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PubMed1994

Epidemiology of hepatitis C virus infection in patients with renal disease.

This study was carried out to determine the prevalence of hepatitis C virus (HCV) antibodies and the epidemiologic factors associated with HCV infection in patients with chronic renal failure before the onset of ESRD. Sex, age, type of renal disease, level of renal function, and history of blood transfusions and invasive procedures were analyzed in 226 patients with renal disease, compared with a population of 1,244 normal subjects and 124 patients with impaired immunity (patients having autoimmune diseases and receiving chemotherapy treatment). Eighteen seropositive patients with renal disease (prevalence, 7.9%) were found, which was significantly higher than the prevalence in the normal population (1.03% in blood donors, 0.98% in pregnant women; P < 0.001, chi 2). There was no significant association of sex, number of blood transfusions, or history of invasive procedures with the presence of HCV antibodies. The prevalence of HCV antibodies was higher (16.6%) in patients with glomerulonephritis compared with patients diagnosed with interstitial nephritis, pyelonephritis, nephrosclerosis, diabetes mellitus, polycystic kidney, and miscellaneous renal diseases (P < 0.01, chi 2). There was a higher prevalence of HCV antibodies in patients with creatinine clearance lower than 30 mL/min (13%) compared with patients with creatinine clearance higher than 30 mL/min (2.7%) (P < 0.01, chi 2). These data suggest that HCV infection may be associated with the pathogenesis of glomerulonephritis. Alternatively, glomerulonephritis or severe renal insufficiency may increase the likelihood of HCV infection.

Adult↗

PubMed1996

Linkage analysis between loci in the renin-angiotensin axis and end-stage renal disease in African Americans.

The factors that initiate chronic renal failure in patients with hypertension, diabetes mellitus, and chronic glomerular disease are largely unknown. The likely genetic contribution to ESRD, particularly in African Americans, suggests that linkage analysis may be useful to evaluate the role of candidate genes in the pathogenesis of chronic renal failure. The renin-angiotensin-aldosterone (RAA) axis has been intensively evaluated for its contribution to cardiovascular disease and nephropathy. This study tested for linkage between candidate genes in the RAA axis and chronic renal failure, using 85 African-American sibling pairs (from 65 families) concordant for ESRD. Angiotensinogen was selected because of the putative link between it and mild to moderate essential hypertension and nephrosclerosis; angiotensin-converting enzyme because of its possible contribution to diabetic nephropathy; and renin, the angiotensin II receptor, and kallikrein because of their roles in hypertension and renal perfusion. These candidate loci did not demonstrate linkage to either diabetic or nondiabetic renal disease in this study's collection of sibling pairs. These results suggest that polymorphisms at these RAA axis loci do not make major contributions to the pathogenesis of renal disease in African Americans.

Angiotensinogen↗

PubMed1987

The epidemiology of end-state renal disease: the six-year South-Central Los Angeles experience, 1980-85.

Using the End-Stage Renal Disease Medical Information System and 1980 census information, the crude cumulative incidence among Blacks, Hispanics, and Whites in south central Los Angeles was determined to be 160.1, 49.28, and 55.3 per 100,000 respectively. Sex-specific rates were slightly greater in males. Among Blacks, nephrosclerosis and diabetes represented 41.5 and 30.2 per cent of the cases respectively and increased during the period 1980-85.

Adolescent↗

PubMed1985

Cardiovascular pathophysiology of essential hypertension: a clue to therapy.

