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• W2000799738 abstract "It has been known for considerable time1.Mogensen C.E. Microalbuminuria predicts clinical proteinuria and early mortality in maturity-onset diabetes.N Engl J Med. 1984; 310: 356-360Crossref PubMed Scopus (1706) Google Scholar that microalbuminuria increases the risk of cardiovascular events and cardiovascular death in diabetic patients. It has only been relatively recently, however, that the adverse effect of microalbuminuria on cardiovascular risk in nondiabetic patients has been recognized2.Damsgaard E.M. Froland A. Jorgensen O.D. Mogensen C.E. Microalbuminuria as predictor of increased mortality in elderly people.BMJ. 1990; 300: 297-300Crossref PubMed Scopus (549) Google Scholar. The largest evidence in this respect has been provided by studies in the general population (e.g., in Groningen3.Hillege H.L. Fidler V. Diercks G.F. et al.Urinary albumin excretion predicts cardiovascular and noncardiovascular mortality in general population.Circulation. 2002; 106: 1777-1782Crossref PubMed Scopus (1287) Google Scholar, in Tröndelag4.Romundstad S. Holmen J. Kvenild K. et al.Microalbuminuria and all-cause mortality in 2,089 apparently healthy individuals: A 4.4-year follow-up study. The Nord-Trondelag Health Study (HUNT), Norway.Am J Kidney Dis. 2003; 42: 466-473https://doi.org/10.1016/S0272-6386(03)00742-XAbstract Full Text Full Text PDF PubMed Scopus (211) Google Scholar, and Copenhagen5.Borch-Johnsen K. Feldt-Rasmussen B. Strandgaard S. et al.Urinary albumin excretion. An independent predictor of ischemic heart disease.Arterioscler Thromb Vasc Biol. 1999; 19: 1992-1997Crossref PubMed Scopus (365) Google Scholar). Hillegeet al reported that among 40,856 individuals in the general population of Groningen (North Holland), 7.2% had microlbuminuria. The great majority had no comorbidity, and no less than 6.6% had microalbuminuria without diabetes or hypertension. It is very likely that the high normal range of albuminuria already carries cardiovascular risk, as recently reported by Gersteinet al6.Gerstein H.C. Mann J.F. Yi Q. et al.Albuminuria and risk of cardiovascular events, death, and heart failure in diabetic and nondiabetic individuals.JAMA. 2001; 286: 421-426https://doi.org/10.1001/jama.286.4.421Crossref PubMed Scopus (1925) Google Scholar in the HOPE study, and Wachtell7.Wachtell K. Ibsen H. Olsen M.H. et al.Albuminuria and cardiovascular risk in hypertensive patients with left ventricular hypertrophy: The LIFE study.Ann Intern Med. 2003; 139: 901-906Crossref PubMed Scopus (466) Google Scholar in the LIFE study. They noted that the risk of cardiovascular events started to increase at albumin excretion rates well below the formal limit of microalbuminuria (i.e., 20–200 μg/mL or 30–300 mg/day). Such findings in the general population are well in line with observations of Rachmani, who noted that for diabetic patients with albumin excretion rates 20 to 300 mg/day (i.e., the high normal range), the risk to develop microalbuminuria or a cardiovascular event was higher by a factor of 12.4 and 9.8 compared to albuminuria 0 to 10 mg/day8.Rachmani R. Levi Z. Lidar M. et al.Considerations about the threshold value of microalbuminuria in patients with diabetes mellitus: Lessons from an 8-year follow-up study of 599 patients.Diabetes Res Clin Pract. 2000; 49: 187-194https://doi.org/10.1016/S0168-8227(00)00155-8Abstract Full Text Full Text PDF PubMed Scopus (64) Google Scholar. It is of note that the prediction of CV risk by albuminuria is independent of established risk factors, such as smoking, gender, blood pressure, and others, as noted in the Copenhagen study by Borch-Johnsen5.Borch-Johnsen K. Feldt-Rasmussen B. Strandgaard S. et al.Urinary albumin excretion. An independent predictor of ischemic heart disease.Arterioscler Thromb Vasc Biol. 1999; 19: 1992-1997Crossref PubMed Scopus (365) Google Scholar. Of particular interest is the known link between microalbuminuria and the metabolic syndrome. Verhaveet al9.Verhave J.C. Hillege H.L. Burgerhof J.G. et al.Cardiovascular risk factors are differently associated with urinary albumin excretion in men and women.J Am Soc Nephrol. 