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PubMed1997

Effects of early and late antihypertensive treatment on extracellular matrix proteins and mononuclear cells in uninephrectomized SHR.

The efficacy of an early and late treatment with the angiotensin converting enzyme inhibitor lisinopril or the angiotensin II receptor blocker ICI D8731 was investigated in uninephrectomized spontaneously hypertensive rats (SHR). Rats that underwent uninephrectomy (UNX) at six weeks of age were randomly assigned to receive no treatment, lisinopril shortly after UNX, lisinopril starting 16 weeks after UNX, ICI D8731 shortly after UNX, and ICI D8731 starting 16 weeks after UNX. Blood pressure was normalized with both treatments. After six months inulin clearance was not significant different, while proteinuria and prevalence of interstitial fibrosis were significantly reduced in all treatment groups. Immunohistochemical studies revealed an interstitial, periglomerular and perivascular increase of extracellular matrix proteins in all rats, but a markedly reduced expression of collagen I, IV and fibronectin after early and late treatment compared to untreated controls. We found a significant reduction of infiltrating macrophages and T-lymphocytes in all treated animals compared to untreated controls after 2, 4 and 6 months. Especially early treatment was associated with lower numbers of infiltrating cells. Both treatments reduced proliferation of tubular and interstitial cells. There were no striking differences with regard to nephroprotection between the ACE inhibitor and angiotensin II receptor blocker. These findings show that both treatments have beneficial effects on kidney structure and function. They suggest that both ACE inhibition and angiotensin II blockade decrease renal cell proliferation and suppress the infiltration of mononuclear cells that may trigger expression of extracellular matrix proteins and progressive nephrosclerosis.

Angiotensin Receptor Antagonists↗

PubMed1997

Genetic linkage analysis of growth factor loci and end-stage renal disease in African Americans.

Hypertension, diabetes mellitus and chronic glomerular diseases reportedly cause in excess of 80% of the incident cases of end-stage renal disease (ESRD) in the U.S. The factors that initiate progressive renal failure in patients with these disorders remain unknown. Several investigators have reported enhanced synthesis and activity of cytokines in the kidneys of patients with renal failure. The ensuing inflammation and fibrosis have been postulated to contribute to the development of progressive renal failure. There is also abundant evidence supporting the contribution of genetic factors in ESRD susceptibility based upon the strong familial clustering of ESRD, particularly in African Americans. Therefore, genetic linkage analysis may be useful to evaluate the role of candidate genes in several cytokine cascades that could contribute to the pathogenesis of chronic renal failure. We tested for genetic linkage between eight cytokine candidate genes and chronic renal failure in a collection of African American sibling pairs concordant for ESRD. Epidermal growth factor (EGF), platelet-derived growth factor (PDGF), transforming growth factor (TGF) beta 1, TGF-beta 2 and TGF-beta 3, and tumor necrosis factor (TNF)-alpha and TNF-beta candidate genes were selected for analysis due to their putative roles in diabetic renal disease and chronic glomerulonephritis. The interleukin-1 receptor antagonist gene (IL1RN) was also genotyped due to its reported association with diabetic nephropathy. Non-parametric (genetic model independent) affected sib pair linkage analysis was used to evaluate evidence for linkage. In order to genotype TGF-beta 3, we identified four closely linked, previously unidentified, highly polymorphic microsatellite loci near the TGF-beta 3 gene. Linkage of ESRD and transforming growth factor beta 2 polymorphisms on human chromosome 1 approached significance for non-diabetic nephropathy (predominantly chronic glomerular disease, hypertensive nephrosclerosis and unknown etiology) (P = 0.08), but showed no linkage to diabetic nephropathy. The other candidate loci did not demonstrate linkage to ESRD in the total population or in the subgroups with diabetic or non-diabetic etiologies of ESRD. The IL1RN gene did not show significant evidence for linkage to ESRD; however, we did confirm an association between allele 2 of IL1RN and ESRD (as reported in diabetic nephropathy). Overall, these results suggest that these growth factor loci do not make major contributions to the pathogenesis of ESRD in African Americans.

Base Sequence↗

PubMed1997

Latent transforming growth factor-beta: structural features and mechanisms of activation.

