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PubMed2003

ACE inhibition is effective and renoprotective in hypertensive nephrosclerosis: the African American Study of Kidney Disease and Hypertension (AASK) trial.

An interim analysis of the AASK trial at three years demonstrates a renoprotective effect [slower decline in glomerular filtration rate (GFR), delayed onset of significant decrease in GFR, end-stage renal disease (ESRD) or death, and a decrease in urinary protein excretion] of the angiotensin converting enzyme (ACE) inhibitor, ramipril, as compared to the dihydropyridine calcium channel blocker (DHP-CCB), amlodipine, in patients with mild-to-moderate renal insufficiency. The beneficial effect occurred in the presence of similar levels of blood pressure control and was apparent in patients with proteinuric (beyond the threshold of "dipstick positive" proteinuria, 300 mg/day) and non-proteinuric hypertensive nephrosclerosis. At the time of the interim analysis, the effectiveness of the beta-blocker metoprolol was not significantly different from that of the ACE inhibitor. The data suggest that DHP-CCBs should be used with caution in the presence of mild-to-moderate renal insufficiency.

Adrenergic beta-Antagonists↗

PubMed2001

Comparison of cross-sectional renal function measurements in African Americans with hypertensive nephrosclerosis and of primary formulas to estimate glomerular filtration rate.

Renal function measurements were obtained in 1,703 African Americans with presumed hypertensive nephrosclerosis who were screened for entry into the African-American Study of Hypertension and Kidney Disease (AASK). We examined the effect of race on relationships involving renal variables by comparing African Americans enrolled into the AASK with non-African Americans enrolled into the Modification of Diet in Renal Disease (MDRD) study. We examined the effect of gender on renal variables by comparing African American men and women. We compared various methods for estimating glomerular filtration rate (GFR) with iodine 125-labeled ((125)I)-iothalamate GFR. AASK data were also used to derive a new formula for estimating GFR in African Americans. After adjusting for age, sex, and baseline GFR, African American patients on the AASK study were heavier and had larger body surface areas and body mass indices than either MDRD African Americans or non-African Americans. African Americans had greater serum creatinine levels and urinary creatinine excretions for any given level of GFR. Mean GFR was greater in African American men than African American women (59.7 versus 51.7 mL/min/1.73 m(2)), although serum creatinine levels were also greater in men (1.91 versus 1.73 mg/dL). Seventy-eight percent of women with serum creatinine levels between 1.2 and 1.5 mg/dL had GFRs less than 65 mL/min/1.73 m(2). For African Americans in the AASK, GFR was overestimated by the 24-hour creatinine clearance and underestimated by the Cockcroft-Gault formula. A prediction formula developed in the MDRD study more accurately predicted GFR in AASK patients than these measurements. AASK data were also used to derive a new five-term formula for estimating GFR that was slightly more accurate in the African Americans in the AASK than the MDRD formula (median percentage of error, 12.4% for the MDRD formula versus 12.1% for the AASK formula). Important differences exist in renal variables between African Americans and non-African Americans and between African American men and African American women. Formulas using demographic data and readily measured serum values estimate (125)I-iothalamate GFR.

Adolescent↗

PubMed1976

[Oral contraceptives, hypertension and nephrosclerosis (author's transl)].

Five personal cases and many reports in the literature demonstrate the not rare development of hypertension after oral contraceptives or an increase of an existing hypertension. In addition, the drug may also cause vascular changes in the kidneys with development of benign or malignant nephrosclerosis, similar to the increased risk of thrombo-embolic complications of the venous-arterial system. It is, therefore, necessary to check the blood pressure of women on oral contraceptive and, if hypertension exists or develops, discontinue these drugs.

Adult↗

PubMed1977

[Renal transplantation in malignant nephrosclerosis (author's transl)].

Renal transplantation was performed 3 to 64 months after the onset of dialysis in 6 patients with histologically ascertained malignant nephrosclersosis and malignant hypertension, as well as terminal renal failure. Three patients were nephrectomized on both sides before and one after the transplantation. 24 to 105 months after the transplantation all patients were normotensive. Only one patient required low-dosage antihypertensive medication. There was evidence for marked improvement of cardiovascular complications, and no evidence for recurrence of malignant nephrosclerosis in the transplanted kidney.

Adult↗

PubMed1986

Quantitation of hypertensive nephrosclerosis on an objective rational scale of measure in adults and children.

The development of a precise, mathematical relationship between blood pressure and renal microvascular abnormalities would be highly desirable. Such a relationship would require that abnormalities be quantitative on a rational scale. The dominant abnormality in nephrosclerosis occurs in arcuate and cortical arteries of 50 to 400 micron outer diameter. This abnormality consists of acquired inner layers of fibroplastic tissue accompanied by variable fibrosis or withering of the preexisting vessel wall. It is this pathologic variable of interest, the amount of fibroplasia, that can be measured by its thickness in a direction perpendicular to the arterial axis. A method for quantitating the fibroplasia is described. Use of this method in a series of 93 autopsies suggests two tentative conclusions. The outer diameter of 141 micron marks the size of artery in which fibroplasia best correlates with blood pressure. The linear function, mean blood pressure = 1.60 X microvascular lesions +79.7, with correlation coefficient 0.698, governs a relationship similar at all ages. This relationship can be used to compute expected blood pressure from measurements of microvascular abnormalities in kidneys obtained at autopsy. Because all ages include ages 14 to 21 years, the observations imply that the initial tissue changes of hypertensive disease occur early in life.

