meet the burgeoning health, economic, and societal challenges of chronic kidney disease.

Humans↗
PubMed2006

Obesity is associated with family history of ESRD in incident dialysis patients.

BACKGROUND: Obesity is an established risk factor for chronic kidney disease and aggregates in families. The objective of this study is to examine the relationship between obesity and family history of end-stage renal disease (ESRD). METHODS: Data were collected from 25,883 incident patients with ESRD in US ESRD Network 6 (Georgia, North Carolina, and South Carolina) dialysis clinics between 1995 and 2003. Family history is defined as a first- or second-degree relative with ESRD. Body mass index (BMI) at dialysis therapy initiation was classified as underweight (BMI < 18.5 kg/m2), normal (BMI, 18.5 to <25 kg/m2), overweight (BMI, 25 to < 30 kg/m2), obese (BMI, 30 to <35 kg/m2), or morbidly obese (BMI > or = 35 kg/m2). RESULTS: Twenty-three percent of patients reported a family history of ESRD. Of patients reporting a family history of ESRD, 5.5% were underweight, 32.5% had normal BMI, 28.0% were overweight, 17.3% were obese, and 16.7% were morbidly obese. After controlling for age, race, sex, primary cause of ESRD, history of diabetes, history of hypertension, and estimated glomerular filtration rate at dialysis therapy initiation, reported family history of ESRD was associated with being overweight (odds ratio [OR], 1.17; 95% confidence interval [CI], 1.08 to 1.26), obese (OR, 1.25; 95% CI, 1.14 to 1.37), and morbidly obese (OR, 1.40; 95% CI, 1.27 to 1.55). CONCLUSION: Obesity at dialysis therapy initiation was associated independently with reported family history of ESRD. This finding suggests that behavioral factors, adiposity-related genes, and gene-by-BMI interaction may contribute to familial risk for ESRD. This finding also suggests that management of obesity may be even more important for patients with a family history of ESRD than for the general population.

Adult↗
PubMed2005

A public health action plan is needed for chronic kidney disease.

In 2005, chronic kidney disease (CKD) meets all criteria for classification as a public health problem in the United States. It imposes a large burden on society that is increasing despite ongoing efforts to control the disease. The burden is unevenly distributed by race and economic status, whereas evidence suggests that preventive strategies could substantially reduce the burden. Finally, there are indications that such strategies are not yet in place. A broad and coordinated public health approach to the burgeoning health, economic, and societal challenges of CKD is needed to complement present clinical approaches, increase awareness, promote early detection, and facilitate prevention and treatment.

Humans↗
PubMed2003

Chronic kidney disease: issues and establishing programs and clinics for improved patient outcomes.

The spectrum of chronic kidney disease (CKD) extends from the point at which there is slight kidney damage, but normal function, to the point at which patients require either a renal transplant or renal replacement therapy to survive. Epidemiological studies suggest there are approximately 20,000,000 patients with various stages of CKD. These patients have many comorbidities, including cardiovascular disease, hypertension, diabetes, anemia, nutritional and metabolic derangements, and fluid overload. Unfortunately, evidence shows that current CKD care in the United States is suboptimal, and late referral to a nephrologist is often the rule and not the exception. Roles of primary care physicians (PCPs) and nephrologists in the care of patients with CKD remain undefined. Several studies have suggested that care provided by multidisciplinary nephrology teams can improve patient outcomes. Currently, there are published evidence-based clinical practice guidelines for anemia management, nutritional therapy, and vascular access placement, with other CKD guidelines under development. The intent of this review includes providing compelling evidence for earlier screening, identification, and management of patients with CKD; showing that current CKD care is suboptimal; encouraging the development of multidisciplinary teams that provide collaborative care to patients with CKD, suggesting roles for PCPs and nephrologists in the care of these patients; describing CKD initiatives from national organizations; and providing a comprehensive checklist that can guide the development of CKD clinics and programs.

Comorbidity↗
PubMed2003

PPARgamma ligand attenuates PDGF-induced mesangial cell proliferation: role of MAP kinase.

BACKGROUND: Mesangial proliferation is a key feature in the pathogenesis of a number of renal diseases and can be experimentally induced by the mitogen platelet-derived growth factor (PDGF). Mitogen-activated protein kinase (MAPK) signaling plays a key role in mesangial cell proliferation. In the present study we examined whether peroxisome proliferator-activated receptor gamma (PPARgamma) activators/ligands, thiazolidinediones such as ciglitazone, troglitazone, and rosiglitazone, can inhibit cell proliferation by modulating individual steps in the MAPK pathway. METHODS: Mouse mesangial cells were made quiescent and proliferation was measured following the application of PDGF. Using ciglitazone as the model compound, the mechanism of the antiproliferative effect of PPARgamma activators on MAPK and specific cell cycle regulatory proteins were examined by Western blot analysis and transfection studies. RESULTS: Ciglitazone inhibited PDGF-induced mesangial cell proliferation in a dose-dependent manner (1 to 20 micromol/L). The inhibitory effect was blocked by a peroxisome proliferator-activated receptor element (PPRE) decoy oligonucleotide, indicating that the observed effect of ciglitazone was via PPARgamma activation. Ciglitazone (1 to 20 micromol/L) did not affect extracellular signal-regulated protein kinase (ERK) activation but inhibited the activation of serum response element (SRE) by 85 +/- 6% (P < 0.01). This effect was associated with a reduction in c-fos expression (80 +/- 9%, P < 0.01). Ciglitazone (1, 10, and 20 micromol/L) also inhibited cyclin D1 expression by 37 +/- 8%, 79 +/- 15%, and 87 +/- 12%, respectively (P < 0.001 to 0.001), and p21 expression by 45 +/- 6% (P < 0.01), 61 +/- 10% (P < 0.001), and 72 +/- 8% (P < 0.001), respectively. Ciglitazone inhibited PDGF-mediated up-regulation of p27. In addition, the antiproliferative effect of ciglitazone was potentiated by PD98059, a mitogen-activated protein (MAP) kinase kinase (MEK) inhibitor that acts at a step upstream from ERK. CONCLUSION: These data indicate that PPARgamma activation may inhibit mesangial growth directly by affecting MAPK and cell cycle regulatory proteins. Furthermore, a MAP kinase inhibitor can potentiate the antiproliferative effect.

