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There is in the Western World a progressive ageing of the population, and consequently haemodialysis patients are also getting older. Some ethical questions have been raised as a consequence of the economic issues related to the scarcity of available resources. In this paper we review our experience in the treatment of very old chronic haemodialysis patients. Fifty patients (7.2% of our haemodialysis patients) aged over 80 years at the beginning of dialysis were included (f = 25, m = 26, age = 82.6 +/- 0.3 years). In 42% of the patients the aetiology of renal disease was unknown. In the remainder, the aetiology was: interstitial nephritis 26%, hypertensive nephrosclerosis 14%, chronic glomerulonephritis 8%, diabetes 8% and polycystic disease 2%. There was a great comorbidity: intradialytic hypotension 82%, cardiac disease 74%, gastrointestinal disease 32%, cerebrovascular disease 26%. Vascular access related problems were the main reason for hospitalization. The major cause of death was vascular (cardiac and cerebral disease). Actuarial survival was 89%, 78%, 56% and 48% at 6, 12, 24 and 36 months, respectively. We think that haemodialysis is the best available choice for treating very old chronic renal failure patients. However further studies are needed to improve the quality of life of these patients.
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PMID:Chronic haemodialysis for very old patients. 782 79

Angiotensin-converting enzyme (ACE) inhibitors represent a major therapeutic breakthrough for treatment of hypertension, congestive heart failure and various chronic renal diseases. They are effective generally well tolerated and safe for most patients. However, acute renal insufficiency or overt renal failure occurs in some patients with underlying critical renal artery stenosis (RAS), hypertensive nephrosclerosis, autosomal dominant polycystic kidney disease, diabetes mellitus, and chronic congestive heart failure. Diuretic-induced sodium depletion and underlying chronic renal insufficiency are the major predisposing factors for renal insufficiency in all of these patient populations. Renal insufficiency is usually asymptomatic, nonoliguric, associated with hyperkalemia, and in nearly every case completely reversible after discontinuation of the offending agent. Moreover, it can usually be managed in the outpatient setting by discontinuation of the ACE inhibitor, concomitant diuretic or both. An asymptomatic increase in serum creatinine in patients administered ACE inhibitors should raise the possibility of RAS; however, more common renal diseases should be considered. The decision to pursue testing for RAS should be done on an individual basis; moreover, it is imperative that patient willingness to undergo invasive procedures including angioplasty and/or surgery should be determined prospectively.
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PMID:Renal insufficiency due to angiotensin-converting enzyme inhibitors. 784 22

Progressive renal failure is conditioned by a number of factors, including type of renal disease, sex, level of arterial pressure, insulin deficiency and/or hyperglycemia in diabetes mellitus, and dietary protein intake. Elevated arterial pressure may cause a progressive renal disease, hypertensive nephrosclerosis, and accelerate the rate of progression of all other chronic renal disease. Hypertension contributes to progressive renal failure by inducing myointimal hyperplasia of arcuate and afferent arterioles, causing glomerular ischemia, and by increasing pressure in the glomerular capillaries. The latter leads to hyperfiltration of protein, increased mesangial ingestion of protein, and glomerular sclerosis. Increased glomerular pressure may also be induced by protein feeding, insulin deficiency and hyperglycemia, especially in the presence of reduced nephron number. Thus at least one common mechanism underlies the effect of hypertension, protein feeding, and diabetes on the progression of chronic renal disease.
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PMID:Pathophysiology of progressive renal failure. 793 15

High levels of tissue advanced glycation end products (AGEs) that result from the spontaneous modification of proteins by glucose occur in diabetes and aging. To address the potential pathogenic role of AGEs in the glomerulosclerosis of diabetes or nephrosclerosis of aging, doses of AGE-modified rat albumin (25 mg per kg per day, i.v.) sufficient to elevate circulating AGE levels to the range of diabetic serum were administered daily to healthy rats alone or in combination with the AGE inhibitor aminoguanidine. After 5 months, the AGE content of renal tissues in AGE-treated rats rose to 50% above controls (P < 0.025), whereas serum contained 2.8-fold greater AGE levels (P < 0.025). Light and electron microscopy of kidneys from AGE-treated rats revealed a more than 50% increase in glomerular volume compared to controls (P < 0.001), significant periodic acid/Schiff reagent-positive deposits, basement membrane widening, and mesangial extracellular matrix increase and indicated significant glomerulosclerosis compared to untreated (P < 0.002) or albumin-treated controls (P < 0.002). These changes were associated with significant loss of protein (P < 0.005) and albumin (P < 0.002) in the urine of AGE-treated rats compared to controls. Cotreatment with aminoguanidine markedly limited both the structural and functional defects. These in vivo data demonstrate that AGEs influence glomerular structure and function in a manner leading to glomerulosclerosis. The effects are AGE-specific, as they are ameliorated by a pharmacological AGE inhibitor, aminoguanidine.
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PMID:Advanced glycation end products induce glomerular sclerosis and albuminuria in normal rats. 797 28