Arterial hypertension is by definition a haemodynamic disorder. At least 3 different subsets of cardiovascular pathophysiological features can be identified in so-called essential hypertension: The young lean patient characterised by an elevated cardiac output and renal blood flow, elevated plasma renin activity and circulating catecholamine levels, as well as symptoms and signs of hyperadrenergic hypertension. The elderly patient characterised by a low cardiac output often with left ventricular hypertrophy, elevated total peripheral resistance, nephrosclerosis, and symptoms and signs of target organ disease. The obese patient (and to a lesser degree the black patient) characterised by expanded fluid volume state, elevated cardiac output, a normal to low total peripheral resistance, and symptoms and signs of volume overload. To initiate antihypertensive therapy, the drug of choice in the young patient is a beta-adrenergic receptor blocker; in the elderly it is a haemodynamic vasodilator (anti-adrenergic drug, slow channel calcium blocker, or converting enzyme (ACE) inhibitor), and in black or obese patients it remains a thiazide diuretic. Enalapril, a new ACE inhibitor is indicated as a first-step agent in the great majority of hypertensive patients in whom the elevated arterial pressure should be reduced by a decrease in total peripheral resistance, without compromising systemic or regional blood flow. In contrast to other antihypertensive agents, enalapril will lower preload and afterload to the left ventricle while improving systemic and regional flow in elderly patients with latent or manifest congestive heart failure.

Angiotensin-Converting Enzyme Inhibitors↗

PubMed1990

Antihypertensive therapy. Is it different in the elderly?

Pathophysiological mechanisms of pressure elevation are different in the elderly hypertensive patient than in middle-aged or young patients. The elderly patient is characterised by a decrease in cardiac output, renal blood flow, and intravascular volume and an increase in total peripheral resistance and vascular resistance. Elderly patients also, quite often, have target organ disease such as left ventricular hypertrophy and nephrosclerosis. Because of impaired baroreflexes and latent or overt cerebrovascular disease, the elderly patient is particularly susceptible to abrupt falls in arterial pressure. Clearly, these physiological findings have to be taken into account when prescribing antihypertensive therapy. Calcium channel blockers and converting enzyme inhibitors seem to be particularly useful in the geriatric population. A close match between the underlying pathophysiology of pressure elevation in a given patient and the pharmacological effects of a selected antihypertensive drug will provide more rational and convenient control of arterial pressure in our senior citizens.

Age Factors↗

PubMed1992

Calcium overload--an important cellular mechanism in hypertension and arteriosclerosis.

Arterial hypertension and arteriosclerosis are dramatic consequences of vascular calcium overload. Acute intracellular calcium overload of vascular smooth muscle cells produces hypercontractility. Hypertension develops if a general increase in systemic arteriolar tone leads to a rise in peripheral flow resistance. Moreover, progressive elevation of calcium destroys the structural integrity of the arterial and arteriolar walls. Thus, in various animals models, calcium overload initiates lesions of an arteriosclerotic character. Interestingly, conventional human coronary plaques also represent a calcium-dominated type of arteriosclerosis. With the advent of specific calcium antagonists, the pathogenic effects of calcium overload and its deleterious consequences have become, for the first time, accessible to therapeutic intervention. Accordingly, adequate treatment with calcium antagonists prevents calcium overload and can thereby protect arteries and arterioles from functional disturbances and structural damage. In spontaneously hypertensive rats, specific calcium antagonists of the verapamil, nifedipine and diltiazem type normalise blood pressure (BP) by reducing transmembrane calcium influx into vascular smooth muscle cells. However, in addition to controlling BP, these drugs also act as tissue protective agents. The long term effects of calcium antagonists such as verapamil in experimental hypertension include the prevention of severe arteriosclerosis, myocardial hypertrophy, and malignant nephrosclerosis. In humans, the antihypertensive efficacy of verapamil is well documented. Further clinical studies have yet to evaluate the antiarteriosclerotic and tissue protective potential of verapamil in humans.

Animals↗

PubMed1997

Treatment of patients with essential hypertension and microalbuminuria.