Transforming growth factor-beta are cytokines with a wide range of biological effects. They play a pathologic role in inflammatory and fibrosing diseases such as nephrosclerosis. TGF-beta s are secreted in a latent form due to noncovalent association with latency associated peptide (LAP), which is a homodimer formed from the propeptide region of TGF-beta. LAP is disulfide linked to another protein, latent TGF-beta binding protein (LTBP). LTBP has features in common with extracellular matrix proteins, and targets latent TGF-beta to the matrix. Activation of latent TGF-beta can be accomplished in vitro by denaturing treatments, plasmin digestion, ionizing radiation and interaction with thrombospondin. The mechanisms by which latent TGF-beta is activated physiologically are not well understood. Results to date suggest an important role for proteases, particularly plasmin, although other mechanisms probably exist. A general model of activation is proposed in which latent TGF-beta is released from the extracellular matrix by proteases, localized to cell surfaces, and activated by cell-associated plasmin.

Animals↗

PubMed1999

Improvement in treatment of hypertension has not reduced incidence of end-stage renal disease.

Hypertension is an important cause of end-stage renal disease (ESRD) in the USA and in Sub-Saharan Africa. Antihypertensive therapy has led to a substantial decrease in incidence of stroke (42%) and to a lesser extent of myocardial infarction (16%), yet there has been an increase in hypertension related ESRD. In 1991, about 190 000 persons in the USA either underwent dialysis or received a transplant for ESRD. Hypertension was found to be the underlying cause in 29% of these patients, second only to diabetes mellitus (36%). Both in the USA and South Africa hypertension was found to be the most common cause of ESRD, but it is not clear whether this is related to the higher incidence and severity of hypertension in black people. Moreover blood pressure (BP) control in black patients does not necessarily lead to improved renal function. These findings suggest that factors other than BP elevation participate in the progression of nephrosclerosis. They include misdiagnosis, black race (socio-economic status, physiologic differences, severity of hypertension), BP control (adequate control of BP and type of antihypertensive therapy), and possibly other factors like genetics. The lack of reduction in ESRD may be that currently accepted standards for BP control are not adequate and that different antihypertensive agents affect glomerular haemodynamics in different ways. These factors need an in-depth analysis to improve the important public health issue of increasing morbidity and mortality from ESRD.

Humans↗

PubMed2004

Sustained beneficial effects on blood pressure during long time retrospective follow-up after endovascular treatment of renal artery occlusion.

We retrospectively evaluated short- and long-term effects of percutaneous transluminal renal angioplasty (PTRA) with or without stent placement of renal artery occlusion (RAO) upon blood pressure (BP), serum (s)-creatinine, and the need for antihypertensive treatment in 34 RAO patients who underwent PTRA during 1996-2002. In 24/34 (71%) treatment was considered technically successful, 22/24 (92%) were treated with PTRA + stent, two with only PTRA. Patients were followed for mean 2.6 (range 0-8) years, during which 14/34 (41%) patients died. In all 34 patients, systolic and diastolic BP (SBP and DBP) before treatment were 184 +/- 30/95 +/- 15 mmHg and had decreased at discharge (to 157 +/- 21/80 +/- 10 mmHg; P < 0.001 for both SBP and DBP), and remained lower after 1 year (154 +/- 20/83 +/- 7 mmHg; P < 0.001 for SBP and P < 0.01 for DBP), and at last follow-up (148 +/- 20/80 +/-12 mmHg; P < 0.001 for both SBP and DBP). No changes occurred in s-creatinine or the number of antihypertensive drugs. Similar results were seen in the subgroup of 24/34 (71%) patients in whom treatment was technically successful. Among the 24 patients undergoing technically successful PTRA, absence of nephrosclerosis (P = 0.035) and a shorter duration of hypertension (P = 0.020) predicted favourable clinical outcome. No adverse effects upon s-creatinine or the need for antihypertensive medication were seen in patients in whom treatment was considered a technical failure. Seven of these patients were treated with PTRA of another renal artery than the occluded, or with embolisation. In conclusion, RAO can be treated with endovascular techniques. Technically successful results with decreasing blood pressure levels were obtained in 71% of patients.

Adolescent↗

PubMed2003

Acrolein produced from polyamines as one of the uraemic toxins.