Animals↗
PubMed2002

The role of the renin-angiotensin system in cholesterol and puromycin mediated renal injury.

BACKGROUND: Puromycin aminonucleoside (PAN) nephropathy is a widely studied model of glomerular sclerosis (GS) in the rat, and cholesterol feeding exacerbates the injury induced by PAN. The importance of the interaction of angiotensin II (Ang II) with the AT2 receptor is unclear. We investigated the role of the renin-angiotensin system, particularly with regard to AT1 and AT2 receptor dynamics, in PAN and cholesterol-mediated GS. METHODS: Sprague-Dawley rats were given a 4% cholesterol diet (group II), subcutaneous PAN (group III), or a 4% cholesterol diet and PAN (group IV) and compared with a control group given PAN vehicle (group I). After 16 weeks, kidneys were harvested and tissue Ang II concentration, angiotensin-converting enzyme (ACE) activity, and ACE, AT1, and AT2 mRNA levels were determined. RESULTS: Compared with control rats, proteinuria was significantly higher in groups II to IV. Kidney ACE activity and ACE mRNA levels in groups III and IV were 2- and 3-fold higher than in groups I and II, respectively. Kidney Ang II concentration also was increased in the experimental groups. Whereas kidney AT1 mRNA was significantly lower in groups III and IV, kidney AT2 mRNA was significantly increased in groups II to IV. CONCLUSION: In these experimental models of GS, there is significant activation of the tissue-based renin-angiotensin system. Puromycin with and without cholesterol decreased the AT1 receptor mRNA and increased the AT2 receptor mRNA. Up-regulation of AT2 receptors may be important in ameliorating the proliferative effects of Ang II, which presumably occur through the AT1 receptor.

Angiotensin II↗
PubMed2002

Part 1. Uric acid and losartan.

PURPOSE OF REVIEW: To characterize the mechanism and clinical impact of the angiotensin-receptor blocker losartan on both renal uric acid handling and thereby serum uric acid. RECENT FINDINGS: Losartan effect on serum uric acid has been demonstrated at various stages of renal failure including most recently observations obtained in end-stage renal disease patients. Other angiotensin-receptor blockers do not alter renal handling of uric acid. The uricosuria, which accompanies losartan administration, has not been associated with adverse renal consequences, in part, because of the increase in urinary pH that follows its administration. SUMMARY: Hyperuricemia is closely linked to both hypertension and cardiovascular disease. The development of hyperuricemia and its persistence are clearly renal processes. Likewise, the correction of hyperuricemia is often accomplished by increasing its renal excretion. A number of medications, by way of varying mechanisms, can alter renal urate handling and thereby influence serum uric acid values. Most recently, the angiotensin-receptor blocker losartan has been shown to reduce serum uric acid. The mechanism of this process relates to losartan alone and does not involve the E-3174 metabolite of this compound. This probenecid-like effect of losartan occurs shortly after drug administration, and is both transient and dose-dependent. This property of losartan, touted by some as a meaningful pharmacological distinction among the angiotensin-receptor blockers, remains to be proved, since, to date, the hypothesis that a reduction in serum uric acid alters the natural history of cardiovascular disease has not been formally tested.

Angiotensin-Converting Enzyme Inhibitors↗
PubMedDate not supplied

The epidemiology and outcome of acute renal failure and the impact on chronic kidney disease.

Acute renal failure (ARF) is a common condition, especially among the critically ill, and confers a high mortality. Recent publications have highlighted changes in the epidemiology and improvement in mortality that was long thought to be static despite improvements in clinical care. The incidence of ARF is increasing. Efforts, such as the Acute Dialysis Quality Initiative, are being undertaken to establish a consensus definition of ARF, and to distinguish between varying degrees of acute kidney injury. Data are emerging to allow comparison of the epidemiology of ARF across institutions internationally. There is ongoing recognition of the important interaction between ARF and chronic kidney disease. Two brief case reports are offered to help frame the context and clinical impact of this disorder, followed by a review of some of the recent literature that addresses these points.

Acute Kidney Injury↗
PubMedDate not supplied

Electrolyte disturbances in the intensive care unit.

The development of many electrolyte disturbances in the ICU can be prevented by attention to the use of intravenous fluids and nutrition. Hyponatremia is a relative contraindication to the use of hypotonic intravenous fluids and hypernatremia calls for the administration of water. Formulae have been devised to guide the therapy of severe hyponatremia and hypernatremia. All formulae regard the patient as a closed system, and none takes into account ongoing fluid losses that are highly variable between patients. Thus, therapy of severe hyponatremia and hypernatremia must be closely monitored with serial electrolyte measurements. The significance of hypocalcemia in the critically ill is controversial. Hypokalemia, hypophosphatemia, and hypomagnesemia should be corrected.

Humans↗