There has been increasing interest in the question of whether microalbuminuria can be used in the risk stratification of patients with essential hypertension. A cluster of cardiovascular and/or renal risk factors may be associated with microalbuminuria in hypertension. Despite this, prospective data about the potential role of microalbuminuria as a prognostic marker of cardiovascular and/or renal risk have been sparse and inconclusive until now. Blood pressure values have been considered the most important determinant of microalbuminuria in essential hypertension; however, hyperinsulinaemia--a metabolic component-was noted to be present in conjunction with high blood pressure. Furthermore, 2 other factors may be also related to microalbuminuria: salt sensitivity and renal structural changes (nephrosclerosis). We are now aware that the clinical and physiological implications of abnormal urinary albumin excretion (UAE) are much broader than anticipated, possibly involving haemodynamic, metabolic and vascular components overlapping several clinical syndromes. Achievement of short term UAE reduction with antihypertensive treatment depends on structural abnormalities established in the glomerulus, the extent of blood pressure reduction and the antihypertensive drug class used. In terms of UAE reduction, better results are obtained with ACE inhibitors or angiotensin II antagonists such as losartan and valsartan, than with other antihypertensive classes, although their true impact in preserving renal function needs to be assessed. The capacity of new calcium antagonists, such as amlodipine, lacidipine or mibefradil, to reduce UAE also needs to be assessed further. Thus, microalbuminuria may be seen as an integrated marker of risk and should be assessed in recently diagnosed patients with essential hypertension. In microalbuminuric patients, the target should be to decrease blood pressure < 135/85 mm Hg, reduce salt intake to around 100 mmol/day and prescribe a low-calorie diet if obesity is present. ACE inhibitors or angiotensin II antagonists have more potential benefits than the other classes of antihypertensive drugs in reducing UAE. Finally, a yearly assessment of microalbuminuria is recommended during treatment, to monitor the impact of therapy.

Albuminuria↗

PubMed2002

Cardiovascular risk in patients with early renal insufficiency: implications for the use of ACE inhibitors.

Patients with end-stage renal disease die from cardiovascular disease at a much younger age than people in the general population do. Here, we review the evidence linking early renal insufficiency (ERI) to an increased cardiovascular risk. A number of cardiovascular risk factors become prevalent with ERI, including night-time hypertension, increase in serum levels of lipoprotein (a), homocysteine and asymmetric dimethyl-arginine, and insulin resistance. Also, an epidemiologic association between coronary artery disease (CAD) and nephrosclerosis, a frequent cause of ERI in the elderly, is documented. In the middle-aged, general population ERI, found in 8% of women and 9% of men, was not associated with cardiovascular disease. However, in a representative sample of middle-aged British men the risk of stroke was 60% higher for the subgroup of individuals with ERI. In people at high cardiovascular risk (mostly CAD), the Heart Outcomes Prevention Evaluation (HOPE) study found a 2-fold (unadjusted) or 1.4-fold (adjusted) higher incidence of cardiovascular outcomes with ERI. The incidence of primary outcome increased with the level of serum creatinine. At least four studies have determined the cardiovascular risk associated with ERI in hypertension. In Hypertension Detection and Follow-up Program, as in HOPE, cardiovascular mortality increased with higher serum creatinine levels (5-fold difference in cardiovascular mortality between the lowest and the highest creatinine strata). In patients with hypertension with low risk, the Hypertension Optimal Treatment and a small Italian trial found about a doubling in cardiovascular outcomes in ERI. However, in the Multiple Risk Factor Intervention Trial, not baseline serum creatinine level, but its increase on follow-up predicted future cardiovascular disease. These observational data suggest that ERI, independent of etiology, is a strong predictor of cardiovascular disease, present in 10% of a population at low, and up to 30% at high, cardiovascular risk. No prospective therapeutic trials aimed at reducing the cardiovascular burden in individuals with ERI are available. Subgroup analyses of the HOPE study indicate that ACE inhibition with ramipril is beneficial without an increased risk of adverse effects like acute renal failure or hyperkalemia. Thus the frequent practice of withholding ACE inhibitors from patients with mild renal insufficiency is unwarranted, especially since this identifies a group at high risk who appears to benefit most from treatment. In addition, there is evidence that ACE inhibitors improve renal outcomes in renal insufficiency. Prospective studies should test the predictive power of ERI for cardiovascular disease and therapeutic options.

