Anemia in diabetic patients at an internal medicine ward: clinical correlates and prognostic significance.

BACKGROUND: Characteristics and prognostic significance of anemia in hospitalized diabetic patients are unknown. METHODS: We studied 3145 unselected patients admitted to two Internal Medicine Departments, 872 (27.7%) of whom were diabetic. Forty diabetic patients died during the first hospitalization period. Out of the remaining 832 patients, 334 (40.2%) were anemic and evaluated for survival. In 87 diabetic patients, the cause of anemia was evident on admission, whereas the other 247 had to be further investigated for etiology of anemia. RESULTS: Compared to non-anemic diabetic patients, the diabetic anemic patients were older (mean age 71.4 vs. 64.4 years, P<.001) and predominantly females (52.4% vs. 44.4%, P<.02). Of the 247 evaluated patients, 38% were deficient in iron, 12% in vitamin B(12) and/or folate, 54% had anemia of chronic disease, 47% suffered from heart failure, 39% had renal dysfunction and 22% were complex nursing care patients and/or had diabetic foot. On median follow-up of 19.2 months, mortality rate was higher in anemic compared to non-anemic diabetic patients (17.3% vs. 4%, P<.001), the main cause of death being infection. Male sex (P=.03), albuminuria (P=.01) and heart failure (P=.06) were associated with shorter survival, male sex being the most significant (OR 2.02, 95% CI 1.04-4.00). CONCLUSION: Frequency of anemia was increased in diabetic patients admitted to the Internal Medicine Departments, compared to the studies performed on ambulatory patient populations. Anemia was multifactorial and associated with higher mortality, predominantly from infections. Males with albuminuria and heart failure were at higher risk of death.

Clinical variables affecting survival in patients with decompensated diastolic versus systolic heart failure.

BACKGROUND: The impact of various clinical variables on long-term survival of patients with acutely decompensated diastolic heart failure (DHF) compared to systolic heart failure (SHF) has not been sufficiently investigated. METHODS: Clinical, laboratory, electrocardiographic and echocardiographic data were collected and analyzed for all-cause mortality in 473 furosemide-treated patients aged >or=60 years, hospitalized for acutely decompensated HF. RESULTS: Diastolic heart failure patients (n = 183) were more likely to be older, female, hypertensive, obese, with shorter preexisting HF duration, atrial fibrillation, lower New York Heart Association (NYHA) class, lower maintenance furosemide dosages, and to receive calcium antagonists. The SHF group (290 patients) demonstrated prevailing coronary artery disease, nitrate or digoxin treatment, and electrocardiographic conduction disturbances (P

Seating-induced postural hypotension is common in older patients with decompensated heart failure and may be prevented by lower limb compression bandaging.

BACKGROUND: Postural hypotension induced by transition from supine to sitting position and measures for its prevention in heart failure has not been investigated. OBJECTIVE: Our purpose was to evaluate the prevalence of postural hypotension and associated clinical manifestations as well as the contribution of various risk factors for postural hypotension on transition from lying to sitting in older patients with decompensated heart failure, and to study the eventual preventive effect of leg bandaging. METHODS: Seating-induced postural hypotension (>or=20 mm Hg systolic and/or >or=10 mm Hg diastolic blood pressure fall) was assessed on the first study day in 108 patients aged >or=60 years, hospitalized for acutely decompensated heart failure. On the next day, in patients manifesting postural hypotension, compression bandages were applied along both legs before seating. Blood pressure, heart rate, O(2) saturation, and the occurrence of dizziness or palpitations were recorded prior to and 1, 3 and 5 min following seating. RESULTS: Postural hypotension occurred in 49.1% of patients. Dizziness and/or palpitations manifested in 25%. Diastolic (36.1%) versus systolic (23.1%) postural hypotension prevailed (p=0.05). On univariate analysis, postural hypotension was associated with female sex (p=0.03), more severe heart failure (p=0.05), longer bedrest (p=0.04), higher supine systolic (p=0.01) or diastolic (p=0.002) blood pressure, nonischemic heart failure (p=0.002), and not using nitrates (p = 0.01). On multivariate analysis, longer bedrest (OR=1.58, 95% CI=1.13-2.2, p<0.001), higher supine diastolic blood pressure (OR=1.33, 95% CI=1.1-1.61, p=0.001), and nonischemic heart failure (OR=3.48, 95% CI=1.4-8.63, p=0.009) were the most predictive of postural hypotension. Compression bandages prevented postural hypotension in 21 of 49 patients and decreased the degree of postural blood pressure fall (p<0.001). CONCLUSION: Seating-induced postural hypotension is common among older inpatients with decompensated heart failure, especially with longer bedrest, higher supine diastolic blood pressure and non-ischemic etiology. Leg compression bandaging may be useful for the prevention of postural hypotension in these patients.