It is well known that the addition of spermine or spermidine to culture medium containing ruminant serum inhibits cellular proliferation. This effect is caused by the products of oxidation of polyamines that are generated by serum amine oxidase. Among the products, we found that acrolein is a major toxic compound produced from spermine and spermidine by amine oxidase. We then analysed the level of polyamines (putrescine, spermidine and spermine) and amine oxidase activity in plasma of patients with chronic renal failure. It was found that the levels of putrescine and the amine oxidase activity were increased, whereas spermidine and spermine were decreased in plasma of patients with chronic renal failure. The levels of free and protein-conjugated acrolein were also increased in plasma of patients with chronic renal failure. An increase in putrescine, amine oxidase and acrolein in plasma was observed in all cases such as diabetic nephropathy, chronic glomerulonephritis and nephrosclerosis. These results suggest that acrolein is produced during the early stage of nephritis through kidney damage and also during uraemia through accumulation of polyamines in blood due to the decrease in their excretion into urine.

Acrolein↗

PubMed2003

Current status of dialytic therapy in Korea.

The status of dialytic therapy in Korea at the end of 2001 was reported by the end-stage renal disease (ESRD) registry committee of Korean Society of Nephrology, where data were collected through an internet on-line registry program. The number of dialysis centres was 335 and the number of haemodialysis machines was 5529. The total number of patients with dialysis was 23,057 (haemodialysis 17,568, peritoneal dialysis 5489). Prevalence and incidence of dialysis patients were 477.5 and 96.4 patients per million population. The most common primary cause of end-stage renal diseases was diabetic nephropathy (41.5%), hypertensive nephrosclerosis (15.4%), and chronic glomerulonephritis (13.6%). Eighty-six percent of haemodialysis patients were on dialysis therapy three times a week, the mean urea reduction ratio was 66.7 +/- 8.68% and mean Kt/V was 1.250 +/- 0.292 in male patients; 1.526 +/- 0.361 in female patients. The technical survival of haemodialysis in 5 years was 30.2% and peritoneal dialysis was 13.8%. The common complication of haemodialysis patients was hypertension (43.3%), gastrointestinal disease other than peptic ulcer (8.0%), congestive heart failure (7.6%), and of peritoneal dialysis patients were also hypertension (28.8%), congestive heart failure (5.0%), and peritonitis (4.8%). The most common causes of death were cardiac diseases (26.9%), vascular diseases, including cerebrovascular accidents (22.7%), and infection (17.8%).

Female↗

PubMed2003

Marked diffuse dilations of the biliary tree associated with intrahepatic calculi, biliary sludges and a mucinous cyst of the pancreatic head in a 99-year-old woman.

A 99-year-old woman was admitted to Shizuoka Shimizu Municipal Hospital because of fever and anasarca. Imaging and laboratory tests showed pneumonia, urinary tract infection, and cardiac failure. The patient died 20 days after admission. An autopsy revealed marked diffuse dilations of the biliary tree ranging from the lower common bile duct to intrahepatic bile ducts. Intrahepatic calcium bilirubinate stones and biliary sludges were recognized within the dilated bile ducts. A unilocular cyst (2 cm in diameter) was present in the pancreatic head adjacent to the lower common bile duct, and it appeared to compress the common bile duct. Histologically, the walls of the dilated biliary tree showed proliferation of peribiliary glands, fibrosis, and infiltration of lymphocytes and neutrophils (cholangitis). The lumens of the dilated biliary ducts contained neutral and acidic mucins, fibrinous materials, bacteria, neutrophils, and Aspergillus fungi, in addition to the calculi and sludges. The background liver showed atrophy (400 g). The pancreatic unilocular cyst was composed of mucous columnar cells with a few infoldings, and the pancreas also showed foci of mucinous duct hyperplasia and ectasia; the pathological diagnosis of the cyst was cystic dilations of a pancreatic duct branch (mucinous ductal ectasia or mucinous cyst). Other lesions included aspiration pneumonia, emaciation, atrophy of systemic organs, gastric leiomyoma, serous cystadenoma of the right ovary, and arteriosclerotic nephrosclerosis. The present case suggests that a mucinous cyst of the pancreas may compress the biliary tree and lead to marked diffuse dilations of the biliary tree. Alternatively, the dilations of the bile ducts may be associated with aging or may be of congenital origin. The dilated bile ducts may, in turn, give rise to bacterial and fungal cholangitis and formation of biliary sludges and intrahepatic calcium bilirubinate stones.