International and geographical differences in the survival rates of chronic dialysis patients can be explained by differences in primary renal disease, in the acceptance rate of elderly patients, and in predialysis comorbid conditions. Several studies have shown the effects of these factors on survival. However, in most studies, a large number of patients may leave for renal transplantation or transfer to other centers, so that precise analysis becomes impossible. Although the number of patients in our registry is not so large (n = 1,982), we have few such problems and were able to examine the effects of the above-mentioned factors on patient survival using the Cox proportional hazard model. Hazard ratios (HR) and 95% confidence intervals were 0.739 and 0.366-1.491 in patients with polycystic kidney disease (n = 38), 2.669 and 1.513-4.708 in patients with systemic lupus erythematosus (n = 39), 1.245 and 0.935-1.660 in patients with nephrosclerosis (n = 122), 1.815 and 1.447-2.229 in patients with diabetes mellitus (n = 374), and 1.595 and 1.201-2.117, respectively, in patients with other renal diseases (n = 146) when the HR in patients with chronic glomerulonephritis (n = 1,263) was taken as 1.00. HR and 95% confidence intervals were 1.222 and 1.016-1.470 in patients with one comorbid condition (n = 217) and 1.494 and 1.033-2.160, respectively, in patients with two comorbid conditions (n = 24) when the HR of patients with no predialysis comorbid conditions (n = 1,741) was taken as 1.00. Our data demonstrate the effects of renal diseases and number of predialysis comorbid conditions on the survival in chronic dialysis patients.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of renal diseases and comorbid conditions on survival in chronic dialysis patients. 799 Oct 45

The reasons for the increased annual incidence of end-stage renal disease (ESRD) in blacks compared with whites are unclear, but may include lack of access to treatment of the causative disease, which likely relates closely to socioeconomic status (SES). End-stage renal disease rates for diabetic glomerulosclerosis, hypertensive nephrosclerosis, and glomerulonephritis were determined in the 9,390 black and white New York State residents who began treatment within the Medicare program between 1982 and 1988. The relationship between the incidence of ESRD, age, and SES, as measured by the race-specific median family income in the patient's zip code, was estimated using a series of logistic-regression models for 12 populations: three causes of renal failure by two races by two sexes. For whites, incidence rates of diabetic glomerulosclerosis and hypertensive nephrosclerosis were significantly negatively associated with declining SES for the 45 to 65 year and 25 to 55 year age groups, respectively. In contrast, there was no relationship between the incidence of these diseases and SES in blacks. For glomerulonephritis, effects of SES were minor for both races. Better access to treatment of diabetes and hypertension might well decrease the annual incidence of ESRD due to diabetic glomerulosclerosis and hypertensive nephrosclerosis in whites. If the SES measures used for blacks are adequate, predisposition to progressive renal damage in response to renal injury or environmental factors other than SES are stronger risk factors for ESRD than SES.
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PMID:Race, socioeconomic status, and the development of end-stage renal disease. 828 92

Prepregnancy counselling for diabetics includes an assessment of the metabolic condition,-and if present-angiopathy and nephropathy. Complications in previous pregnancies worsen the prognosis, particularly if they involve the kidneys. A case story is presented of a diabetic woman (White group F/R), who in her first pregnancy had shown several signs of increasing nephropathy. At the beginning of her third pregnancy her diabetes is badly regulated and her kidneys show signs of nephrosclerosis. Nevertheless, the pregnancy runs relatively smoothly until the thirty-third week where she delivers prematurely. The case story shows the difficulties in predicting the course of present and future pregnancies in a diabetic with angio- and nephropathy.
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PMID:[Repeated pregnancy in a patient with diabetes, nephrotic syndrome and hydronephrosis in an earlier pregnancy]. 832 70