Magnesium and C-reactive protein in heart failure: an anti-inflammatory effect of magnesium administration?

BACKGROUND: Little is known about the relationship between serum magnesium (Mg) and C-reactive protein (CRP) in heart failure (HF). AIM OF THE STUDY: To investigate the relationship, if any, between serum Mg and CRP in HF patients and, concomitantly, to test a hypothesis that Mg supplementation might affect serum CRP levels. METHODS: Serum Mg and CRP were evaluated in 68 patients with chronic systolic HF leading to hospital admission and 65 patients requiring hospitalization for other causes. Following 5 weeks, serum Mg, CRP and intracellular Mg were reevaluated in 17 HF patients after administration of oral Mg citrate 300 mg/day (group A), and 18 untreated HF patients (group B). In order to obtain Gaussian distribution, logarithmic transformation of CRP was performed. RESULTS: Inverse correlation was found between serum Mg and log CRP (r = -0.28, P = 0.002). Compared to controls, patients with HF demonstrated higher baseline CRP levels, independent of coexisting conditions, and lower serum Mg values. Following Mg treatment, log CRP decreased from 1.4 +/- 0.4 to 0.8 +/- 0.3 in group A (P < 0.001). No significant changes in log CRP were demonstrable in group B. Serum Mg (mmol/l) rose significantly in group A (0.74 +/- 0.04-0.88 +/- 0.08, P < 0.001), and to a lesser extent in group B (0.82 +/- 0.08-0.88 +/- 0.08, P = 0.04). Intracellular Mg significantly increased only in Mg-treated group A (P = 0.01). CONCLUSIONS: Oral Mg supplementation to HF patients significantly attenuates blood levels of CRP, a biomarker of inflammation. Targeting the inflammatory cascade by Mg administration might prove a useful tool for improving the prognosis in HF.

Patient-dependent variables affecting treatment and prediction of acute coronary syndrome are age-related. A study performed in Israel.

BACKGROUND: Acute coronary syndrome (ACS) prevails in older patients and is associated with higher morbidity and mortality. Little is known about patient-related variables that may affect course and treatment of ACS in older vs. younger with acute chest pain. METHODS: Situational, circumstantial, and other patient-related variables were assessed in 1000 unselected consecutive older (> or =70 years) and younger (<70 years) patients admitted with chest pain and possible ACS. RESULTS: In 182 older vs. 818 younger patients, prevalence of females, those not speaking the local language, living alone, lower education level, non-smokers, diabetes, hypertension, preexisting coronary artery disease, and attempting some form of self-treatment before seeking medical help were significantly greater (P<0.001). Interval from chest pain onset to emergency department arrival was longer (P=0.05), and a higher proportion of the older considered hospitalization mandatory, suspecting ACS (P<0.001). ACS eventually developed in 19.1% of younger and 39% of older patients (P<0.001). On multivariate analysis, most predictive of ACS in the younger group were: preexisting coronary artery disease (OR 5.27; 95% CI 3.44-8.07, P<0.001), current smoking (OR 1.78; 95% CI 1.16-2.75, P=0.002), male sex (OR 1.57; 95% CI 1.0-2.59, P=0.07), and older age (OR 1.25; 95% CI 1.11-1.42, P=0.005). In the older group, these were: not speaking the local language (OR 2.39; 95% CI 1.19-4.79, P=0.005), preexisting coronary artery disease (OR 1.95; 95% CI 1.0-3.87, P=0.026), direct emergency department arrival (OR 1.9; 95% CI 1.0-3.77, P=0.066), and diabetes (OR 1.84; 95% CI 1.0-3.56, P=0.079). CONCLUSIONS: We defined age-associated differences in patient-related variables that may predict ACS and affect treatment negatively. These variables might improve risk stratification upon hospitalization.

