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Vasoactive hormones and renal sclerosis.
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Renal vascular sclerosis is associated with inherited thrombophilias.
Vascular sclerosis is often seen in renal biopsies. It is usually associated with diabetes mellitus, hypertension, smoking, etc. However, whether inherited thrombophilic states such as factor V gene mutation, prothrombin gene mutation, and methylenetetrahydrofolate reductase (MTHFR) gene mutation are associated with the vascular sclerosis is not known. Renal biopsies that showed vascular disease were grouped into five groups: (1) diabetic patients, (2) hypertensive patients, (3) diabetic and hypertensive patients, (4) smokers, and (5) vascular sclerosis of unknown etiology (idiopathic renal disease). Renal biopsies with no vascular sclerosis were used as controls. Frozen tissue was analyzed for factor V Leiden mutation, prothrombin G20210A mutation, and MTHFR C677T. Factor V Leiden mutation and prothrombin G20210A mutation was not seen in patients with diabetes, hypertension, or smoking, whereas MTHFR C677T polymorphism in these groups was not significant, compared to the controls. In the idiopathic renal disease group, three of the 17 patients (17.6%) had prothrombin G20210A mutation, two of the 17 patients (11.8%) had the factor V Leiden mutation, and five of the 17 (29.4%) were homozygous for the MTHFR C677T polymorphism. When the data were evaluated as a whole, 10 mutations were found in 17 patients (P<0.0005 compared to controls) or eight of the 17 patients (47%) were observed to have at least one of the three forms of inherited thrombophilia (P<0.001 compared to controls). These findings indicate that renal vascular lesions, in the absence of diabetes, hypertension, or smoking appears to be associated with inherited thrombophilias.
Prevention of mesangial sclerosis by bone marrow transplantation.
Previously we have shown that bone marrow (BM) transplantation (BMT) can attenuate progression of and even ameliorate mesangial sclerosis (MS) in Wt1-heterozygous mice. However, it is unclear whether BMT performed before the onset of disease will prevent the development of MS. To investigate whether intravenous (i.v.) or intrarenal (i.r.) administration of BM have equal effects on the progression of MS in Wt1-heterozygous mice, young Wt1-heterozygous mice that had not yet developed renal disease were used as recipients for BMT. After preconditioning with 750 cGy radiation, mice were transplanted with one million wild-type BM via i.v. or i.r. administration. All recipients and untreated controls were assessed for urinary albumin loss, renal pathology, and BM donor-derived renal cells over time. Representative kidney samples were subjected to transmission electron microscopy (TEM) analysis. Interestingly, i.r. and i.v. administration of BM cells gave comparable hematopoietic engraftment levels, and both were able to prevent the onset of MS as assessed by improved lifespan, renal function, renal histology, and TEM analysis. Taken together, we show for the first time that MS can be prevented if BMT is performed before disease onset. Similar therapeutic effects were obtained whether the BM was administered i.v. or i.r.
The clot thickens.
Vascular sclerosis has been linked to many risk factors, including smoking, family history, low birth weight, and hypertension. In interesting studies, Goforth et al. show an increased rate of mutations in thrombophilic molecules in patients with vascular sclerosis in renal biopsies, suggesting yet another mechanism.
Studies on hypertension in spontaneously hypertensive rats.
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Renal vascular responses to dopamine: haemodynamic and angiographic observations in normal man.
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The vicious circle in acute malignant hypertension of rats.
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Acute renal failure due to hypertension: malignant hypertension in an adolescent.
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Angiotensin converting enzyme gene I/D polymorphism in essential hypertension and nephroangiosclerosis.