2003; 14: 1330-1335https://doi.org/10.1097/01.ASN.0000060573.77611.73Crossref PubMed Scopus (107) Google Scholar noted a striking relation, more so in male than in female individuals, between fasting blood glucose concentration and urinary albumin excretion, as well as between BMI and urinary albumin excretion. What is of great interest is the observation that this is true not only for elevated glucose or BMI values; the correlation extends well into the range of normal values. Apparently, the metabolic syndrome and microalbuminuria are tightly correlated with each other. This relation is of considerable interest because in patients with renal disease insulin resistance is found even in the very early stages10.Fliser D. Pacini G. Engelleiter R. et al.Insulin resistance and hyperinsulinemia are already present in patients with incipient renal disease.Kidney Int. 1998; 53: 1343-1347https://doi.org/10.1046/j.1523-1755.1998.00898.xAbstract Full Text Full Text PDF PubMed Scopus (284) Google Scholar, and even when GFR is still within the normal range (unpublished observations). Conversely, in a population sample it was found that insulin resistance (according to the HOMA index) was associated with a higher risk of chronic kidney disease11.Chen J. Muntner P. Hamm L.L. et al.Insulin resistance and risk of chronic kidney disease in nondiabetic US adults.J Am Soc Nephrol. 2003; 14: 469-477Crossref PubMed Scopus (293) Google Scholar. The information obtained from microalbuminuria cannot be replaced by estimating the glomerular filtration rate. Although the reports in the literature are not entirely consistent, the study in Groningen showed that with increasing quantiles of urinary albumin excretion, the creatinine clearance tended to be higher and was lower only in the uppermost quantiles12.Pinto-Sietsma S.J. Janssen W.M. et al.Urinary albumin excretion is associated with renal functional abnormalities in a nondiabetic population.J Am Soc Nephrol. 2000; 11: 1882-1888PubMed Google Scholar. Although the creatinine clearance is not a reliable index of glomerular filtration, this observation would be plausible in view of a similar relation between GFR and albuminuria noted previously in diabetic patients13.Mogensen C.E. Prediction of clinical diabetic nephropathy in IDDM patients. Alternatives to microalbuminuria?.Diabetes. 1990; 39: 761-767Crossref PubMed Google Scholar. There has been much discussion whether microalbuminuria reflects primarily a generalized endothelial cell dysfunction, as suggested by the Steno hypothesis14.Deckert T. Feldt-Rasmussen B. Borch-Johnsen K. et al.Albuminuria reflects widespread vascular damage. The Steno hypothesis.Diabetologia. 1989; 32: 219-226https://doi.org/10.1007/BF00285287Crossref PubMed Scopus (1260) Google Scholar, or whether it reflects a podocyte defect, as proposed more recently15.Pereira A.C. Pereira A.B. Mota G.F. et al.NPHS2 R229Q functional variant is associated with microalbuminuria in the general population.Kidney Int. 2004; 65: 1026-1030https://doi.org/10.1111/j.1523-1755.2004.00479.xAbstract Full Text Full Text PDF PubMed Scopus (93) Google Scholar. The observation that the rate of albumin escape from the plasma space is increased in patients with microalbuminuria16.Parving H.H. Nielsen S.L. Lassen N.A. Increased transcapillary escape rate of albumin, IgG, and IgM during angiotensin-II-induced hypertension in man.Scand J Clin Lab Invest. 