Apoptosis and proliferation of mesangial cells isolated from kidneys undergoing compensatory growth following contralateral nephrectomy: role of the renin-angiotensin system.

BACKGROUND: Contralateral nephrectomy stimulates compensatory growth of the remaining kidney. Intensive growth is frequently associated with increased apoptosis. The proliferation and apoptosis of cultured rat mesangial cells isolated from the remaining kidney following contralateral nephrectomy were evaluated. The involvement of the renin-angiotensin system was concomitantly assessed. MATERIAL/METHODS: Apoptosis was assessed by TUNEL assay and hematoxylin staining, proliferation by (3)H-thymidine incorporation, angiotensin-II (A-II) production by RIA, bradykinin synthesis by specific EIA, and AT-1/AT-2 receptor mRNA expression by RT-PCR.( 125)I-A-II labeling was applied for AT-1/AT-2 receptor density evaluation. RESULTS: Apoptosis of unstimulated control cultures progressively increased from a baseline of 2.02+/-0.55% to 8.3+/-1.19% in 30-min and 12.8+/-4.11% in 24-h cultures (p<0.0001 in each comparison), accompanied by augmented cell proliferation and both could be abolished by captopril treatment. Endogenous A-II synthesis was increased in postnephrectomy cultures. Exogenous A-II enhanced apoptosis of control, but not of postnephrectomy cells. Bradykinin synthesis was elevated in cultures treated with captopril, but not with losartan or PD123319. AT-1 mRNA was increased 24 h following nephrectomy. Total A-II receptor density was decreased 30 min and 24 h following nephrectomy, while blockade of AT-1/AT-2 receptors was ineffective. CONCLUSIONS: 1. Contralateral nephrectomy stimulates apoptosis and proliferation of mesangial cells in the remaining kidney via increased endogenous A-II. 2. The mechanism by which A-II triggers apoptosis and proliferation of mesangial cells is not related to the AT-1/AT-2 receptor pathway. 3. The effects of angiotensin-II can be abolished by ACE inhibition and are, at least in part, mediated via bradykinin activity.

Intracellular magnesium in elderly patients with heart failure: effects of diabetes and renal dysfunction.

Hypomagnesemia is frequent in diabetes mellitus (DM), while renal dysfunction (RD) may be associated with hypermagnesemia. Severe cardiac arrhythmias and other adverse clinical manifestations are frequent in heart failure (HF), in DM and in RD. Depletion of intracellular magnesium (icMg), which may coexist with normal serum Mg, might contribute to these deleterious effects. However, icMg content in normomagnesemic HF patients with RD or DM has not been studied. We assessed total icMg in peripheral blood mononuclear cells (PBMC) from 80 normomagnesemic furosemide-treated HF patients who were divided as follows: subgroups A (DM), B (RD), C (DM and RD), and D (free of DM or RD). PBMC from 18 healthy volunteers served as controls. IcMg content (microg/mg cell protein) in HF was lower compared to controls (1.68+/-0.2 vs. 2.4+/-0.39, p<0.001). In the entire HF group, a significant inverse correlation was evident between icMg and serum creatinine (r=-0.37) and daily furosemide dosages (r=-0.121). IcMg in the HF subgroups A, B, C, and D was 1.79+/-0.23, 1.57+/-0.23, 1.61+/-0.25, and 1.79+/-0.39, respectively (p=0.04 between A and B, p=0.08 between B and D, and non-significant in the remaining comparisons). Serum Mg, potassium, calcium, furosemide dosages and left ventricular ejection fraction were comparable in all subgroups. In conclusion, icMg depletion was demonstrable in PBMC, which may be responsible for some of the adverse clinical manifestations in HF patients. In particular, icMg depletion in RD might contribute to cardiac arrhythmias in this patient group. Mg supplementation to normomagnesemic HF patients might therefore prove beneficial.

Patient-related variables predicting acute coronary syndrome following admission for chest pain of possible coronary origin.

