The Evolving Scenario of COVID-19 in Hemodialysis Patients.

Coronavirus disease 2019 (COVID-19) is a rapidly changing disease. Therefore, in this study, to evaluate the evolution of COVID-19 in hemodialysis patients, we retrospectively compared patients affected by COVID-19 during the first pandemic waves of 2020 (from March to December 2020-Group 1) with patients with COVID-19 from September 2021 to February 2022 (Group 2) after the full completion of vaccination. Group 1 was constituted of 44 patients (69.3 ± 14.6 years), and Group 2 of 55 patients (67.4 ± 15.3 years). Among Group 2, 52 patients (95%) were vaccinated. Patients of Group 2, compared with Group 1, were more often asymptomatic (38 vs. 10%, p = 0.002) and reported less frequent fever and pulmonary involvement. At diagnosis, Group 2 showed a significantly higher number of lymphocytes and lower levels of circulating IL-6 (16 ± 13.3 vs. 41 ± 39.4 pg/mL, p = 0.002). Moreover, in Group 2, inflammatory parameters significantly improved after a few days from diagnosis. Patients of Group 2 presented a lower hospitalization rate (12.7 vs. 38%, p = 0.004), illness duration (18.8 ± 7.7 vs. 29.2 ± 19.5 days, p = 0.005), and mortality rate (5.4 vs. 25%, p = 0.008). Finally, responders to the vaccination (80% of vaccinated patients) compared with nonresponders showed a reduction in infection duration and hospitalization (5 vs. 40%, p = 0.018). In conclusion, we found that COVID-19 presentation and course in hemodialysis patients have improved over time after the implementation of vaccine campaigns. However, due to the evolving nature of the disease, active surveillance is necessary.

New Treatment Options for Hyperkalemia in Patients with Chronic Kidney Disease.

Hyperkalemia may cause life-threatening cardiac and neuromuscular alterations, and it is associated with high mortality rates. Its treatment includes a multifaceted approach, guided by potassium levels and clinical presentation. In general, treatment of hyperkalemia may be directed towards stabilizing cell membrane potential, promoting transcellular potassium shift and lowering total K+ body content. The latter can be obtained by dialysis, or by increasing potassium elimination by urine or the gastrointestinal tract. Until recently, the only therapeutic option for increasing fecal K+ excretion was represented by the cation-exchanging resin sodium polystyrene sulfonate. However, despite its common use, the efficacy of this drug has been poorly studied in controlled studies, and concerns about its safety have been reported. Interestingly, new drugs, namely patiromer and sodium zirconium cyclosilicate, have been developed to treat hyperkalemia by increasing gastrointestinal potassium elimination. These medications have proved their efficacy and safety in large clinical trials, involving subjects at high risk of hyperkalemia, such as patients with heart failure and chronic kidney disease. In this review, we discuss the mechanisms of action and the updated data of patiromer and sodium zirconium cyclosilicate, considering that the availability of these new treatment options offers the possibility of improving the management of both acute and chronic hyperkalemia.

Pemetrexed-induced acute kidney failure following irreversible renal damage: two case reports and literature review.

BACKGROUND: Pemetrexed (PEM) is a new-generation multitargeted antifolate agent with a demonstrated broad-spectrum activity in several types of human cancers, including non-small cell lung cancer (NSCLC) and mesothelioma. Major side effects include dose-limiting hematologic toxicities. PEM nephrotoxicity is well known; however, its frequency is considered to be low. CASE PRESENTATION: Here we report two cases of acute kidney injury (AKI) related to PEM administration (500 mg/m2) in patients with NSCLC. The first patient required hemodialysis treatment and was submitted to renal biopsy which showed acute tubular damage and interstitial edema without acute tubular necrosis. No other potential nephrotoxic agents were identified. The second patient developed AKI, not proven by biopsy and did not require renal replacement therapy. Both patients, on regular supplementation with folic acid and vitamin B12, concomitantly developed myelosuppression and even several months after PEM withdrawal, showed only a modest improvement of renal function. CONCLUSIONS: PEM is an antifolate antineoplastic agent with a broad-spectrum activity in locally advanced or metastatic NSCLC. It has been shown that PEM allows longer survival. The risk of acute or chronic kidney disease may be one of the prices to be paid for this success.