Aged↗

PubMed1998

Hypertension as cause of end-stage renal disease: lessons from international registries.

The incidence of hypertension as cause of ESRD has doubled in the ERA-EDTA Registry in the past two decades, going from 7 to 13%. It is very possible that this is not a real increase in the incidence of hypertension as cause of ESRD, but rather a consequence of greater acceptance of older patients, a phenomenon that has simultaneously occurred. There are geographic differences in the incidence of hypertension as cause of ESRD, from 6% in Japan to 28.5% in the U.S., and 13% in Europe. With the present data, it is impossible to know if these differences are real. The diagnostic criteria used are not uniform and a consensus would be necessary to establish uniform diagnostic criteria for nephrosclerosis or ischemic nephropathy. The percentage of patients starting renal replacement therapy (RRT) with unknown primary renal disease is very different in the U.S. and Europe. This could be a critical factor in explaining these differences. Survival of patients at 5 and 10 years with renal vascular disease did not improve from 1977 to 1989. The same occurs with survival of patients with standard primary renal disease, although this is better than that of patients with renal vascular disease. To interpret this lack of improvement in survival of patients over a decade, we must take into account that at the same time there has been a significant increase in the age of patients starting RRT. Therefore, when the population of patients of under 55 is analyzed, there is evidence that those starting treatment in the 80's have much better survival than those starting in the 70's. However, survival of patients with renal vascular disease continues to be poorer than that of patients with standard primary renal disease. This lower survival of patients with renal vascular disease seems to be related to higher cardiac mortality, which is in alignment with the diagnosis of hypertension as cause of renal failure.

Global Health↗

PubMed2000

Glomerular type IV collagen in patients with diabetic nephropathy with and without additional glomerular disease.

BACKGROUND: Type IV collagen is a constituent of mesangial matrix and is increased in amount in many forms of glomerular injury. METHODS: We performed renal biopsies in patients who (1) were donating a kidney to a relative (LRD, N = 6), (2) had diabetic glomerulopathy with or without nephrosclerosis (DM, N = 6), or (3) had diabetic glomerulopathy with a superimposed glomerular lesion (DM+, N = 5). Glomerular collagen alpha2(IV) and control glyceraldehyde-3-phosphate dehydrogenase (GAPDH) mRNAs were measured, and the former correlated with clinical and morphological data to assess its usefulness in reflecting glomerular injury. RESULTS: Collagen alpha2(IV) mRNA levels were lowest in LRD (2.9 +/- 0.6 attomol/glomerulus), higher in DM (5.9 +/- 1.6, P = 0.05), and highest in DM+ (12.7 +/- 2.8 attm/glomerulus, P < 0.05 vs. LRD and vs. DM). Control GAPDH mRNA levels were not significantly different (P > 0.05). Levels of proteinuria, serum creatinine, and glomerular size did not correlate with collagen alpha2(IV) mRNA levels. The fractional mesangial area and the fractional mesangial area occupied by type IV collagen were higher in both diabetic groups than in LRD (P < 10-6), but the intensity of type IV collagen staining in the diabetic patients was significantly less than that seen in the LRD (P < 0.01). In DM+ patients, extramesangial type IV collagen was present. Fractional mesangial area and glomerular collagen alpha2(IV) mRNA levels correlated (r = 0.45, P < 0.05). CONCLUSION: These data are consistent with a view of diabetic nephropathy as a lesion of increased alpha2 type IV collagen transcription, increased total amount of collagen present, but decreased mesangial density relative to other matrix molecules. These data further demonstrate that glomerular injury superimposed on diabetic nephropathy contributes to additional structural damage by inducing increased synthesis of type IV collagen at extramesangial sites.

Adult↗

PubMed2001

Increased importin alpha protein expression in diabetic nephropathy.