African Americans have higher overall incidence rates of end-stage renal disease (ESRD) compared with American whites. Hypertensive nephrosclerosis (HN), nephropathy secondary to diabetes mellitus types I and II, and chronic glomerulonephritis (CGN) all occur more frequently in African Americans. To explore the possibility that hereditary factors may play a role in the increased risk of ESRD in African Americans, the family history of 131 African American hemodialysis patients (cases) was compared with 115 age-, sex-, and race-matched non-ESRD controls. Odds ratios (ORs) were calculated to define the prevalence of a relative with ESRD among cases versus controls. Chi-square values were estimated from a log-linear model, while controlling for gender, to test for significance of ORs. Forty percent (12/30) of HN cases, 35% (18/51) of type II diabetes mellitus-induced renal failure cases, and 13% (5/38) of CGN cases had a first-, second-, or third-degree relative with ESRD. The presence of a first-degree relative with ESRD increased an African American's risk for developing ESRD ninefold (OR, 9.13; 95% confidence interval [CI], 2.6 to 31.8; P < 0.001). The presence of a first- or second-degree relative increased the risk fivefold (OR, 5.23; 95% CI, 2.2 to 12.3; P < 0.0002). First-, second-, or third-degree relatives with ESRD were more prevalent among cases with ESRD due to hypertension and type II diabetes mellitus compared with CGN (P < or = 0.05). Gender differences among the ORs were nonsignificant (P > 0.2) and socioeconomic class (level of education and income) did not differ markedly between cases and controls.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The familial risk of end-stage renal disease in African Americans. 846 18

Hyperinsulinemia is potentially associated with the development of vascular sclerosis. On the other hand, the relationship between hyperinsulinemia and nephrosclerosis has not been elucidated. In this investigation clinicopathological studies were performed in 40 patients with nephrosclerosis, with special attention to the relationship between hyperinsulinemia and glomerular hypertrophy. Forty patients with biopsy-proven nephrosclerosis were divided into two groups by the 75-g oral glucose tolerance test (OGTT): group A, 2-hr plasma glucose concentration > 140 mg/dL (n = 25); group B, 140 < or = 2-hr plasma glucose < 200 mg/dL (n = 15). Patients with diabetes mellitus or diabetic nephropathy were not included. Morphometric analysis of the glomeruli revealed a significantly larger mean glomerular volume in subjects with nephrosclerosis in both subgroups. In addition, the mean glomerular volume was significantly correlated with the fasting insulin level, while no significant correlation was observed between the mean glomerular volume and creatinine clearance or degree of global sclerosis. These results indicate that hyperinsulinemia may be intimately related to glomerular hypertrophy in patients with nephrosclerosis.
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PMID:Possible relationship between hyperinsulinemia and glomerular hypertrophy in nephrosclerosis. 872 65

To update 2 National High Blood Pressure Education Program working group reports on hypertension and chronic renal failure and renovascular hypertension, a working group was appointed by the director of the National Heart, Lung, and Blood Institute. Literature was searched through MEDLINE and the National Heart, Lung, and Blood Institute information center library. Scientific evidence was given precedence over clinical anecdotal experience. The working group members produced initial draft documents that were circulated to additional experts on hypertension and renal disease. This reiterative process occurred for 18 draft documents. The final report was sent to the representatives of the 44 organizations on the Coordinating Committee for vote and unanimously approved September 1, 1995. The report recommended treatment of hypertension to the goal of 130/85 mm Hg with whatever therapy is necessary to prevent the development of hypertensive nephrosclerosis or the progression of established renal disease of diverse causes. It seems reasonable to recommend angiotensin-converting enzyme inhibitors as initial therapy for patients with diabetes and microalbuminuria or overt diabetic nephropathy with and without hypertension. Renovascular disease has emerged as a major cause of end-stage renal disease, especially in the elderly. Newer screening procedures for the noninvasive screening of renovascular disease include the captopril test, renal scintigraphy following captopril administration, duplex scanning, and magnetic resonance angiography.
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PMID:1995 update of the working group reports on chronic renal failure and renovascular hypertension. National High Blood Pressure Education Program Working Group. 882 47


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