Pemetrexed induced acute kidney injury in patients with non-small cell lung cancer: reversible and chronic renal damage.

BACKGROUND: Pemetrexed (Alimta(®)) (PEM) is an antifolate antineoplastic agent effective in several tumor types, such as non-small-cell lung cancer (NSCLC) and mesothelioma, among others. It is almost exclusively excreted by the kidney and an eGFR lower 45 mL/min is a contraindication for its use: above this level PEM administration is considered safe and dose adjustment is not required. Although there are some reported cases of PEM-induced renal injury, its incidence and the negative effects on patients' outcome has not been systematically evaluated. METHODS: We report a retrospective evaluation on the incidence of PEM-induced renal injury in patients affected by NSCLC. Between June 2010 and March 2012 a total of 38 NSCLC patients were treated at our hospital. In 29 of them other possible cause of renal injury were excluded and thus they were eligible to be analysed. RESULTS: Although by protocol all of them had eGFR >45 mL/min at baseline, six patients (average eGFR 56.2 ± 11.5 mL/min/1.73 m(2)) developed AKI (21 %). In these six patients PEM-induced myelosuppression was more severe and hospitalization was longer. Kidney function completely recovered in four patients whereas in the other two deterioration of renal function was irreversible. The number of patients with baseline eGFR <60 mL/min/1.73 m(2) was higher (4/6) in the group that developed AKI as compared to those who did not (6/23) (p < 0.05). CONCLUSIONS: There is no clear cut eGFR above which PEM may be used without potential risks of renal toxicity. If PEM has to be used, all the coexisting risk factors for AKI should be possibly corrected.

Rosuvastatin-induced acute interstitial nephritis.

We report a case of acute interstitial nephritis (AIN), most likely induced by rosuvastatin, in an 83-year-old male patient. The patient underwent angioplasty of the left internal carotid artery, after which he began a regimen of rosuvastatin (20 mg/day). After 3 weeks the patient was admitted to our unit for acute renal failure with mild proteinuria with negligible urinary sediment. A left kidney biopsy showed dense interstitial infiltrates, mainly composed of lymphocytes with evident tubulitis. Rosuvastatin withdrawal plus prednisolone (1 mg/kg/day) treatment, which was slowly tapered over a period of 4 weeks, allowed for a complete recovery of renal function. To our knowledge, this is the first case report of rosuvastatin-induced AIN. Acute renal failure is associated with a clear increase in morbidity, length of hospital stay and mortality. Moreover, since statins are among the most widely prescribed drugs in Western countries, we think that the risk of AIN should be taken into account as a possible side effect of rosuvastatin.

Divert to ULTRA: differences in infused volumes and clearance in two on-line hemodiafiltration treatments.

BACKGROUND: Mixed diffusive-convective dialysis therapies offer greater removal capabilities than conventional dialysis. The aim of this study was to compare two different on-line, post-dilution hemodiafiltration (HDF) treatments with regard to achieved convective volume and middle-molecule dialysis efficiency: standard volume control (sOL-HDF) and automated control of the transmembrane pressure (TMP) (UC-HDF). METHODS: We enrolled 30 ESRD patients (55.9 ± 14.0 years, 20/10 M/F) in a randomized, prospective, cross-over study. The patients received a 3-month period of sOL-HDF followed by UC-HDF for a further 3 months, or vice versa, using the same dialysis machine. In sOL-HDF, fixed exchange volumes were set according to a filtration fraction greater than or equal to 25%. In UC-HDF therapy, the exchanged volume was driven by a biofeedback system controlling the TMP and its set point in a double loop. Patients maintained their treatment time, dialyzer, blood flow rate, and anticoagulant regimen unchanged throughout the study. RESULTS: Greater convective volumes were achieved in UC-HDF than in sOL-HDF (23.8 ± 3.9 vs.19.8 ± 4.8 L; p<0.001) with high pre-dialysis Ht value (sOL-HDF 34.0 ± 4.5% and UC-HDF 34.0 ± 4.4%; p = 0.91). The average clearance values of ß2m and P were higher in UC-HDF than in sOL-HDF (respectively 123 ± 24 vs. 111 ± 22 ml/min, p<0.002 and 158 ± 26 vs. 152 ± 25 ml/min, p<0.05). Moreover, the UC-HDF mode led to a significantly increased rate of call-free sessions from 88% to 97% (p<0.0001). CONCLUSIONS: This study showed that the biofeedback module, applied to the automatic control of TMP in on-line HDF, results in higher convective volumes and correspondingly higher ß2m and P clearances. By making the HDF treatment more automated and less complex to perform, it significantly reduced the staff workload.