1974; 34: 111-118Crossref PubMed Google Scholar argues for the former possibility. The observation that the risk of being microalbuminuric was significantly higher for carriers of the Q-genotype of the 229 polymorphism of the podocin gene at any given level of body mass index or other correlates of microalbuminuria is more in favor of a podocyte problem15.Pereira A.C. Pereira A.B. Mota G.F. et al.NPHS2 R229Q functional variant is associated with microalbuminuria in the general population.Kidney Int. 2004; 65: 1026-1030https://doi.org/10.1111/j.1523-1755.2004.00479.xAbstract Full Text Full Text PDF PubMed Scopus (93) Google Scholar. To the best of our knowledge, one of the first studies to clearly document the relation between serum creatinine concentration and mortality was the observation of Shulman17.Shulman N.B. Ford C.E. Hall W.D. et al.Prognostic value of serum creatinine and effect of treatment of hypertension on renal function. Results from the hypertension detection and follow-up program. The Hypertension Detection and Follow-up Program Cooperative Group.Hypertension. 1989; 13: I80-93Crossref PubMed Google Scholar in the Hypertension Detection and Follow-Up program. Over 96 months of follow-up, the cumulative life mortality increased progressively with increasing serum creatinine concentration between 1.2 to 2.5 mg/dL. This information is important because recent studies based mainly on NHANES data show that minor renal dysfunction is extremely prevalent in the United States population. Three percent of the population is estimated to have chronic kidney disease stage 2 (i.e., eGFR 60–89 mL/min), and 4.3% stage 3 (i.e., eGFR of 30–59 mL/min). Meanwhile, the relation between reduced glomerular filtration and cardiovascular risk has been shown in the general population, in hypertensive patients, in individuals at high cardiovascular risk, and in patients with cardiac dysfunction, specifically congestive heart failure. Furthermore, substantial evidence indicated that during and after acute cardiac ischemic events, the mortality is strongly dependent on renal function. In a prospective population-based study in the Dutch city of Hoorn in individuals age 50 to 75 years, Henry18.Henry R.M. Kostense P.J. Bos G. et al.Mild renal insufficiency is associated with increased cardiovascular mortality: The Hoorn Study.Kidney Int. 2002; 62: 1402-1407https://doi.org/10.1046/j.1523-1755.2002.00571.xAbstract Full Text Full Text PDF PubMed Scopus (417) Google Scholar found that the relative risk of a cardiovascular death increased by 26% per 5 mL/min/1.73m2 lower GFR. This indicates that a difference in eGFR of 20 mL/min is associated with a 2-fold increase in the risk of CV death. Ruilope19.Ruilope L.M. Salvetti A. Jamerson K. et al.Renal function and intensive lowering of blood pressure in hypertensive participants of the hypertension optimal treatment (HOT) study.J Am Soc Nephrol. 2001; 12: 218-225PubMed Google Scholar found in individuals recruited for the HOT study (Hypertension Optimal Treatment) that patients with an estimated creatinine clearance less than 60 mL/min. consistently had almost double the events per 1000 patient years compared to patients with creatinine clearance >60 mL/min, independent of the target diastolic blood pressure to which these patients had been randomized. The HOPE study20.Yusuf S. Sleight P. Pogue J. et al.Effects of an angiotensin-converting-enzyme inhibitor, ramipril, on cardiovascular events in high-risk patients. The Heart Outcomes Prevention Evaluation Study Investigators.N Engl J Med. 2000; 342: 145-153https://doi.org/10.1056/NEJM200001203420301Crossref PubMed Scopus (7858) Google Scholar investigated individuals at high cardiovascular risk. The analysis of the relation between serum creatinine concentration