OBJECTIVE: Improving risk stratification of patients experiencing acute chest pain with non-revealing electrocardiogram and cardiac biomarkers could reduce missed acute coronary syndrome and avoid unnecessary hospitalization. METHODS: We assessed the ability of situational, circumstantial, and other patient-related variables in predicting acute coronary syndrome in 921 consecutive patients randomly admitted to this medical department with chest pain of possible coronary origin. A reference group comprised 107 patients referred promptly to the coronary care unit with acute myocardial infarction. RESULTS: Acute coronary syndrome eventually developed in 219 (23.7%) patients. Age and proportions of male patients and those with diabetes, which were significantly lower in the heterogeneous chest pain group than in the reference group, did not differ when re-evaluation was performed between the latter group and the subgroup of patients who eventually developed acute coronary syndrome. Overweight and a family history of premature coronary artery disease remained significantly higher in the reference group, while prevalence of pre-existing coronary artery disease, previous coronary angiography, and coronary intervention remained significantly lower. Variables most significantly predictive of acute coronary syndrome resulted: pre-existing coronary artery disease [odds ratio (OR) 3.2; 95% confidence interval (CI) 2.17-4.71; P<0.001), older age (OR 1.35; 95% CI 1.17-1.57; P<0.001), male sex (OR 1.77; 95% CI 1.19-2.61; P=0.004), diabetes (OR 1.6; 95% CI 1.11-2.32; P=0.01), self-initiation of pain relief treatment before seeking medical help (OR 1.54; 95% CI 1.07-2.23; P=0.02), and conviction that hospitalization for acute coronary disease was mandatory (OR 1.46; 95% CI 1.03-2.07; P=0.03). CONCLUSIONS: Easily obtainable patient-related variables might improve risk stratification and assist physicians to decide on policy in the emergency department and upon hospitalization.

Renal functional deterioration is not affected by the magnitude of sodium consumption in a normotensive model of moderate renal failure.

BACKGROUND/AIMS: High sodium consumption has been repeatedly reported to exert deleterious effects on severe chronic renal failure progression, mainly via glomerular mechanisms. However, the role of high sodium intake in renal function deterioration in a model of moderate chronic tubulointerstitial disease has not yet been addressed. We evaluated the effects of exaggerated dietary sodium and the resultant increase in proteinuria on renal function deterioration in experimental tubulointerstitial disease in rats. METHODS: In 48 Sprague-Dawley rats, moderate renal failure (approximately 50% of normal glomerular filtration rate) was induced by administration of lithium chloride in drinking water. The animals were divided into three groups fed low (<0.2% Na(+)), normal (0.5% Na(+)), or high (8% Na(+)) sodium diets. RESULTS: Animals in all groups remained normotensive with a similar course of GFR downslope and 100% survival, irrespective of sodium regimen. Rats consuming high sodium diets developed significantly greater proteinuria compared to their counterparts fed normal or low sodium chow. CONCLUSIONS: (1) Deterioration of renal function in a lithium-induced model of normotensive moderate chronic renal failure was not affected by dietary sodium. (2) Unlike in some other human or experimental renal failure models, the magnitude of proteinuria had no adverse effect on the progression of renal deterioration.

First morning standing up may be risky in acutely ill older inpatients.

Information about orthostatic hypotension (OH) among elderly patients hospitalized for acute conditions in short-term facilities is scarce. Many older inpatients carry various predisposing factors for OH. However, its existence goes frequently unrecognized. In this context, first morning standing up following admission for an acute disease may be dangerous. The aim of this study was to investigate OH and associated manifestations in this situation. OH (> or = 20 mmHg systolic and/or (> or =10 mmHg diastolic blood pressure fall), heart rate, arrhythmias and appearance of dizziness or palpitations were recorded in 121 sequential inpatients aged >65 years, prior to and 1, 3 and 5 min following first morning standing. OH occurred in 64.5% of patients, while dizziness and/or palpitations appeared in 76%. Severe adverse effects were registered in 11.5% of OH patients. Significantly associated with OH were: bed rest lasting 9-24 h (vs (< or = 8 h, p<0.001), appearance of dizziness or palpitations (p<0.001 and p=0.005, respectively), heart failure (p=0.02) and renal dysfunction (p=0.04). OH and/or associated symptoms are frequent in acutely ill older inpatients on first morning standing up following nocturnal bed rest. The ominous potential consequences call for alertness to this phenomenon and application of appropriate preventive measures.

