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PubMed2005

Prediction model of coronary heart disease in patients with chronic kidney disease: role of plasma fibrinogen as a new prognostic variable.

BACKGROUND: The Framingham-Anderson (FA) risk equation can predict coronary heart disease (CHD) risk in the general population. However, this formula's validity in predicting CHD risk in chronic kidney disease (CKD) patients is not extensively evaluated. METHODS: In a group of 96 patients with CKD stage 2 to 4, free of CHD at the time of the start of follow-up, and prospectively followed for 4 to 12 years (7.4 +/- 2.2 years, mean +/- SD), we calculated the FA index. RESULTS: During the follow-up period, twenty-one patients experienced fatal and non-fatal myocardial infarction (CHDobs+), and 75 remain free of CHD (CHDobs-). The median FA index was 7.1% for CHDobs - patients and 10.3% for CHDobs+ patients. The specificity of the model was acceptable (89%), but the sensitivity was low (24%). Sensitivity analysis by adding fibrinogen led to an improvement in the CHD risk index and the sensitivity of the model (48%) as well. However, despite the addition of fibrinogen to the FA risk factors, full CHD risk in CKD patients remains underestimated. CONCLUSIONS: Our results show that the FA index is a weak predictor of CHD in CKD stage 2 to 4 patients, and emphasized the role of inflammation in predicting the CHD risk.

Aged↗
PubMed1998

The level of autoantibodies against oxidized LDL is not associated with the presence of coronary heart disease or diabetic kidney disease in patients with non-insulin-dependent diabetes mellitus.

Oxidation of low-density lipoprotein (LDL) may be an important factor in the development of diabetic macrovascular and renal complications. The level of autoantibodies against oxidized LDL (oxLDL-Ab) can be used as an index of LDL oxidation in vivo. The purpose of this study was to investigate the association between the level of oxLDL-Ab and the presence of coronary heart disease and renal dysfunction in patients with non-insulin-dependent diabetes mellitus (NIDDM). We determined the plasma levels of oxLDL-Ab in 46 NIDDM patients and 48 well matched nondiabetic control subjects. NIDDM patients had a moderately higher level of oxLDL-Ab than control subjects (0.083 +/- 0.051 vs. 0.062 +/- 0.045, p = 0.04). However, there was no difference in the level of oxLDL-Ab between subjects with and without coronary heart disease, and the level of oxLDL-Ab was not associated with indices of glomerular filtration rate or urinary albumin excretion.

Aged↗
PubMed1998

Effect of dietary soy protein and genistein on disease progression in mice with polycystic kidney disease.

The effects of feeding a soy protein isolate or genistein, an isoflavonoid present in soy protein, on cyst development were examined in the DBA/2FG-pcy (pcy) mouse, an accepted animal model of polycystic kidney disease, before the appearance of clinical symptoms. In study 1, 60-day-old male pcy mice were evenly divided into two groups and fed semipurified diets, based on casein or a soy protein isolate (15 g protein/100 g diet) for 90 days. In study 2, the animals were fed a casein-based diet (25 g casein/100 g diet) with or without genistein (0.05 g/100 g diet) for 60 days. In study 1, total kidney weight and kidney weight relative to body weight were significantly reduced (by 24% to 25%) in the animals fed the soy protein-based diet, relative to the casein-fed group, as was kidney water content (by 38%). In addition, mean cyst volume, as measured by morphometry, were lower (by 25%) in kidneys from the soy protein-fed group. No differences were found between these two groups with respect to final body weight, plasma creatinine, and protein content; however, plasma urea values were significantly lower in the soy protein-fed animals. Genistein supplementation of a casein-based diet in study 2 did not reduce the renal enlargement and cyst development associated with progression of polycystic kidney disease. These results suggest that soy protein is effective in retarding cyst development in the pcy mouse and that this beneficial effect may be unrelated to its genistein content.

Animals↗
PubMed2005

Metabolic acidosis: an unrecognized cause of morbidity in the patient with chronic kidney disease.

In patients with chronic kidney disease, metabolic acidosis can occur as a result of insufficient ammoniagenesis within the damaged kidney. This, in turn, can bring about a variety of sequella that have their basis in hormonal and cellular abnormalities that effect stunted growth, loss of muscle and bone mass, and negative nitrogen balance. Cellular mechanisms accounting for these findings are reviewed. In bone, metabolic acidosis causes direct dissolution of bone; ostoeclastic activity is increased while osteoblastic activity is suppressed. In muscle, branched-chain amino acid oxidation is increased and the ubiquitin-proteasome pathway is activated: muscle wasting results. Even a modest degree of metabolic acidosis can be harmful and can initiate a series of maladaptive responses that are not easily reversed, although there is evidence that alkali therapy can be beneficial in reversing these responses.