An insertion/deletion (I/D) polymorphism of the angiotensin converting enzyme (ACE) gene significantly influences circulating ACE levels and plays a role in the development of target organ damage, that is, left ventricular hypertrophy in essential hypertension (EH), and microalbuminuria in diabetes mellitus. We have examined the role of the I/D polymorphism in essential hypertensive patients with renal involvement. The study was divided in two independent protocols. In protocol 1, we retrospectively analyzed the ACE genotypes in 37 essential hypertensive patients with a clinical and histopathological diagnosis of nephroangiosclerosis. In protocol 2, ACE genotypes as well as microalbuminuria and renal hemodynamic parameters were investigated in 75 patients with EH with normal renal function and a strong family history of hypertension. As control group, 75 healthy subjects with BP < 130/85 mm Hg and no family history of cardiovascular diseases were studied. The ACE variants were determined by PCR and the genotypes were classified as DD, DI and II. In protocol 1, patients with nephroangiosclerosis displayed a significant difference in the genotype distribution (57% DD, 27% DI, 16% II) when compared to the control population (25% DD, 64% DI, 11% II; P < 0.001). There was no significant difference in genotype distribution between hypertensive patients with normal renal function (protocol 2; 33% DD, 59% DI, 8% II) and the control group. There were no differences in age, blood pressure, microalbuminuria and duration of the disease among the three genotypes in the EH group from protocol 2. Taken together, these findings suggest that the DD genotype of ACE is associated with histopathologic-proven kidney involvement in patients with EH and that this polymorphism could be a potential genetic marker in hypertensives at risk of renal complications.
Ischemic renal diseases: new insights into old entities.
Vascular nephropathies are a steadily increasing cause of end-stage renal failure. Arterionephrosclerosis and arteriolonephrosclerosis are common features in the hypertensive patient. This is especially true for blacks of African descent, in whom hypertension and nephrovasculopathies are a major cause of renal insufficiency. That primary hypertension leads to renal vascular lesions, glomerular obsolescence and interstitial fibrosis has long been established. It should not, however, obscure the fact that renal vascular lesions can be observed in animal models as well as in some humans, especially young blacks, in the absence of, or anticipating the onset of hypertension. This leads to considering the hypothesis that nephroangiosclerosis might stem from a genetic defect in the renal vascular bed and that this defect is strongly associated with the hypertensive trait. Atherosclerotic renal disease is a major, potentially treatable cause of chronic renal disease is a major, potentially treatable cause of chronic renal failure, especially in whites. It leads to renal atrophy, but the ischemic kidney retains a vigorous potential for tubular cell regeneration, which pleads for early recognition and treatment. Recent data suggest that renal ischemia, be it due to renal artery stenosis or to cholesterol crystal embolism, ranks among the multiple causes of secondary focal segmental glomerulosclerosis. Irrespective of its initial mechanism, ischemia induces renal fibrosis, the pathophysiology of which is centered on increased generation of angiotensin II. Finally, renal vascular lesions are commonly observed in the course of various nephropathies, even in the absence of hypertension, and the relationship between these lesions and the unfavorable prognosis of glomerulopathies, especially primary focal-segmental glomerulosclerosis, membranous glomerulopathy and IgA glomerulonephritis, remains to be elucidated. Expanding knowledge of the spectrum of nephrovasculopathies opens perspectives for investigating, understanding and treating a major mechanism of progressive renal insufficiency.
A stereological study of glomerular number and volume: preliminary findings in a multiracial study of kidneys at autopsy.
BACKGROUND: This report describes preliminary results of a study of glomerular number and volume and their associations, in kidneys of people coming to autopsy. METHODS: Both kidneys were weighed at autopsy and the right kidney was perfusion-fixed and sub-sampled for stereological estimation of total glomerular number, and of mean renal corpuscle volume, using the physical disector/fractionator combination. RESULTS: The 78 kidneys studied so far were from Australian Aborigines, Australian non-Aborigines, US blacks and US whites, ages newborn to 84 years. Glomerular number ranged almost ninefold (from 210,332 to 1,825,380), with mean (SD) of 784,909 (314,686); it decreased throughout adult life (r=-0.32, P=0.009). Mean renal corpuscle volume varied 5.6-fold in adults and was inversely correlated with glomerular number (r=-0.38, P=0.001). Total renal corpuscle volume varied in adults by a factor of 15.8. Kidney weight correlated with body surface area (BSA) at all ages (r=0.76, P < 0.001); it varied 3.4-fold among adults, while kidney weight/m2 varied 3.7-fold. The percentage of sclerosed glomeruli varied from 0 to 23%, and it correlated strongly with age (r=0.58, P < 0.001). Females had smaller kidneys than males, and, marginally, fewer glomeruli. There were no significant variations by ethnic group. CONCLUSIONS: These extraordinary ranges of glomerular number and size among ostensibly "normal" people, and their inverse relationship, probably have important implications for susceptibility to renal insufficiency. People with low glomerular (nephron) numbers are likely to be particularly predisposed, with the process marked by compensatory hypertrophy of residual nephrons, which, in turn, accelerates their obsolescence. Much, however, remains to be done, including evaluation of history, clinical features, accompanying pathology, detailed renal morphology, and further pursuit of potentially defining characteristics in high risk groups.