BACKGROUND: Importins transport kinases, transcription factors, and viral proteins into the nucleus. Since the expression of several genes is increased in diabetic nephropathy, we tested the hypothesis that importin protein expression is increased in diabetic kidneys. METHODS: Immunohistochemistry and Western blotting were used in kidneys from streptozotocin-treated diabetic rats and from spontaneously diabetic Goto-Kakizaki rats. The effects of high glucose and mannose also were tested in cell culture experiments. RESULTS: In normal rat kidneys, importin alpha isoforms were differentially expressed in glomerular cells and tubular segments, while importin alpha1/Rch1 was expressed only in tubules and peritubular cells. In diabetic rat kidneys from both models, the importin alpha isoform expression was markedly up-regulated. Western blotting revealed strong up-regulation of importin alpha7 and minor up-regulation of other isoforms. Exposure of various cell types to high glucose or mannose (25 mmol/L) led to increased expression of importins alpha3, alpha5/hSRP1, and alpha7 in different cultured cells, while up-regulation of other importin alpha isoforms was less consistent. CONCLUSIONS: A specific importin alpha isoform up-regulation takes place in kidneys of diabetic rats. Diabetes is a stimulus for increased importin alpha7 expression. Thus, nuclear transport in diabetes may be increased in glomerular and tubular cells. The signaling pathways appear differentially regulated in glomeruli, proximal, and distal tubules. The enhanced nuclear transport may participate in increased gene expression and nephrosclerosis in diabetes.

Animals↗

PubMed2003

Validation of endogenous controls for gene expression analysis in microdissected human renal biopsies.

BACKGROUND: The appropriate choice of an internal reference is critical for quantitative RNA analysis. However, no comparison of frequently used "housekeeping" genes is available for renal biopsy studies. METHODS: Microdissected biopsies from 165 patients, including a wide range of histopathologic diagnoses, were analyzed [immunoglobulin A (IgA) nephritis, membranous glomerulopathy, rapid progressive glomerulonephritis, minimal change disease, focal segmental glomerulosclerosis (FSGS), nephrosclerosis, diabetic nephropathy, interstitial nephritis, and controls]. Expression of three frequently used housekeeping genes [glyceraldehyde-3-phosphate dehydrogenase (GAPDH), 18S rRNA, and cyclophilin A] was examined by real-time reverse transcription-polymerase chain reaction (RT-PCR). RESULTS: Absolute expression values of reference genes obtained from the renal biopsies were related to each other. In tubulointerstitial compartment, a positive correlation coefficient (r) of 0.96 was observed between 18S rRNA and cyclophilin A. However, a subset of samples showed lower expression levels for GAPDH in relation to 18S rRNA or cyclophilin A, resulting in a decrease to r = 0.77 and r = 0.73, respectively, consistent with considerable mRNA regulation of GAPDH. In glomerular samples, a comparable low correlation between GAPDH versus 18S rRNA (r = 0.75) was obtained. CONCLUSION: Using a single housekeeper gene as reference for renal biopsy studies, differences in gene expression ratios may reflect regulation of the internal control rather than the mRNA under investigation. Relating the gene expression to several housekeepers in parallel (i.e., 18S rRNA and cyclophilin A) should result in robust expression data.

Biopsy↗

PubMed2003

Enlarged nephrons and severe nondiabetic nephropathy in hepatocyte nuclear factor-1beta (HNF-1beta) mutation carriers.

BACKGROUND: Mutations in hepatocyte nuclear factor-1beta (HNF-1beta) lead to a syndrome with diabetes and urogenital malformations [maturity onset of diabetes of the young, type 5 (MODY5)]. The aim of this study was to perform a clinicopathologic investigation of the renal disease in members of a Norwegian family with the HNF-1beta mutation R137-K161del. METHODS: The study was based on long-term clinical observations of five mutation carriers, combined with renal biopsies from four of these. The biopsies were examined by light microscopy, immunohistochemistry, and transmission electron microscopy. The diameter of the glomerulus, proximal and distal tubules, in addition to thickness of the glomerular basement membrane (GBM), were measured in light microscopic slides and transmission electron micrographs. The results were compared with biopsies from adult patients with diabetic glomerulopathy, glomerulonephritis, and/or benign nephrosclerosis, and children with minimal-change glomerulopathy or glomerulonephritis, respectively. RESULTS: Clinically, there was a wide intrafamilial variation from stable or slightly increasing serum creatinine to progressive renal failure and end-stage renal disease (ESRD). In all cases, the kidney disease was diagnosed prior to diabetes. Hypertrophy of the proximal and distal tubules as well as enlarged glomeruli were found in three of four mutation carriers. Essentially normal nephrons were found in the 10-year-old boy. The thickness of the GBM was considered near normal in all mutation carriers. Oligomeganephronia was found in one patient. CONCLUSION: Histopathologic and morphometric studies of kidney biopsies from four carriers of an HNF-1beta mutation revealed enlarged glomeruli and tubular structures. Long-term clinical follow-up demonstrated that the renal disease developed prior to and independently of diabetes. Finally, there is a wide phenotypic variation of the renal disease caused by HNF-1beta mutations.