Lanthanum carbonate: a postmarketing observational study of efficacy and safety.

BACKGROUND: Hyperphosphatemia is associated with morbidity and mortality in hemodialysis patients. The use of calcium chelators is restricted by the risk of hypercalcemia and vascular calcifications. Sevelamer, a non-calcium chelator, is associated with risks of metabolic acidosis and poor compliance. Lanthanum carbonate is a non-calcium chelator not associated with these issues. However, accumulation in liver and bone has been a reason for concern. METHODS: Adult patients (n=112) from 9 hemodialysis centers, with serum phosphorus >5.5 mg/dL and on hemodialysis for >1 year, were selected to switch to lanthanum carbonate (mean dosage: 2,189 ± 491 mg/day); 103 completed the study. Laboratory assays for serum phosphate, calcium, parathyroid hormone, alkaline phosphatase, gamma-glutamyl transpeptidase (gammaGT), aspartate transaminase, alanine transaminase and plasma bicarbonate were performed monthly. Seven patients underwent a bone biopsy for evaluation of lanthanum bone content. RESULTS: Switching to lanthanum carbonate led to a reduction in mean serum phosphate levels (-18.2%; p<0.001) and calcium × phosphorus product (-17.6%; p<0.0001). There were no important changes in other variables, except for an increase in transaminases in 2 patients with preexisting liver disease, who discontinued therapy. An increase in plasma bicarbonate concentration was observed (p=0.001). Although some lanthanum was detected in bone, its distribution did not follow the mineralization front. CONCLUSIONS: Lanthanum carbonate is effective and well tolerated, provided that recipients do not have preexisting liver disease. After 8 months of treatment, lanthanum was not detected in the mineralization front of bone. In hemodialysis patients, lanthanum carbonate does not seem to be involved in metabolic bone disease.

Vascular permeability, blood pressure, and organ damage in primary hypertension.

Sub-clinical organ damage is a strong independent predictor of cardiovascular mortality in primary hypertension, and its changes over time parallel those in risk of cardiovascular events. A better understanding of the pathogenetic mechanisms underlying the development of target organ damage may help us devise more effective therapeutic strategies. We therefore investigated the relationship between the presence of organ damage and some of its potential determinants, such as blood pressure severity and early atherosclerotic abnormalities. Thirty-seven untreated, non-diabetic hypertensive patients were enrolled. Target organ damage was assessed by albuminuria and left ventricular mass index; systemic vascular permeability was evaluated by transcapillary escape rate of albumin (TERalb); and blood pressure was measured by 24h ambulatory blood pressure monitoring. The albumin-to-creatinine ratio and left ventricular mass index were directly related to TERalb (r = 0.48, p = 0.003 and r = 0.39, p < 0.020, respectively) and 24-h systolic blood pressure values (r = 0.54, p < 0.001; r = 0.60, p < 0.001). The simultaneous occurrence of increased blood pressure load and TERalb was associated with higher left ventricular mass index values (p = 0.012) and entailed an increased risk of having at least one sign of damage (chi2 = 17.4; p < 0.001). Logistic regression analysis showed that the risk of presenting at least one sign of organ damage increased more than ten-fold when TERalb was above the median and more than five-fold with each 10 mmHg increase in 24-h systolic blood pressure. Blood pressure load and vascular permeability are potentially modifiable factors that are independently associated with the occurrence of sub-clinical signs of renal and cardiac damage in hypertensive patients.