and cardiovascular events21.Mann J.F. Gerstein H.C. Pogue J. et al.Renal insufficiency as a predictor of cardiovascular outcomes and the impact of ramipril: The HOPE randomized trial.Ann Intern Med. 2001; 134: 629-636Crossref PubMed Scopus (1207) Google Scholar showed a strong correlation between serum creatinine and the event rate. The hazard ratio for a patient with a serum creatinine 1.4 to 2.0 mg/dL was higher by 40%, for the patient with microalbuminuria by 59%, and for the patient with both increased serum creatinine and microalbuminuria by 108%. This should be compared to diabetes, per se, which increased the risk only by 42%. In patients with congestive heart failure (CHF), eGFR emerged as a potent and independent predictor of cardiovascular risk. Hillege22.Hillege H.L. Girbes A.R. de Kam P.J. et al.Renal function, neurohormonal activation, and survival in patients with chronic heart failure.Circulation. 2000; 102: 203-210Crossref PubMed Scopus (816) Google Scholar analyzed 1906 patients with CHF who had been enrolled in a prospective randomized survival trial. Baseline eGFR, according to Cockcroft-Gault, was the single most potent predictor of risk, followed by NYHA class and use of ACE inhibitors. The negative impact of low eGFR on survival was found for each category of NYHA class and EF, so that eGFR is not merely a surrogate marker for the severity of heart failure, but an independent predictor of risk. Patients undergoing an ischemic event have much more adverse outcomes if serum creatinine concentrations are elevated. In a Medicare sample, Shlipaket al23.Shlipak M.G. Fried L.F. Crump C. et al.Cardiovascular disease risk status in elderly persons with renal insufficiency.Kidney Int. 2002; 62: 997-1004https://doi.org/10.1046/j.1523-1755.2002.00522.xAbstract Full Text Full Text PDF PubMed Scopus (155) Google Scholar noted a strong dependence of post-discharge survival on serum creatinine concentrations in the range <1.5 to 3.9 mg/dL. In a single center study, Wright24.Wright R.S. Reeder G.S. Herzog C.A. et al.Acute myocardial infarction and renal dysfunction: A high-risk combination.Ann Intern Med. 2002; 137: 563-570Crossref PubMed Scopus (504) Google Scholar analyzed 3106 patients and found a strong relation between eCcr and in-hospital mortality, ranging from 2% at eGFR >75 mL/min, 6% at 50 to 75 mL/min, 14% at 35 to 50 mL/min, up to 30% in end-stage renal disease. Similarly, a high post-discharge death hazard ratio was noted (2.4 at eCcr 50–75 mL/min compared to >75 mL/min and 5.4 with end-stage renal disease). The risk of in-hospital death increased already when eCcr was 80 compared to 110 mL/min. This observation has recently been confirmed in a large international, prospective, multicenter study covering 11,715 patients. The relative risk of death was 4.7 at an eCcr of 30 to 60 mL/min, and 9.92 at <30 mL/min compared to patients with eCcr >60 mL/min25.Santopinto J.J. Fox K.A. Goldberg R.J. et al.Creatinine clearance and adverse hospital outcomes in patients with acute coronary syndromes: Findings from the global registry of acute coronary events (GRACE).Heart. 2003; 89: 1003-1008https://doi.org/10.1136/heart.89.9.1003Crossref PubMed Scopus (213) Google Scholar. Reineke26.Reinecke H. Trey T. Matzkies F. et al.Grade of chronic renal failure, and acute and long-term outcome after percutaneous coronary interventions.Kidney Int. 2003; 63: 696-701https://doi.org/10.1046/j.1523-1755.2003.00784.xAbstract Full Text Full Text PDF PubMed Scopus (82) Google Scholar noted a striking relation between serum creatinine concentration and cumulative mortality in patients who had undergone PTCA. The risk increased from 5% at S-creatinine <1.0, and 6.3% at 1.1 mg/dL, and 9% at 1.2 mg/dL, to no less than 31% at a serum creatinine >2 mg/dL. Serum creatinine is a notoriously insensitive reflection of glomerular filtration. It is strikingly influenced by muscle mass and other confounding factors. It has therefore been recommended to use algorithms to estimate routinely the GFR with the help of the Cockroft-Gault formula27.Cockcroft D.W. Gault M.H. Prediction of creatinine clearance from serum creatinine.Nephron. 