Acidosis↗
PubMed2004

Recent trends in hospital management practices and prognosis after acute myocardial infarction in patients with kidney disease.

Patients who have kidney disease receive aspirin, beta blockers, lipid-lowering therapy, thrombolytic agents, and coronary interventions less often than patients who have normal kidney function. The odds of dying during hospitalization for acute myocardial infarction were significantly higher among patients who had kidney disease than among those who did not have kidney disease after adjusting for several demographic and clinical confounders and year of hospitalization.

Aged↗
PubMed1995

Methylprednisolone retards the progression of inherited polycystic kidney disease in rodents.

Polycystic kidney disease in adult laboratory animals and humans is associated with enlarged kidneys and a progressive decline of renal function, resulting in death from uremia. Interstitial inflammation and fibrosis typically are observed in association with the development of renal insufficiency. To determine whether amelioration of interstitial inflammation and fibrosis may diminish cyst expansion/kidney enlargement and stabilize renal function, we administered methylprednisolone, an anti-inflammatory drug with antifibrogenic effects, to mice and rats with hereditary polycystic kidney disease. The experiment was repeated once for each species. Mice were studied both in America and in Japan. Weanling male and female mice (DBA/FG pcy/pcy [cystic] and +/+ [normal], n = 87 and 20, respectively) and rats (Han:SPRD Cy/+ and +/+, n = 70 and 33, respectively) were administered methylprednisolone (1 to 2 mg/kg/d) in the drinking water for 100 days (mice) or 42 days (rats). Control animals drank distilled water. In normal DBA +/+ mice, methylprednisolone had no effect on serum urea nitrogen (SUN) levels, kidney weight, or kidney/body weight. Untreated male and female mice developed cystic kidneys and azotemia to an equal extent. Methylprednisolone administered in America to mice with renal cystic disease decreased kidney weight, kidney/body weight, SUN levels, volume density of cysts, and severity of interstitial fibrosis. In Japan, methylprednisolone decreased kidney weight and SUN levels of animals with cystic disease, but the effect on kidney/body weight did not reach statistical significance. In contrast to mice, male rats developed more severe renal cystic changes and were more azotemic than female rats. Methylprednisolone administered to male rats with cystic disease decreased SUN levels, kidney weight, kidney/body weight, volume density of cysts, and severity of interstitial fibrosis. Methylprednisolone had no effect on kidney/body weight or SUN levels in female rats with renal cystic disease. In normal Han:SPRD (+/+) rats of both sexes, kidney and body weight were decreased by methylprednisolone, but kidney/body weight and SUN levels were unchanged. On the basis of this study, we conclude that methylprednisolone decreased the extent of renal enlargement, reduced renal interstitial fibrosis, and preserved kidney function in mice and rats with relatively severe forms of inherited polycystic kidney disease.

Animals↗
PubMed2004

Predictors of new-onset kidney disease in a community-based population.