Global risk stratification in primary hypertension: the role of the kidney.

OBJECTIVE: Microalbuminuria and a reduction in creatinine clearance are well known, independent predictors of unfavourable cardiovascular prognosis. Our aim was to evaluate the impact of renal damage on global risk stratification in 459 non-diabetic, untreated hypertensive patients (64% men, mean age 47.3 years). METHODS: Renal damage was defined as creatinine clearance < 60 ml/min per 1.73 m2 (Cockcroft-Gault formula) or the presence of microalbuminuria (albumin to creatinine ratio). Cardiac and vascular organ damage was assessed by ultrasound scan. We evaluated the impact of renal damage, left ventricular hypertrophy and carotid atherosclerosis on risk stratification as recommended by the 2007 European Society of Hypertension-European Society of Cardiology Guidelines. RESULTS: The prevalence of renal damage, microalbuminuria and creatinine clearance < 60 ml/min per 1.73 m2 was 24, 12 and 13%, respectively. There was no correlation between albuminuria and estimated creatinine clearance, and only 0.9% of patients showed microalbuminuria and reduced creatinine clearance simultaneously. The presence of renal damage entailed a 3.3 times higher risk of having cardiovascular abnormalities. Based on routine work-up, 58% of our study patients were classified as high-very high risk. The simultaneous evaluation of albuminuria and creatinine clearance resulted in a significant change in risk stratification, since 68% of patients were classified in the high-very high risk class. The search for left ventricular hypertrophy or carotid atherosclerosis by ultrasonography did not improve risk stratification significantly as compared to the assessment of renal damage. CONCLUSIONS: Our findings support the assessment of renal abnormalities as the first step when evaluating target organ damage for cardiovascular risk assessment in hypertensive patients.

Inappropriate left ventricular mass is associated with microalbuminuria independently of left ventricular hypertrophy in primary hypertension.

OBJECTIVE: Inappropriate left ventricular mass (LVM) and microalbuminuria predict cardiovascular events in hypertension. We attempted to evaluate the relationship between inappropriate LVM and albuminuria in hypertensive patients. PATIENTS AND METHODS: Four hundred and two nondiabetic, untreated patients with primary hypertension were studied. The appropriateness of LVM to cardiac workload was calculated by the ratio of observed LVM to the predicted value using the reference equation. Albuminuria was evaluated by the urinary albumin to creatinine ratio. RESULTS: The deviation of LVM from the predicted value was positively related to albuminuria (P < 0.0001). Multiple regression analysis showed that albuminuria (0.0182), pulse pressure (P < 0.0001) and left ventricular hypertrophy (LVH) (P < 0.0001) were the only independent predictors of observed/predicted LVM. When subjects were divided into subgroups on the basis of the presence/absence of inappropriate LVM, patients with inappropriate LVM showed higher urinary albumin excretion (P < 0.0001), regardless of potential confounding factors, including LVH (analysis of covariance, P = 0.0453), and higher prevalence of microalbuminuria (P = 0.0024) compared to those without it. Analogous results were obtained by looking at the study patients on the basis of the presence of micro- or normoalbuminuria. Indeed, patients with microalbuminuria showed higher prevalence of inappropriate LVH compared to other left ventricular geometries (appropriate LVH and absence of LVH) (P < 0.0001). After adjusting for confounders, microalbuminuria entailed a three- and five-fold greater risk of having appropriate and inappropriate LVH, respectively. CONCLUSIONS: Inappropriate LVM is associated with albuminuria in hypertension. These data strengthen the role of microalbuminuria as an indicator of high cardiovascular risk.