Angiotensin-Converting Enzyme Inhibitors↗

PubMed2001

Aldosterone as a mediator of progressive renal dysfunction: evolving perspectives.

End-stage renal disease (ESRD) comprises an enormous public health burden, with an incidence and prevalence that are increasingly on the rise. This escalating prevalence suggests that newer therapeutic interventions and strategies are needed to complement current therapeutic approaches. Although much evidence demonstrates conclusively that angiotensin II mediates progressive renal disease, recent evidence also implicates aldosterone as an important pathogenetic factor in progressive renal disease. Recently, several lines of experimental evidence demonstrate that selective blockade of aldosterone, independent of renin-angiotensin blockade, reduces proteinuria and nephrosclerosis in the spontaneously hypertensive stroke-prone rat (SHRSP) model and reduces proteinuria and glomerulosclerosis in the subtotally nephrectomized rat model (ie, remnant kidney). Whereas pharmacologic blockade with angiotensin II receptor blockers and angiotensin-converting enzyme (ACE) inhibitors reduces proteinuria and nephrosclerosis/glomerulosclerosis, selective reinfusion of aldosterone restores these abnormalities despite continued renin-angiotensin blockade. Aldosterone may promote fibrosis by several mechanisms, including plasminogen activator inhibitor-1 (PAI-1) expression and consequent alterations of vascular ribrinolysis, by stimulation of transforming growth factor-beta1 (TGF-beta1), and by stimulation of reactive oxygen species (ROS). Based on this formulation, randomized clinical studies will be initiated to delineate the potential renal-protective effects of aldosterone receptor blockade.

Aldosterone↗

PubMed2004

Mechanisms of tubulointerstitial injury in the kidney: final common pathways to end-stage renal failure.

There are many different glomerular disorders, including glomerulonephritis, diabetic nephropathy, and hypertensive nephrosclerosis. However, once glomerular damage reaches a certain threshold, the progression of renal disease is consistent and irreversible. Recent studies emphasized the crucial role of tubulointerstitial injury as a mediator of progression of kidney disease. One common mechanism that leads to renal failure via tubulointerstitial injury is massive proteinuria. Accumulating evidence suggests critical effects of filtered macromolecules on tubular cells, including lysosomal rupture, energy depletion, and tubular injury directly induced by specific components such as complement components. Another common mechanism is chronic hypoxia in the tubulointerstitium. Tubulointerstitial damage results in the loss of peritubular capillaries, impairing blood flow delivery. Interstitial fibrosis also impairs oxygen diffusion and supply to tubular cells. This induces chronic hypoxia in this compartment, rendering a vicious cycle. Development of novel therapeutic approaches against these final common pathways will enable us to target any types of renal disease.

Adult↗

PubMed2005

Insulin resistance contributes to obesity-related proteinuria.

OBJECTIVE: Proteinuria is a recognized complication of obesity, but the pathogenesis remains unclear. We undertook the present study to clarify the factors contributing to proteinuria associated with obesity. METHODS: We studied 12 obese patients with proteinuria. Twenty-seven age-matched obese subjects without proteinuria served as controls. A glucose tolerance test and renal biopsy were performed in all patients. Fasting serum insulin and homeostasis model assessment-insulin resistance (HOMA-IR) were regarded as reflecting insulin resistance. To delineate the relation between insulin resistance and proteinuria, troglitazone, which acts an insulin sensitizer was given to 6 of 12 patients with a regular diet for 8 weeks. The 6 others were observed without receiving troglitazone. RESULTS: The 12 patients showed the presence of a cluster of insulin resistance factors: higher blood pressure, higher body mass index, higher fasting plasma glucose, higher fasting serum insulin, and higher HOMA-IR than controls. The renal biopsy specimens exhibited no histological abnormalities in 7, focal segmental glomerulosclerosis in 3 and benign nephrosclerosis in 2. Troglitazone attenuated HOMA-IR and ameliorated proteinuria, but did not affect body weight, creatinine clearance, or blood pressure. In contrast, the parameters in the patients not given troglitazone did not change. CONCLUSION: Insulin resistance is a factor contributing to obesity-related proteinuria. The role of insulin resistance as a factor reducing proteinuria remains to be clarified.