Control of hypertension with captopril affords better renal protection as compared with irbesartan in salt-loaded uremic rats.

BACKGROUND/AIM: Hypertension induced by exaggerated sodium consumption accelerates the progression of renal failure. We investigated the effects of a high-sodium (HS) diet on the progression of renal failure in rats maintained normotensive by angiotensin-converting enzyme inhibition or AT-1 blockade. METHODS: In 70 Sprague-Dawley rats, renal failure was induced by five-sixths nephrectomy. They were fed isocaloric normal-sodium (NS), low-sodium (LS), or HS diets. HS rats prone to develop hypertension were divided into three subgroups: treated to normotension by irbesartan (HS-1) or captopril (HS-2) or left untreated (HS-0). RESULTS: All HS animals developed significant proteinuria which strongly correlated with the 24-hour sodium excretion. HS-0 rats demonstrated severe hypertension, rapid deterioration of the renal function, and 100% mortality after 3 weeks. In irbesartan-treated HS-1 rats, mortality and decline of the glomerular filtration rate were similar to those of normal- or low-sodium-fed animals (100% mortality after week 12). In captopril-treated HS-2 rats, glomerular filtration rate decline and mortality were significantly blunted as compared with all other groups (50% mortality after week 12). CONCLUSIONS: (1) In five-sixths-nephrectomized uremic rats maintained normotensive by either irbesartan or captopril, the rate of deterioration of the renal function was not aggravated by exaggerated sodium consumption. (2) In this experimental setting, captopril treatment yielded a better survival outcome as compared with irbesartan, despite the similar hypotensive effect.

Heart failure in diabetes mellitus: clinical features and prognostic implications.

We defined the prevalence and impact on survival of clinical bedside variables in 385 patients with symptomatic congestive heart failure (CHF), of whom there were 176 with and 209 without diabetes mellitus. Patients were consecutively hospitalized and admitted for various acute conditions. Following discharge all-cause mortality was recorded. Prevalence and association of various variables with mortality were statistically analyzed. Prevailing in the diabetics versus nondiabetics were younger age (p < 0.05), pulmonary edema on admission (p = 0.002), using furosemide > 80 mg/day (p < 0.01) for > 1 year (p < 0.01) and hyponatremia (p = 0.01). Less prevalent were chronic lung disease (p < 0.01) and cardiac arrhythmias (p = 0.001). On follow-up extending up to 60 months, diabetic patients, especially those with fasting blood glucose levels on admission > or = 180 mg/dl, survived for a shorter period of time than nondiabetics (p = 0.02). Associated with increased mortality in the diabetic group were female gender (p = 0.04), furosemide > or = 80 mg/day (p < 0.001) and renal dysfunction (RD; p = 0.04). The respective variables in the nondiabetics were advanced age (p < 0.001) and RD (p = 0.002). Although they were younger, diabetic patients presented more severe CHF. It is recommended that special attention should be given to diabetic females, those using higher furosemide dosages and those suffering from RD.

Sex-related bedside clinical variables associated with survival of older inpatients with heart failure.

BACKGROUND: Little is known about sex-related differences in factors affecting prognosis of heart failure (HF). We prospectively investigated the relationship between bedside clinical variables and survival of older females vs. males with HF. METHODS: Included were consecutive unselected inpatients, age >/=60 years, admitted for various acute conditions. HF was chronic and of diverse etiologies. Follow-up extended up to 5 years. All-cause mortality was registered and statistically analyzed for association with in-hospital clinical variables. RESULTS: Included were 162 females and 200 males. Survival rates were 52.4% and 59%, respectively, (P=0.1). Advanced age and renal dysfunction (RD) were associated with low survival in both sexes (P<0.03 and 0.02, P<0.001 and 0.01, respectively). An association with low survival was found with respect to; admission for pulmonary edema (P<0.02), using furosemide >/=80 mg/day (P<0.005) and severe HF [NYHA class III-IV (P<0.01)] in females, as well as for hypokalemia (P<0.03) and hypocalcemia (P<0.03) in males. On multivariate analysis RD (P<0.001), increasing age (P=0.008) and furosemide dosage >/=80 mg (P=0.02) were most significantly associated with low survival in females, while RD only was significantly associated with low survival in males (P=0.03). CONCLUSIONS: Several clinical variables, which affect prognosis in older HF patients are sex-related and probably carry practical significance.