CONTEXT: Kidney disease is associated with an increased risk for the development of cardiovascular disease and end-stage renal disease; however, risk factors for kidney disease have not been well studied. OBJECTIVE: To identify predictors of the development of new-onset kidney disease. DESIGN, SETTING, AND PARTICIPANTS: A community-based, longitudinal cohort study of 2585 participants who attended both a baseline examination in 1978-1982 and a follow-up examination in 1998-2001, and who were free of kidney disease at baseline. MAIN OUTCOME MEASURES: Kidney disease was assessed by the Modification of Diet in Renal Disease Study equation and defined by a glomerular filtration rate (GFR) in the fifth or lower percentile (< or =59.25 mL/min per 1.73 m2 in women, < or =64.25 mL/min per 1.73 m2 in men). Stepwise logistic regression was used to determine the impact of risk factors on the occurrence of new-onset kidney disease. Baseline and long-term, 12-year, averaged risk factor models were explored. RESULTS: At baseline, there were 1223 men and 1362 women, with a mean age of 43 years, who were free of preexisting kidney disease. After a mean follow-up of 18.5 years, 244 participants (9.4%) had developed kidney disease. In multivariable models, baseline age (odds ratio [OR], 2.36 per 10-year increment; 95% confidence interval [CI], 2.00-2.78), GFR (<90 mL/min per 1.73 m2: OR, 3.01; 95% CI, 1.98-4.58; 90-119 mL/min per 1.73 m2: OR, 1.84; 95% CI, 1.16-2.93), body mass index (OR, 1.23 per 1 SD; 95% CI, 1.08-1.41), diabetes (OR, 2.60; 95% CI, 1.44-4.70), and smoking (OR, 1.42; 95% CI, 1.06-1.91) were related to the development of kidney disease. In addition to baseline age and GFR, the long-term, averaged risk factors that were predictive of kidney disease included hypertension (OR, 1.57; 95% CI, 1.17-2.12), high-density lipoprotein cholesterol level (OR, 0.80 per 1 SD; 95% CI, 0.69-0.92), and diabetes (OR, 2.38; 95% CI, 1.45-3.92). Compared with a normal GFR (> or =120 mL/min per 1.73 m2), a mildly reduced GFR (<90 mL/min per 1.73 m2) predicted a 3-fold odds of progression to kidney disease (OR, 2.95; 95% CI, 1.94-4.49). CONCLUSIONS: Established cardiovascular disease risk factors are associated with the development of new-onset kidney disease. Patients with a mildly reduced GFR should be monitored for progression to kidney disease.

Adult↗
PubMed2002

Preoperative care of patients with kidney disease.

Patients with chronic kidney disease often require surgical interventions for vascular access and for medical problems related to comorbid conditions. Perioperative morbidity and mortality rates are increased in these patients. Preoperative attention to common medical problems that occur in patients with impaired renal function can lower some surgical risks. Hyperkalemia can be temporarily improved by the intravenous administration of an insulin-dextrose combination or bicarbonate, and polystyrene binding resins or dialysis can remove excess stores of potassium. Increased bleeding related to uremic platelet dysfunction can be managed by the administration of desmopressin, cryoprecipitate, or estrogens, and by avoiding the use of medications with antiplatelet effects close to the time of surgery. Transfusions of red blood cells should be reserved for use in patients with clinically significant anemia, because antibody formation may decrease the likelihood of successful renal transplantation in the future. Cardiovascular disease is the most common cause of death in patients with renal disease. Patients with chronic kidney disease may have hypertension and hypoglycemia in the perioperative period. Preoperative testing may be necessary in patients with cardiac risk factors. If future vascular access grafting is contemplated, intravenous line placement and blood draws should be avoided in a patient's nondominant arm.

Anemia↗
PubMed1982

Prognosis curves for patients with polycystic kidney disease.

In patients with polycystic kidney disease and in many patients with other chronic renal diseases kidney function decreases from year to year. When the increase in serum creatinine concentration is followed graphically, the time for dialysis/transplantation can be predicted long beforehand. Based on the course of azotaemia in 34 patients with polycystic disease prognosis curves have been prepared. By comparing the course of a patient with the average course of similar patients, additional information can be gained. A statistical method for making a prognosis curve for kidney function in end-stage polycystic renal disease is described.

Adult↗
PubMed2004

Combination therapy improves survival after acute myocardial infarction in the elderly with chronic kidney disease.

BACKGROUND: Individuals with chronic kidney disease have a high mortality rate after acute myocardial infarction. It is not known how frequently these individuals are prescribed combination cardioprotective therapy and if survival is affected by such therapy after acute myocardial infarction. METHODS: A retrospective cohort study of 1,342 Medicare recipients with acute myocardial infarction. Data were collected by medical chart abstraction as part of the Cooperative Cardiovascular Project in 60 hospitals in North Carolina during 5/30/1996-12/28/1997. We categorized cardioprotective medication use as aspirin alone, aspirin with beta-blockers, and aspirin with beta-blockers and ace-inhibitors. Chronic kidney disease was defined as a derived glomerular filtration rate (GFR) ranging from 15-89 mL/min/1.73 m2. Cox proportional hazards regression analyses were performed to determine the effect of cardioprotective medication use on survival while controlling for potential explanatory variables. RESULTS: The prevalence of cardioprotective medication use differed among levels of chronic kidney disease. Those with severe kidney disease (GFR 15-29 mL/min/1.73 m2) were less frequently prescribed aspirin with beta-blockers, 27.1%, and only 8.6% were prescribed aspirin with beta-blockers and ace-inhibitors. Survival was improved with prescribed cardioprotective medication use. In severe kidney disease (GFR 15-29 mL/min/1.73 m2), the hazards risk for death was 0.21 (0.08, 0.53) for aspirin alone, 0.17 (0.06, 0.51) for aspirin with beta-blockers, and 0.35 (0.09, 1.42) for aspirin with beta-blockers and ace-inhibitors. CONCLUSIONS: Individuals with chronic kidney disease benefit from combination cardioprotective therapy, but are less likely to be prescribed them after acute myocardial infarction. Further investigation is warranted to identify possible reasons for these observed treatment disparities.