1976; 16: 31-41Crossref PubMed Scopus (12499) Google Scholar or the MDRD formula28.Levey A.S. Bosch J.P. Lewis J.B. et al.A more accurate method to estimate glomerular filtration rate from serum creatinine: A new prediction equation. Modification of Diet in Renal Disease Study Group.Ann Intern Med. 1999; 130: 461-470Crossref PubMed Scopus (12277) Google Scholar. None of these formulas is absolutely satisfactory29.Bostom A.G. Kronenberg F. Ritz E. Predictive performance of renal function equations for patients with chronic kidney disease and normal serum creatinine levels.J Am Soc Nephrol. 2002; 13: 2140-2144Crossref PubMed Scopus (321) Google Scholar, but their use is a decided progress compared to reliance on serum creatinine alone, and has now been more widely proposed in consensus statements30.Sarnak M.J. Levey A.S. Schoolwerth A.C. et al.Kidney disease as a risk factor for development of cardiovascular disease: A statement from the American Heart Association Councils on Kidney in Cardiovascular Disease, High Blood Pressure Research, Clinical Cardiology, and Epidemiology and Prevention.Hypertension. 2003; 42: 1050-1065https://doi.org/10.1161/01.HYP.0000102971.85504.7cCrossref PubMed Scopus (864) Google Scholar,31.Sarnak M.J. Levey A.S. Schoolwerth A.C. et al.Kidney disease as a risk factor for development of cardiovascular disease: A statement from the American Heart Association Councils on Kidney in Cardiovascular Disease, High Blood Pressure Research, Clinical Cardiology, and Epidemiology and Prevention.Circulation. 2003; 108: 2154-2169Crossref PubMed Scopus (2675) Google Scholar. The high cardiovascular risk conferred by minor renal dysfunction could possibly be explained by the known endothelial cell dysfunction in incipient renal disease. There are several observations that point in this direction. First, Kielsteinet al found that the concentrations of asymmetric dimethyll-arginine are increased in renal patients, even when the inulin clearance is still within the normal range32.Kielstein J.T. Boger R.H. Bode-Boger S.M. et al.Asymmetric dimethylarginine plasma concentrations differ in patients with end-stage renal disease: Relationship to treatment method and atherosclerotic disease.J Am Soc Nephrol. 1999; 10: 594-600PubMed Google Scholar. We have found a striking relation between symmetric dimethyl-l-arginine and serum creatinine, but not between ADMA and serum creatinine. Therefore, we postulated that it is not (only) impaired renal excretion, but also impaired catabolism that contributes to high ADMA concentrations in renal disease33.MacAllister R.J. Rambausek M.H. Vallance P. et al.Concentration of dimethyl-L-arginine in the plasma of patients with end-stage renal failure.Nephrol Dial Transplant. 1996; 11: 2449-2452Crossref PubMed Scopus (190) Google Scholar. This postulate is in line with recent demonstrations that endothelial dysfunction is associated with dysregulation of dimethyl-l-arginine dimethylaminohydrolase34.Ito A. Tsao P.S. Adimoolam S. et al.Novel mechanism for endothelial dysfunction: Dysregulation of dimethylarginine dimethylaminohydrolase.Circulation. 1999; 99: 3092-3095Crossref PubMed Scopus (607) Google Scholar. With respect to the cardiovascular risk, it is particularly important that even at normal GFR, hypertensive individuals with ADPKD have strikingly increased sympathetic activity when measured by microneurography35.Klein I.H. Ligtenberg G. Oey P.L. et al.Sympathetic activity is increased in polycystic kidney disease and is associated with hypertension.J Am Soc Nephrol. 