Hypertension but not sodium intake determines progression of renal failure in experimentally uremic rats.

BACKGROUND/AIMS: High sodium intake is implicated in contributing to progression of chronic renal failure. We studied the effect of high sodium consumption on progression of rat experimental renal failure while sodium-induced hypertension was pharmacologically controlled. METHODS: 64 Sprague-Dawley rats underwent 5/6 nephrectomy. Subsequently, they were divided in three groups which were fed either low, normal, or high sodium diet. Only the high sodium-consuming group developed hypertension. This group was further divided in two subgroups in which hypertension was either untreated or titrated to normotension by hydralazine alone or with propranolol. RESULTS: Sequential GFR values did not differ between the respective normotensive groups. Survival downslopes of all three normotensive groups (including the pharmacologically treated, high sodium-consuming subgroup) were also similar, extending over 10 weeks. By contrast, pharmacologically untreated animals exhibited severe hypertension and 100% mortality within 3 weeks. In all experimental groups, 24-hour urinary sodium excretion paralleled sodium intake. Proteinuria rose similarly and significantly in all animals on high sodium. A significant correlation between 24-hour sodium and proteinuria was evident throughout the experimental period. CONCLUSIONS: (1) In 5/6 nephrectomized rats, renal function deterioration was not affected by dietary sodium, provided hypertension was pharmacologically controlled. (2) Enhanced proteinuria secondary to high sodium consumption had no adverse effect on progression of renal failure in this model.

Lower limb compression bandaging is effective in preventing signs and symptoms of seating-induced postural hypotension.

BACKGROUND AND AIMS: Data concerning postural hypotension (PH) induced by transition from supine to sitting position are scarce and measures for its prevention have not been investigated. Our objective was to assess the preventive role of lower limb compression bandaging on PH and associated manifestations in older inpatients when seated from lying position. METHODS: In a randomized crossover study, 61 patients aged >65 years were enrolled. Following bed rest lasting >36 h, each patient was seated and studied for 2 consecutive days, unbandaged or bandaged. PH was defined as a fall of >/=20 mm Hg and/or >/=10 mm Hg in systolic/diastolic blood pressure, respectively. Compression bandages were applied along both legs before seating; the pressure was approximately 30 mm Hg. Blood pressure, heart rate, O(2) saturation, dizziness and palpitations were recorded prior to and 1, 3, and 5 min following seating. RESULTS: Prevalence of PH was identical in the unbandaged versus bandaged state (55.7%). However, dizziness, palpitations, accelerated heart rate and decreased O(2) saturation over 5 min were more prevalent in the unbandaged versus bandaged state (p < 0.01, <0.001, <0.05, <0.001, respectively). In the unbandaged state, presence versus absence of PH was associated with significantly greater incidence of palpitations, tachycardia and decline of O(2) saturation over time (p < 0.04, <0.03, <0.03, respectively). In the bandaged state, O(2) saturation over 5 min tended to rise irrespective of PH, but mean values were higher in patients without PH (p < 0.02). CONCLUSIONS: Lower limb compression bandaging does not reduce the incidence of PH. However, associated manifestations are largely prevented.

Seated postural hypotension is common among older inpatients.

Bed-rest > 12 hours produced postural hypotension (PH) in 54% of seated older inpatients. PH was multifactorial, equally initiated throughout 5 minutes and symptoms arised frequently following small blood pressure drops. In this context PH should be anticipated and prevented.

Dietary intake of various nutrients in older patients with congestive heart failure.