Hypertension and end-stage renal disease in the developing world.
Hypertension is an important primary etiology of end-stage renal disease as well as a major factor responsible for progression of renal disease due to other causes. Multiple genetic and environmental factors are responsible for the variable prevalence of hypertension in various parts of the world. Although the frequency of hypertension awareness and control is very modest in the developing world, nephroangiosclerosis seems to be more common in the developed countries. Factors responsible for this discrepancy as well as various strategic measures to control hypertension and its impact on renal disease are discussed.
Evidence for high incidence of end-stage renal disease in patients after stroke and acute myocardial infarction at age 60 or younger.
The impact of stroke and acute myocardial infarction (AMI) on the incidence of end-stage renal disease (ESRD) is unknown. Two community-based registries, one of patients with stroke or AMI and another of patients with ESRD who undergo dialysis, are available in Okinawa, Japan. Whether survivors after stroke and AMI who were registered from April 1988 through March 1991 entered an ESRD dialysis program by the end of December 1999 was determined. Among 4,556 patients (3,809 patients with stroke, 747 patients with AMI) who survived at least 28 days after the event onset, 44 patients (36 patients, stroke; 8 patients, AMI) entered an ESRD dialysis program during the study period. The 10-year cumulative incidence of ESRD was approximately 2.0% in those who survived stroke or AMI. The observed-expected ratio was 4.1 in men (P < 0.01) and 5.8 in women (P < 0.01) aged 30 to 59 years and 0.8 in men (not significant) and 0.4 in women (not significant) 60 years and older. The present results confirm that survivors after stroke or AMI have a greater incidence of ESRD than those in the general population, in particular, those who had stroke or AMI at 60 years or younger.
Osteocalcin and myoglobin removal in on-line hemodiafiltration versus low- and high-flux hemodialysis.
BACKGROUND: Removal of medium and large solutes is poor with low-flux (LF-HD) and limited with high-flux hemodialysis (HF-HD) and on-line hemodiafiltration (OL-HDF). In clinical practice, there are few in vivo solute markers. Osteocalcin is a protein with a molecular mass of 5,800 daltons, and myoglobin is a large molecule with a molecular mass of 17,200 daltons. The aim of this study was to evaluate the impact of OL-HDF on in vivo removal of a wide spectrum of solutes (urea, creatinine, osteocalcin, beta2-microglobulin, and myoglobin) in comparison to LF-HD and HF-HD. METHODS: Twenty-three patients (15 men, 8 women) were studied. Every patient underwent three dialysis sessions with routine HD parameters. We compared 1.8-m2 polysulfone LF-HD and 1.8-m2 polysulfone HF-HD versus OL-HDF. Predialysis and postdialysis solute concentrations were measured. The percentage of reduction ratio for each solute was calculated. RESULTS: Mean values for predialysis osteocalcin, beta2-microglobulin, and myoglobin were 16.3 +/- 21 ng/mL, 27.4 +/- 5 mg/L, and 239 +/- 162 ng/mL in LF-HD, respectively. Urea and creatinine reduction ratios were similar in LF-HD and HF-HD and only 1.2% higher in OL-HDF. Osteocalcin, beta2-microglobulin, and myoglobin reduction ratios for LF-HD were negligible. Mean osteocalcin reduction rates were 54.2% +/- 12% for HF-HD versus 63.5% +/- 9% for OL-HDF (reinfusion volume, 26.8 +/- 5 L/session; P < 0.01). Mean beta2-microglobulin reduction rates were 60.1% +/- 9% for HF-HD versus 75.4% +/- 9% for OL-HDF (P < 0.01). Mean myoglobin reduction rates were 24.5% +/- 6% and 62.7% +/- 9% for HF-HD and OL-HDF, respectively (P < 0.01). CONCLUSION: LF-HD does not seem to remove solutes with a molecular weight greater than 5,800 daltons. OL-HDF provides marked enhancement of convection volume and enables a significant increase in osteocalcin and beta2-microglobulin removal. Myoglobin extraction is nil with LF-HD, very low with HF-HD, and only adequate with OL-HDF.