Improving cardiovascular risk stratification: the case for redefining microalbuminuria.

Large epidemiological studies have pointed out that regardless of the degree of hypertension, the cost-effectiveness of antihypertensive treatment increases in parallel with the global burden of risk. Therefore, there has been growing interest in developing sensitive and easy-to-perform ways to accurately and inexpensively identify patients at high cardiovascular risk. Numerous studies over the past years have provided evidence that microalbuminuria is a concomitant of extrarenal signs of hypertensive organ damage, as well as a strong, independent predictor of cardiovascular and cerebrovascular events. Recent clinical data indicate that the risk of cardiovascular morbidity and mortality is linearly related to the degree of urinary albumin excretion, with no identifiable threshold or plateau. Furthermore, it has been demonstrated that a reduction in albuminuria under antihypertensive treatment is paralleled by changes in cardiovascular risk. Therefore, the routine search for microalbuminuria could lead to a significant improvement in the evaluation and treatment of patients with primary hypertension.

Blood pressure load, vascular permeability and target organ damage in primary hypertension.

BACKGROUND: Target organ damage (TOD) is an often reversible subclinical condition that may precede major cardiovascular events in primary hypertensive patients. Furthermore, TOD has been shown to be a complex, multifactorial process which does not depend on blood pressure (BP) reduction alone. We therefore investigated the relationship between BP load, vascular permeability and the occurrence of TOD. PATIENTS AND METHODS: Thirty-seven never-treated, nondiabetic hypertensive patients were enrolled. Albuminuria was measured as the albumin to creatinine ratio (ACR), left ventricular mass index (LVMI) was assessed by echocardiography, systemic vascular permeability was evaluated by transcapillary escape rate of albumin (TERalb), and BP was measured by means of 24-hour ambulatory BP monitoring. RESULTS: Patients with microalbuminuria showed higher levels of body mass index (BMI) (p<0.034), 24-hour systolic BP levels (p<0.001), left ventricular mass index (LVMI) (p=0.003) and capillary permeability to albumin (p<0.005), as compared with normoalbuminurics. Increased BP load and vascular permeability were associated with higher LVMI (p=0.012) and with an increased risk of having microalbuminuria and/or left ventricular hypertrophy (Chi square=17.4; p<0.001). Logistic regression analysis showed that the risk of having at least 1 sign of TOD was 10-fold higher in patients with TERalb above the median, and almost 5-fold higher for each 10 mm Hg increase in systolic blood pressure. CONCLUSIONS: Abnormal vascular permeability and increased BP load are potentially modifiable risk factors that are independently associated with the development of subclinical cardiac and renal damage.

Mild hyperuricemia and subclinical renal damage in untreated primary hypertension.

BACKGROUND: Subclinical renal damage and hyperuricemia are not uncommon in patients with primary hypertension. Whether mild hyperuricemia reflects a subclinical impairment of renal function or contributes to its development is currently debated. We investigated the relationship between serum uric-acid levels and the occurrence of early signs of kidney damage. METHODS: Four hundred eighteen patients with primary hypertension were studied. Albuminuria was measured as the albumin-to-creatinine ratio, and creatinine clearance was estimated by the formula of Cockcroft and Gault. Interlobar resistive index and renal abnormalities, ie, the renal volume-to-resistive index ratio, were evaluated by renal Doppler and ultrasound. RESULTS: Uric acid was directly related to resistive index (P = .007) in women and to albuminuria (P = .04) in men, and was inversely related to the renal volume-to-resistive index ratio in both men (P = .005) and women (P = .02). Patients with uric-acid levels above the median showed a higher prevalence of microalbuminuria (14% v 7%, P = .012) and of renal abnormalities (41% v 33%, P = .007). Moreover, when creatinine clearance was taken as a covariate, patients with increased uric-acid levels showed higher albuminuria and resistive indices, and a lower renal volume-to-resistive index ratio. Even after adjustment for several risk factors, each standard deviation increase in serum uric acid entailed a 69% higher risk of microalbuminuria, and a 39% greater risk of ultrasound detectable renal abnormalities. CONCLUSIONS: Mild hyperuricemia is associated with early signs of renal damage, ie, microalbuminuria and ultrasound-detectable abnormalities, regardless of the glomerular filtration rate in primary hypertension.