Adrenergic beta-Antagonists↗
PubMed2006

Cardiovascular disease in early stages of chronic kidney disease in a Chinese population.

Cardiovascular disease (CVD) is one of the most serious complications of kidney disease, yet studies of CVD in early stage of chronic kidney disease (CKD) in Asian patients are very limited. Therefore, this study determined the prevalence and the spectrum of CVD in individuals with early-stage CKD and compared them with data of individuals without CKD. Compared with individuals with estimated GFR (eGFR) >90 ml/min per 1.73 m2, the prevalence of myocardial infarction, stroke, and total CVD of individuals with eGFR 60 to 89 ml/min per 1.73 m2 was increased by 91.4, 71.7, and 67.6%, respectively. For individuals with eGFR 30 to 59 ml/min per 1.73 m2, the percentage was 105.2, 289.1, and 200.7%, respectively. For each eGFR category, stroke was more prevalent than myocardial infarction. Compared with individuals with eGFR >90 ml/min per 1.73 m2, participants with eGFR 60 to 89 and 30 to 59 ml/min per 1.73 m2 tended to have more cardiovascular risk factors, and there were strong unadjusted and adjusted associations between CVD with different stages of eGFR (eGFR >90 ml/min per 1.73 m2 as reference). This is the first report on the prevalence and the spectrum of CVD in early stages of CKD in a community-based Chinese population. The spectrum of CVD in this Chinese population is different from reports of Western countries. Individuals with subtle decreased renal function seem much more likely to have multiple cardiovascular risk factors and have higher prevalence of CVD than those without CKD.

Adult↗
PubMed2005

Increased activity of activator protein-1 transcription factor components ATF2, c-Jun, and c-Fos in human and mouse autosomal dominant polycystic kidney disease.

Autosomal dominant polycystic kidney disease is a common inherited disorder that predominantly manifests with the formation of fluid-filled cysts in both kidneys. The disease can be accounted for by a mutation in either the PKD1 or the PKD2 gene. It was demonstrated previously that aberrant expression of the PKD1 gene product, polycystin-1, results in modification of activator protein-1 (AP-1) transcription factor activity in cultured renal epithelial cells. Here, it is reported that activity of the AP-1 components c-Jun, ATF2, and c-Fos is altered in renal cystic tissue of patients with autosomal dominant polycystic kidney disease and of hypomorphic Pkd1 mice with polycystic kidney disease. Data were obtained using immunohistochemical and Western blot analysis. Significant upregulation of Thr71- and Thr69/71-phosphorylated ATF2 and Ser73-phosphorylated c-Jun and increased c-Fos were detected in small cysts and (dilated) ducts and tubules surrounded by fibrotic interstitium. The data indicate that various AP-1 components are constitutively activated in polycystic kidney disease and suggest that aberrant AP-1 activity is relevant for cyst formation.

Activating Transcription Factor 2↗
PubMed2006

Predominant extrahepatic biliary disease in autosomal recessive polycystic kidney disease: a new association.

Autosomal recessive polycystic kidney disease (ARPKD) is characterized by dilation of ectatic renal collecting ducts, intrahepatic biliary dysgenesis, and portal fibrosis. Portal hypertension and recurrent bacterial cholangitis can dominate the clinical picture in long-term survivors. Predominant extrahepatic bile duct disease was revealed in four patients who underwent magnetic resonance cholangiopancreatography. All four patients had portal hypertension, although liver biochemistries did not suggest biliary disease. In two of the patients, cholangitis was clinically ascribed to the bile duct disease. Western blot analysis of plasma membranes from normal rat extrahepatic bile duct and kidney revealed the presence of polyductin as a single approximately 440 kDa protein. Although the exact function of polyductin in the extrahepatic duct is unknown, it may have a role in the development and control of lumenal size. Clinical management of patients with ARPKD should include consideration of potential problems related to extrahepatic bile duct disease.

Adolescent↗