Prevalence and progression of CRF in Iceland: a population-based study.
BACKGROUND: The prevalence of end-stage renal disease (ESRD) is lower in Europe than in the United States. The purpose of this study was to examine whether this difference results from a lower prevalence or slower progression of chronic renal failure (CRF) in a European cohort. METHODS: We studied 18,912 subjects (9,773 women, 9,139 men) aged 33 to 81 years who participated in the Reykjavik Study between 1967 and 1991. Subjects with serum creatinine (SCr) levels of 1.7 mg/dL (150 micromol/L) or greater were considered to have CRF. We determined the crude prevalence of CRF, as well as age-standardized prevalence for 5-year age groups, in individuals aged 30 to 79 years. Progression of CRF was defined as a decrease in estimated glomerular filtration rate greater than 1 mL/min/1.73 m2/y. RESULTS: Of 49 individuals who had an SCr of 1.7 mg/dL (150 micromol/L) or greater at entry, 41 individuals (26 men, 15 women) had a persistent elevation in SCr levels. Thirty-four individuals had mild CRF (SCr, 1.7 to 2.8 mg/dL [150 to 250 micromol/L]), 6 individuals had moderate CRF (SCr, 2.8 to 5.6 mg/dL [250 to 500 micromol/L]), and 1 individual had ESRD. The crude prevalence of CRF was 0.22% (220/100,000); 0.15% among women and 0.28% among men. The age-standardized prevalence was 0.23% (95% confidence interval [CI], 0.04 to 0.42) for women and 0.42% (95% CI, 0.18 to 0.66) for men. Eighty-five percent of patients with CRF were 50 years or older. Twenty-seven subjects had progressive renal failure, 17 of whom progressed to ESRD during a median of 7 years (range, 3 to 21 years). CONCLUSION: The prevalence of CRF is markedly lower in Iceland than in the United States. Furthermore, 27% of subjects did not show progression of their renal failure. These factors may explain in part the difference in ESRD prevalence between European countries and the United States.
Pseudohyperphosphatemia in a hyperphosphatemic hemodialysis patient.
Hyperphosphatemia is a predictable consequence of end-stage renal disease. Pseudohyperphosphatemia is a spurious elevation of serum phosphate in samples containing a substance that interferes with the laboratory assay for phosphate. The most common cause is a paraprotein in disorders such as Waldenström's macroglobulinemia and multiple myeloma. We report here a case of pseudohyperphosphatemia in a hyperphosphatemic patient with end-stage renal disease on long-term hemodialysis caused by a saline solution containing phosphorus used to dilute the patient's serum sample in the clinical chemistry laboratory. Investigations showed that the phosphorus most likely was introduced at the time of saline manufacture. Pseudohyperphosphatemia resulting from the manufacture and distribution of saline-containing phosphorus could be a cause of abnormally high serum phosphate measurements in hyperphosphatemic dialysis patients whose serum samples must be diluted in the laboratory. Such spuriously elevated results can lead to inappropriate changes in medications and subject patients to additional hemodialysis treatments.
Chloroquine-induced phospholipidosis of the kidney mimicking Fabry's disease: case report and review of the literature.
A 46-year-old female patient with Sjögren's syndrome, hypertension, and stable chronic renal insufficiency (creatinine [CR], 1.9 to 2.1 mg/dL) had a progressive worsening of renal function (CR, 5.0 mg/dL) after 11 months of chloroquine therapy (155 mg/day; cumulative dose of approximately 51 g). Light microscopy revealed nonspecific angionephrosclerosis. Electron microscopy showed accumulations of lamellated myelinoid material and occasionally also of curvilinear bodies, especially in the glomerular podocytes and to a lesser extent in vascular myothelial and endothelial cells. In the tubular system, mainly protein droplets were stored. Activity of alpha-galactosidase A was normal in isolated leukocytes (56 nmol/mg; range, 33.2 to 109 nmol/mg), ruling out Fabry's disease. Clinical, morphological, and biochemical findings were consistent with chloroquine-associated deterioration of renal function that improved considerably after discontinuation of chloroquine treatment. Adverse effects of chloroquine may aggravate preexisting renal disease. Electron microscopy is a worthwhile tool for establishing the correct diagnosis.