Adult↗

PubMed2005

Influence of chronic kidney disease development and renin-angiotensin system inhibition on cardiovascular prognosis.

Recently published guidelines recognize the relevance of the development of chronic kidney disease in the stratification of risk of the hypertensive patient. Adequate assessment of renal function, including estimation of glomerular filtration rate, is mandatory in order to ensure an adequate evaluation of global cardiovascular risk in the hypertensive patient. The presence of subtle elevations of serum creatinine concentrations is a potent predictor of a poor cardiovascular prognosis. Clustering of associated risk factors seems to justify the elevated cardiovascular risk observed in patients with essential hypertension and mild renal function derangement. Chronic kidney disease is associated with a significant increase in cardiovascular risk attributable to the simultaneous existence of other risk factors related to the metabolic syndrome. The inhibition of the effects of angiotensin II is necessary to ensure the best degree of renal protection. It has demonstrated to improve the long-term renal outcome of patients with nephrosclerosis and to reduce the appearance of cardiovascular complications in high risk patients The high prevalence of chronic kidney disease in the general and in the hypertensive populations forces the recognition of its relevance and the need for an integrative therapeutic approach to protect simultaneously renal and cardiovascular systems.

Angiotensin II↗

PubMed1976

The spotted nephrogram of renal scleroderma.

The renal angiographic findings in our two patients with scleroderma and recent onset of hypertension included minor changes in the distal interlobar and arcuate arteries and a nephrogram displaying diffuse, spotty lucencies. Although the spotted nephrogram is occasionally seen in cases of severe nephrosclerosis, we believe that, in the absence of major arterial changes in the arcuate and distal interlobar arteries, it is virtually diagnostic of renal scleroderma.

Adult↗

PubMed1979

Persisting hypertension after renal artery reconstruction. A follow-up study.

Twenty-four patients with persisting hypertension after renal artery reconstruction were re-investigated 1--8 years after surgery. They underwent renal arteriography, determination of plasma renin activity, renography and renal function studies in order to find the causes of the postoperative hypertension. Restenosis was found in 6 patients, in 3 of whom it was of functional significance according to the positive renin tests (renin ratio greater than 1.5). Positive renin tests were found in 2 other patients. One had occlusion of a renal artery branch and the other hypoplasia of the kidney due to chronic nephritis. No explanation of the persisting hypertension could be found in 19 patients at re-examination. In 10 of them, however, biopsy from the affected kidney obtained during operation showed nephrosclerosis, which may explain the outcome. Fourteen of the 19 patients had negative renin tests preoperatively. These negative tests indicate that renal artery stenosis was not the only cause of hypertension. It may be concluded that the renin test is of the utmost value in the selection of patients for renal artery reconstruction and should always be considered. A biopsy from the contralateral kidney may be necessary in order to detect other causes of hypertension than renal artery stenosis. The importance of re-investigating patients with persisting hypertension is confirmed by the present study.

Adolescent↗

PubMed1991

Changing patient characteristics in chronic hemodialysis.