Adult↗

PubMed2003

End-stage renal disease in North Africa.

There are many similarities in the profile of chronic renal disease in the five North African countries, reflecting their close resemblance in ethnic background, bioecology and socioeconomic standards. The incidence of renal disease is much higher than that in the West, yet the prevalence is relatively lower, which mirrors the inadequacy of medical care facilities. The principal causes of end-stage chronic renal disease (ESRD) are interstitial nephritis (14 to 32%), often attributed to environmental pollution and inadvertent use of medications; glomerulonephritis (11 to 24%), mostly mesangioproliferative and focal segmental sclerosis; diabetes (5 to 20%) and nephrosclerosis (5 to 21%). Obstructive/reflux nephropathy, attributed to urinary schistosomiasis, is common in Egypt (7%), Libya and Southern Algeria. Primary urolithiasis is a frequent cause of obstructive nephropathy in the western (hyperoxaluria) and middle (cystinuria) regions. The incidence of tuberculosis is increasing, particularly the diffuse interstitial and hematogenous forms. It is responsible also for 10 to 40% of renal amyloidosis. The latter is also frequently associated with familial Mediterranean fever. Sickle cell anemia is an important health problem in the west, leading to a wide range of glomerular and tubulointerstitial nephropathies. Takayasu disease is increasingly recognized as a cause of ischemic nephropathy and renovascular hypertension. The management of ESRD is largely influenced by late referral, co-morbidities and lack of dialysis facilities. Hemodialysis is the most frequent modality of renal replacement therapy (RRT). CAPD is used sporadically. Renal transplantation, largely from live (often unrelated) donors, is offered to less than 5% of patients with ESRD. The reported outcome of RRT generally conforms with international standards.

Africa, Northern↗

PubMed2003

Cardiovascular risk in patients with mild renal insufficiency.

We reviewed the evidence linking mild renal insufficiency (MRI) to an increased cardiovascular risk. A number of cardiovascular risk factors become prevalent with MRI, including night-time hypertension, increase in lipoprotein(a), in homocysteine, in asymmetric dimethyl-arginine (ADMA), markers and mediators of inflammation, and insulin resistance. Also, an epidemiologic association between coronary artery disease and nephrosclerosis, a frequent cause of mild renal insufficiency in the elderly, is documented. In the middle-aged, general population MRI, 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 people with MRI; in people at high cardiovascular risk (mostly coronary disease), the HOPE study found a 2-fold (unadjusted), or 1.4-fold (adjusted), higher incidence of cardiovascular outcomes with MRI. The incidence of primary outcome increased with the level of serum creatinine. Several studies determined the cardiovascular risk associated with MRI in hypertension. In HDFP, as in HOPE, cardiovascular mortality increased with higher serum creatinine (five-fold difference in cardiovascular mortality between the lowest and the highest creatinine strata). The risk associated with renal insufficiency was independent from other classic cardiovascular risk factors. In hypertensives with low risk, the HOT, and a small Italian trial found about a doubling in cardiovascular outcomes in MRI. However, in MRFIT, increase in follow-up creatinine predicted future cardiovascular disease, not baseline creatinine. These observational data suggest that MRI, independent of etiology, is a strong predictor of cardiovascular disease, present in 10% of a population at low risk, and up to 30% at high cardiovascular risk. No prospective therapeutic trials, aimed at reducing the cardiovascular burden in people with MRI, are available. Subgroup analyses of the HOPE study indicate that ACE inhibition with ramipril is beneficial without an increased risk for side 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 that 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 MRI for cardiovascular disease and therapeutic options.

Cardiovascular Diseases↗

PubMedDate not supplied

Racial inequity in America's ESRD program.