2001; 12: 2427-2433PubMed Google Scholar. There is also recent evidence of increased biomarkers of inflammation such as CRP, fibrinogen, IL-6, and ICAM, as well as indicators of a procoagulatory state (factor VIII, D-dimers)36.Shlipak M.G. Fried L.F. Crump C. et al.Elevations of inflammatory and procoagulant biomarkers in elderly persons with renal insufficiency.Circulation. 2003; 107: 87-92Crossref PubMed Scopus (624) Google Scholar, and this has been confirmed in the Birmingham study37.Landray M.J. Wheeler D.C. Lip G.Y. et al.Inflammation, endothelial dysfunction, and platelet activation in patients with chronic kidney disease: The chronic renal impairment in Birmingham (CRIB) study.Am J Kidney Dis. 2004; 43: 244-253https://doi.org/10.1053/j.ajkd.2003.10.037Abstract Full Text Full Text PDF PubMed Scopus (243) Google Scholar. Furthermore, even when GFR is still normal, Stefanskiet al38.Stefanski A. Schmidt K.G. Waldherr R. Ritz E. Early increase in blood pressure and diastolic left ventricular malfunction in patients with glomerulonephritis.Kidney Int. 1996; 50: 1321-1326Abstract Full Text PDF PubMed Scopus (107) Google Scholar found increased blood pressure values by ambulatory blood pressure measurements, particularly, increased nighttime values, and this was associated with evidence of target organ damage (i.e., thickening of the LV wall and evidence of diastolic LV malfunction). Finally, abnormal lipoprotein patterns are present in renal patients again, even when GFR is still normal39.Kronenberg F. Kuen E. Ritz E. et al.Lipoprotein(a) serum concentrations and apolipoprotein(a) phenotypes in mild and moderate renal failure.J Am Soc Nephrol. 2000; 11: 105-115PubMed Google Scholar,40.Kronenberg F. Kuen E. Ritz E. et al.Apolipoprotein A-IV serum concentrations are elevated in patients with mild and moderate renal failure.J Am Soc Nephrol. 2002; 13: 461-469PubMed Google Scholar. Recently, two groups provided evidence for accelerated atherogenesis in renal failure using the apo-E knockout mouse model41.Buzello M. Tornig J. Faulhaber J. et al.The apolipoprotein e knockout mouse: A model documenting accelerated atherogenesis in uremia.J Am Soc Nephrol. 2003; 14: 311-316Crossref PubMed Scopus (130) Google Scholar,42.Bro S. Moeller F. Andersen C.B. et al.Increased expression of adhesion molecules in uremic atherosclerosis in apolipoprotein-e-deficient mice.J Am Soc Nephrol. 2004; 15: 1495-1503Crossref PubMed Scopus (65) Google Scholar. Slight reduction of functional renal parenchyma by uninephrectomy caused marked acceleration of the rate of growth of plaques. This was associated with expression of nitrotyrosine as an indicator of oxidative stress in aortic endothelial cells41.Buzello M. Tornig J. Faulhaber J. et al.The apolipoprotein e knockout mouse: A model documenting accelerated atherogenesis in uremia.J Am Soc Nephrol. 2003; 14: 311-316Crossref PubMed Scopus (130) Google Scholar, as well as with increased expression of adhesion molecules42.Bro S. Moeller F. Andersen C.B. et al.Increased expression of adhesion molecules in uremic atherosclerosis in apolipoprotein-e-deficient mice.J Am Soc Nephrol. 2004; 15: 1495-1503Crossref PubMed Scopus (65) Google Scholar. We propose the hypothesis that such minor derangements of renal function, as reflected by microalbuminuria or reduced glomerular filtration, cause an increase in oxidative stress, thus provoking dysfunction of endothelial cells. It is plausible to assume that this sensitizes the vasculature to further damage when they are exposed to the injurious effect of hypertension, dyslipidemia, hyperglycemia, or smoking." @default.
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