Patients accepted to chronic hemodialysis have changed. We analyzed these changes and survival, cause of death and other factors during 23 years at the Karolinska Hospital. Between 1965 and 1987, 274 patients were accepted: 60 are alive on dialysis, 75 died, 113 were transplanted, 25 sent to other units and one recovered renal function. The mean age increased from 44 to 55 years (p=0.001), the creatinine level at acceptance decreased from 1191 to 965 mumol/l (p = 0.001), the hemoglobin level rose from 70 to 85 g/l (p = 0.001) and the diastolic blood pressure decreased from 96 to 90 mmHg (p = 0.007). The number of co-morbid conditions increased from 1.2 to 1.4 (p less than 0.005). The diagnoses changed from over 90% primary renal disease to 20% systemic diseases such as nephrosclerosis and diabetes (p = 0.04). The chance of receiving a renal transplant decreased from 46 to 39% (p = 0.28). The transplanted patients were younger than the dialyzed patients 42 vs 47 years (p = 0.03) before 1980 and 49 vs. 56 years (p = 0.0001) after 1980. The cause of death changed. Withdrawal from dialysis increased from 5% of deaths before to 24% after 1980 (p = 0.047), cardiovascular deaths decreased from 85% to 55% (p = 0.01). Although the patients accepted for dialysis after 1980 had more serious renal disease and other degenerative diseases than those before, the mortality rate was reduced to only 1/4 to that before, in all age groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1986

Pharmaco-epidemiological considerations in patients with arthritis and vascular disease of the kidney.

Non-steroidal anti-inflammatory drugs (NSAIDs) may produce acute renal failure, papillary necrosis and interstitial nephritis. These adverse drug reactions are rare but have been reported in patients with congestive heart failure, cirrhosis, renal parenchymal disease, lupus nephritis and hypertension. All these conditions may be associated with hypovolaemia and an activated renin-angiotensin system, when renal blood flow and glomerular filtration depend on local renal prostaglandin biosynthesis. A severe impairment of renal function may occur when this synthesis is inhibited by NSAID treatment. It is possible that 1 in 100 of elderly patients have renal parenchymal disease, 1 in 100 arteriolar nephrosclerosis, 1 in 200 unilateral or bilateral renal artery stenosis and an unknown number suffer from atheroembolic renal disease. Fortunately, only a small proportion of 'at risk' patients given NSAIDs appear to develop renal failure. Perhaps bilateral renal disease or salt depletion are necessary factors? Whatever the explanation, NSAIDs should be used with caution in the elderly.

Adolescent↗

PubMed1993

Hypertension and renal disease.

Chronic renal parenchymal disease is the most common cause of secondary hypertension: By the time end-stage renal disease develops, its prevalence approaches 75-85%. It was previously believed that hypertension caused arteriolar nephrosclerosis and ischemic renal injury superimposed on primary renal parenchymal disease, contributing to progressive renal insufficiency. Recently, the importance of an increased intraglomerular hydraulic pressure due to loss of renal autoregulation has been emphasized. There are several potential explanations concerning clinical studies which have not uniformly demonstrated slowing of progressive renal damage with antihypertensive therapy: Random BP measurements may not adequately reflect average BP levels, or, alternatively, the widely accepted target level of BP control may be inadequate. In a retrospective study, we found that hypertensive nephropathics had higher serum creatinine levels than normotensives; in another prospective trial we have demonstrated that enalapril is an effective antihypertensive agent in patients with IgA nephropathy, and it also ameliorates the evolution of the disease.

Adult↗

PubMed1997

Acute renal failure in pregnancy.

From 1976 to 1994, 57 women were referred to the Centro de Nefrología, Montevideo, with obstetric acute renal failure (ARF). The main causes were hypertensive disorders such as preeclampsia (PE) in 27, acute pyelonephritis of pregnancy (APN) in 26, and idiopathic postpartum renal failure in 3. Severe preeclampsia superimposed on chronic hypertension and acute pyelonephritis of pregnancy complicated by sepsis accounted for more than 50% of the cases of ARF. Chronic renal failure developed in 6 patients: 2 had bilateral renal cortical necrosis, 1 had malignant nephrosclerosis, and 3 had idiopathic postpartum renal failure. Maternal mortality related to ARF was low in this group of patients (less than 2%). In contrast, perinatal mortality was strikingly high (40%).

Acute Kidney Injury↗