C-reactive protein and target organ damage in untreated patients with primary hypertension.

High sensitivity C-reactive protein (hs-CRP) has been recognized as a risk factor for cardiovascular disease. Asymptomatic organ damage is known to precede cardiovascular events in hypertension. The aim of the present study was to investigate the relationship between hs-CRP and signs of organ damage, namely left ventricular mass index (LVMI), albuminuria, and carotid atherosclerosis in a group of hypertensive patients. One hundred and eighty-two untreated patients with primary hypertension were studied. HS-CRP was measured by immunonephelometry. LVMI was assessed by echocardiography, albuminuria was measured as albumin to creatinine ratio, and carotid atherosclerosis by ultrasonography. Patient stratification according to quartiles of hs-CRP showed a significant trend toward higher age, prevalence of left ventricular hypertrophy, and carotid plaques. Moreover, there was a significant correlation among hs-CRP quartiles and left ventricular mass index, carotid cross-sectional area, carotid plaques, and albuminuria. Multiple regression analysis showed that, after adjusting for established cardiovascular risk factors (ie, age, duration of hypertension, smoking habit, body mass index (BMI), 24-hour systolic and diastolic blood pressures, glucose, creatinine, uric acid, triglycerides, total and low-density lipoprotein cholesterol), hs-CRP remained a strong correlate of target organ damage. These results support the importance of chronic microinflammation in the development of atherosclerotic disease in hypertension.

Microalbuminuria, blood pressure load, and systemic vascular permeability in primary hypertension.

BACKGROUND: Microalbuminuria, a powerful predictor of cardiovascular events, is thought to reflect widespread subclinical vascular abnormalities. To explore the pathogenesis of increased urinary albumin excretion in primary hypertension we evaluated systemic capillary permeability and ambulatory blood pressure (BP) measurement in two groups of matched untreated patients with (n = 11) and without (n = 29) microalbuminuria. METHODS: Albuminuria was measured as the mean of albumin-to-creatinine ratio (ACR) in three nonconsecutive first morning urine samples. Systemic capillary permeability was evaluated by transcapillary escape rate of albumin (TERalb) (ie, the 1-h decline rate of intravenous (125)I-albumin). Twenty-four-hour ambulatory BP, renal hemodynamics, and hormones of the renin-angiotensin-aldosterone system (RAAS) were also assessed. RESULTS: Patients with microalbuminuria showed greater body mass index (BMI) (P < .04), higher 24-h systolic and diastolic BP levels (P = .02), and higher capillary permeability to albumin (P < .02) as compared to normoalbuminurics. Renal hemodynamics and RAAS hormones were similar in the two groups. Univariate analysis showed that urinary ACR was related to ambulatory pressure components (P < .02), TERalb (r = 0.31, P < .05), smoking habits (r = 0.36, P = .02), and left ventricular mass index (LVMI) (r = 0.57, P < .001) among the whole study group. Logistic regression analysis showed that each 1% increment in TERalb or 10 mm Hg increase in systolic BP entailed an almost three times higher risk of having microalbuminuria. CONCLUSIONS: Microalbuminuria is associated with greater systemic BP load and increased vascular permeability in patients with primary hypertension.

Ambulatory arterial stiffness index and renal abnormalities in primary hypertension.