BACKGROUND AND AIMS: Anorexia, nausea and premature satiety with eating, prevalent in congestive heart failure (CHF), have been held responsible for reduced dietary intake and deficiency of magnesium, potassium and probably other nutrients. Since solid data is not available, this study was undertaken with the following aims (1) to assess dietary intake in CHF, (2) to compare dietary intake in older CHF patients with a similar patient population free of CHF (control group), and (3) to evaluate these data in patients with moderate versus severe CHF. METHODS AND RESULTS: Dietary intake of 57 consecutively hospitalized furosemide-treated CHF patients over the age of 60 was compared with that of 40 similar patients free of CHF. In addition, a statistical analysis was performed comparing the data of the 37 patients with moderate versus the 20 patients with severe CHF. Dietary content of various nutrients was assessed with the food frequency recall technique. Dietary intake was comparable in the two respective pairs of groups. However, the intake of magnesium, calcium, zinc, copper, manganese, energy, thiamin, riboflavin, and folate in all subgroups fell short of recommended levels for intake, while vitamins A, C and niacin contents exceeded those recommended. Intakes of potassium and proteins were within the recommended values. CONCLUSIONS: CHF per se, even severe CHF, is not responsible for a reduced dietary intake of various nutrients. A population-related dietary culture, old age or other chronic conditions, rather than CHF, might be mainly involved. The increased intake of vitamins A, C and niacin in our patients may be attributed to the high content of fruits and vegetables in the Mediterranean diet. Insufficient intake of the above-mentioned group of electrolytes and essential nutrients may contribute to the frequently observed negative balance of some of them. This is especially relevant in furosemide-treated CHF patients. Therefore, supplementation should be considered.

Contrast media augmented apoptosis of cultured renal mesangial, tubular, epithelial, endothelial, and hepatic cells.

RATIONALE AND OBJECTIVE: Nephrotoxicity of contrast media, resulting in apoptosis and acute necrosis of tubular cells, is well documented. No studies concerning mesangial cells apoptosis have been published yet. AIM: Apoptosis of cultured mesangial, tubular, and hepatic cell lines was investigated following exposure to different contrast media. METHODS: Apoptosis was assessed by TUNEL assay and verified by Mayer Hematoxylin staining. RESULTS: Iopromide, Ioxaglate, and Ioxatalamate induced apoptosis in all cell cultures at final concentrations ranged from 0.1% to 10.0%. However, only 1% to 10% Iomeprol elicited a significant apoptosis. Moreover, at 10% concentration, Iomeprol induced significantly less apoptosis than Iopromide, Ioxaglate, or Ioxatalamate. CONCLUSIONS: First, Iomeprol, which has a different physico-chemical properties, proved to be less proapoptotic compared with other contrast compounds. Second, all types of cells similarly respond by apoptosis to contrast media induced injury. However, apoptosis of mesangial cells might generate additional deleterious effects in vivo.

Cell-associated magnesium and QT dispersion in hemodialysis patients.

BACKGROUND: Impaired magnesium (Mg) homeostasis has been implicated in a variety of cardiovascular disturbances, including ventricular arrhythmias and changes in the interval between the onset of wave Q to the end of wave T (QT interval) on electrocardiogram. Cardiac arrhythmias are common in patients on hemodialysis therapy. METHODS: We investigated the relationship between QT interval corrected for heart rate (QTc) dispersion and Mg content in peripheral blood mononuclear cells (PBMC) of chronic hemodialysis patients treated with high-dose calcium carbonate providing Mg in excess (group I; n = 18) or low-dose calcium carbonate and smaller Mg load (group II; n = 13). RESULTS: Mean Mg content in PBMC of group I patients (27.9 +/- 4.2 [SD] micromol/L/mg protein) was significantly greater than in group II patients (10.4 +/- 4.1 micromol/L/mg protein; P < 0.05) and greater in both groups than in healthy control subjects (2.75 +/- 0.6 micromol/L/mg protein; P < 0.05). Mean QTc dispersion was significantly longer (74.6 +/- 21.4 milliseconds) in group I than group II (37.8 +/- 13.1 milliseconds; P < 0.02) and longer in both groups than in controls (27.3 +/- 9.6 milliseconds; P < 0.05). After dialysis, in both groups of patients, cell-associated Mg (c-a Mg) levels and QTc dispersion were significantly greater (P < 0.05) than before dialysis started. One week after stopping calcium carbonate treatment, group 1 patients showed significant reductions in predialytic c-a Mg levels (to 19.5 +/- 9.8 micromol/L/mg protein; P < 0.05) and QTc dispersions (to 48.9 +/- 23.7 milliseconds; P < 0.05). Plasma Mg and other electrolyte concentrations prior to and during hemodialysis did not correlate with QTc dispersion. CONCLUSION: Prolongation of QTc dispersion in patients on chronic hemodialysis therapy could be, at least in part, a consequence of increased concentrations of c-a Mg resulting from excess daily Mg intake.