The end-stage renal disease (ESRD) program has a significant overrepresentation of racial and ethnic minority groups. The increased susceptibility of nonwhite populations to ESRD has not been fully explained and probably represents a complex interplay of genetic, cultural, and environmental influences. Because the program delivers care under a uniform health care payment system, it represents a unique environment in which to explore variation in health care delivery. A number of disparities in outcomes and delivery of ESRD care have been noted for racial minority participants. These include possible overdiagnosis of hypertensive nephrosclerosis, decreased provision of renal replacement therapy, limited referral for home dialysis modalities, underprescription of dialysis, increased use of synthetic grafts rather than fistulas as permanent angioaccess, and delayed wait-listing for renal transplantation. Transplantation inequities mean that black patients are likely to remain on dialysis relatively longer, so that their susceptibility to less than optimal processes of care increases disproportionately. Improved survival and quality of life (QOL) for blacks with ESRD may have encouraged provider complacency about racial disparities in the ESRD program and in particular about referral for transplantation. It is also apparent that minority ESRD patients may, similar to their non-ESRD counterparts, be referred less frequently for invasive cardiovascular (CV) procedures. Despite these observations of inequality in ESRD care, the adjusted mortality for minority participants in the ESRD program are better than for the majority population. This seeming paradox may define an opportunity to improve outcomes for minorities with ESRD even more.

Black or African American↗

PubMed1998

Hypertension and chronic renal failure: the use of ACE inhibitors.

The incidence of end-stage renal disease (ESRD) has increased 9% a year over the past 10 years, due primarily to diabetic nephropathy and hypertensive nephrosclerosis. Over this period of time, mortality rates for hypertensive heart disease and stroke have decreased substantially, in large part because of greater recognition and improved therapy of hypertension. Why then is there an increasing incidence of ESRD in diseases in which hypertension plays a significant role in causation and/or progression of renal failure? Is it possible that a lower level of blood pressure than usually recommended is necessary to prevent kidney disease (particularly in blacks) or to prevent or slow progression in most forms of renal failure? Furthermore, are there specific renoprotective drugs? This report will focus primarily on large prospective studies that may provide information to answer these questions.

Angiotensin-Converting Enzyme Inhibitors↗

PubMed1998

Incidence, outcome, and risk factors of cerebrovascular events in patients undergoing maintenance hemodialysis.

We retrospectively investigated the incidence and prognosis of and risk factors for cerebrovascular events in 1,064 patients with chronic uremia who received maintenance hemodialysis (HD) for more than 3 months during 24 years in our dialysis units in Miyazaki, Japan. Cerebrovascular events developed in 98 patients (9.2%). The confirmed incidences of cerebral hemorrhage (CH) and infarction were 8.7 and 3.7 per 1,000 patient-years, respectively. Of the 56 patients with CH, 40 (71.4%) died within 3 months of the onset of CH. Ganglio-thalamic lesion was observed in 32 (80.0%) of 40 patients with CH confirmed by a brain computed tomography. The incidence of polycystic kidney disease was higher in the CH group than in the overall HD population (12.5% v 3.9%, P < 0.01). Of the 13 patients with diabetes mellitus and nephrosclerosis, nine (69.2%) developed CH within 36 months of the initiation of HD; 11 (78.6%) of 14 patients with chronic glomerulonephritis developed CH after 36 months. CH developed in six patients (15.0%) within 6 hours of a previous HD session. We compared laboratory values, the supine blood pressure, and electrocardiographic (ECG) findings in 35 patients with CH and a control group (66 patients) matched in age, sex, basal renal disease, age at the initiation of HD, and the duration of HD. Data were obtained before and after HD 3 to 4 months before the first attack of CH. The systolic and diastolic blood pressure (SBP, DBP) before and after HD were significantly higher in the CH group than in the control group (pre-HD SBP: 171 +/- 22.5 v 154 +/- 19.3 mm Hg, P < 0.001; pre-HD DBP: 89 +/- 13.6 v 81 +/- 9.6 mm Hg, P < 0.001). The incidence of left ventricular hypertrophy was higher, and the Kt/V was significantly lower (1.23 +/- 0.26 v 1.38 +/- 0.34, P < 0.05) in the CH group than in the control group. However, there were no significant differences in the serum levels of albumin and cholesterol or the total dose of heparin during HD sessions between groups. In conclusion, the incidence of CH was high, and its prognosis was poor, in patients undergoing maintenance HD. Reversible risk factors include hypertension and possibly the amount of HD prescribed, but not anticoagulation with heparin.

Cerebral Hemorrhage↗