OBJECTIVE: Arterial stiffness is a predictor of cardiovascular mortality in the general population as well as in hypertension and end-stage renal disease. We investigated the relationship between a recently proposed ambulatory blood pressure monitoring-derived index of arterial stiffness and early signs of renal damage in patients with primary hypertension. DESIGN AND SETTING: A total of 168 untreated patients with sustained primary hypertension were studied. Ambulatory arterial stiffness index (AASI) was calculated based on 24-h ambulatory blood pressure readings. Albuminuria was measured as the albumin to creatinine ratio. Creatinine clearance was estimated using the Cockcroft-Gault formula, and the interlobar resistive index was evaluated by renal ultrasound and Doppler examination. RESULTS: AASI was positively related to urinary albumin excretion and resistive index, and was negatively related to estimated creatinine clearance and renal volume to the resistive index ratio. Patients with AASI above the median (i.e. > 0.51) showed a higher prevalence of microalbuminuria and a mild reduction in creatinine clearance. Moreover, patients with microalbuminuria or a mild reduction in creatinine clearance had significantly higher AASI values compared with those without, and the greater the renal involvement, the greater the AASI. After adjusting for several potentially confounding variables, we found that each standard deviation increase in AASI (i.e. 0.16) entails an almost twofold greater risk of renal involvement. CONCLUSION: Increased AASI is independently associated with early signs of renal damage in patients with sustained primary hypertension. These results strengthen the usefulness of AASI and ambulatory blood pressure monitoring in cardiovascular risk assessment.

Increased ambulatory arterial stiffness index is associated with target organ damage in primary hypertension.

Increased arterial stiffness has been shown to predict cardiovascular mortality in patients with primary hypertension. Asymptomatic organ damage is known to precede cardiovascular events. We investigated the relationship between a recently proposed index of stiffness derived from ambulatory blood pressure (BP) and target organ damage in 188 untreated patients with primary hypertension. Ambulatory arterial stiffness index was defined as 1 minus the regression slope of diastolic over systolic BP readings obtained from 24-hour recordings. Albuminuria was measured as the albumin:creatinine ratio, left ventricular mass index was assessed by echocardiography, and carotid abnormalities were evaluated by ultrasonography. The prevalence of microalbuminuria, left ventricular hypertrophy (LVH), and carotid abnormalities was 12%, 38%, and 19%, respectively. Ambulatory arterial stiffness index was positively related to age, triglycerides, office and 24-hour systolic BP, 24-hour pulse pressure, urinary albumin excretion, and carotid intima-media thickness. Patients with microalbuminuria, carotid abnormalities, or LVH showed higher ambulatory arterial stiffness index as compared with those without it. After adjusting for confounding factors, each SD increase in ambulatory arterial stiffness index entails an &2 times higher risk of microalbuminuria, carotid abnormalities, and LVH and doubles the risk of the occurrence of >or=1 sign of organ damage. Ambulatory arterial stiffness index is associated with organ damage in patients with primary hypertension. These data strengthen the role of this index as a marker of risk and help to explain the high cardiovascular mortality reported in patients with high ambulatory arterial stiffness index.

Microalbuminuria and cardiovascular risk assessment in primary hypertension: should threshold levels be revised?

BACKGROUND: Urinary albumin excretion and left ventricular mass are related to each other and to the risk of cardiovascular events in patients with primary hypertension. We aimed to identify a lower threshold for albuminuria that might improve detection of patients with left ventricular hypertrophy (LVH) and cost-effectiveness in cardiovascular risk assessment. METHODS: Albuminuria and left ventricular mass index were assessed in 448 untreated, nondiabetic patients with primary hypertension. The impact that lower albuminuria cut-off levels might have on detecting LVH was evaluated with regard to test cost and sensitivity. This was done by a diagnostic algorithm consisting of albuminuria evaluation followed by echocardiography in the presence of normoalbuminuria. RESULTS: The area under the ROC curve of albuminuria in predicting LVH was 0.73. Using a lower albumin to creatinine ratio threshold than what is recommended by the guidelines (ie, 11.5 mg/g), the sensitivity and specificity of albuminuria in identifying patients with LVH was 39% and 92%, respectively, which translated to positive and negative predictive values of 76% and 69%, respectively. When considering only patients without electrocardiographically detected LVH, routine screening for albuminuria, followed by echocardiography in the presence of albuminuria