Adolescent↗

PubMed1988

Long-term survival after recovery from malignant nephrosclerosis.

Five patients with malignant nephrosclerosis (MNSC) and severe renal failure (mean plasma creatinine 926 micromoles/L) were followed for 52 to 83 months. Blood pressure was controlled by a minoxidil-nadolol-diuretic combination. Combined renal length (CRL) on presentation was greater than 18 cm in four patients and 15.3 cm in one patient. Plasma creatinine values declined into the second year, and improved function persisted into the third and fourth years after presentation. The patient with least renal mass on presentation had evidence of declining renal function at 60 months. The data suggest that CRL and sustained blood pressure control are critical determinants of both short- and long-term recovery and preservation of self-sustaining renal function in patients with MNSC.

Acute Kidney Injury↗

PubMed2000

Inaccuracy of clinical phenotyping parameters for hypertensive nephrosclerosis.

BACKGROUND: Multiple studies suggest that hypertension-induced end-stage renal disease (ESRD) is heritable. Identification of nephropathy susceptibility genes absolutely requires accurate phenotyping, but the clinical hypertensive nephrosclerosis (HN) phenotype is poorly characterized. We hypothesized that many patients with HN as the indicated cause of ESRD on the Health Care Financing Administration (HCFA) 2728 form, fail to satisfy stringent HN phenotyping criteria. METHODS: Since renal biopsy documentation of HN is uncommon, clinical parameters for HN phenotype were applied: family history of hypertension, left ventricular hypertrophy, proteinuria <0.5 g/day, and hypertension preceding renal dysfunction (Schlessinger et al., 1994) or urine protein:creatinine (prot:creat) ratio <2.0 and no evidence of other renal diseases (AASK Trial Group, 1997). RESULTS: ESRD patients (n=607, 73% African American, 25% Caucasian) were enrolled in a study to identify HN susceptibility genes. HN was the most common cause of ESRD according to HCFA 2728 forms (37% prevalence). Phenotyping of randomly selected patients with HN from the total cohort revealed that 4/100 subjects satisfied the Schlessinger criteria, and 28/91 African Americans met AASK criteria for HN. From these figures, the adjusted prevalence of HN was only 1.5-13.5%. Of patients that could not be phenotyped for HN, 14 were misdiagnosed, 14 had urine prot:creat >2.0, and insufficient data were available in the remainder. Four patients underwent renal biopsy, but histology from only one was consistent with HN. If the HN phenotype definitions are revised to exclude 'hypertension preceding renal dysfunction', or proteinuria limits, then 44/100 and 39/91 patients respectively satisfy clinical phenotyping parameters for HN. CONCLUSIONS: (i) We provide the strongest evidence to date that HN is less frequent in an ESRD population than commonly assumed if strict clinical criteria are used; many patients clinically diagnosed with HN may have undetected, treatable renal disease from other causes; (ii) relaxing HN phenotype criteria may erroneously include patients with glomerular diseases and secondary hypertension; (iii) reliance on HCFA 2728 diagnoses will confound identification of HN susceptibility genes; (iv) to attain adequate statistical power for genotype analysis, rigorous HN phenotyping will require screening an extremely large number of patients, which can be reasonably accomplished only in a multi-centre trial design.

Black People↗

PubMed1999

Mibefradil prevents L-NAME-exacerbated nephrosclerosis in spontaneously hypertensive rats.

OBJECTIVE: To determine the potential renal protective effects of a novel calcium channel blocker mibefradil in chronic renal failure. METHOD: We compared the long-term effects of mibefradil with an angiotensin-converting enzyme inhibitor cilazapril on blood pressure, proteinuria, renal function and histological alterations in N-nitro-L-arginine methylester (L-NAME)-treated spontaneously hypertensive rats (SHR). Three groups of SHR were studied for 45 days: group 1 (n = 14), treated with L-NAME only (50 mg/l in the drinking water); group 2 (n = 15) L-NAME plus co-treatment with mibefradil (30 mg/kg per day); group 3 (n = 15), L-NAME plus co-treatment with cilazapril (10 mg/kg per day). RESULTS: Both mibefradil and cilazapril attenuated the increased systolic blood pressure, and prevented the development of proteinuria and the decreased creatinine clearance (Ccr) seen at day 42 in the group treated with L-NAME alone. Notably, mibefradil had similar effects to cilazapril on proteinuria and Ccr, despite a reduced antihypertensive effect All animals receiving mibefradil co-treatment remained alive throughout the experiment, whereas the mortality rate was 43% in SHR treated with L-NAME alone. Both mibefradil and cilazapril completely prevented renal structural damage as assessed by scoring glomerular, tubulo-interstitial and vascular lesions. CONCLUSIONS: Our data show that mibefradil prevented the development of hypertension and proteinuria, renal functional impairment and nephrosclerosis, and also improved animal survival. The renal protective effects of mibefradil were at least equivalent to those of an ACE inhibitor in this animal model of chronic renal failure.

Animals↗

PubMed2002

A 3-hydroxy-3-methylglutaryl co-enzyme A reductase inhibitor reduces hypertensive nephrosclerosis in stroke-prone spontaneously hypertensive rats.

BACKGROUND: Recent studies suggest that 3-hydroxy-3-methylglutaryl co-enzyme A reductase inhibitors (statins) exert their protective effects against cardiovascular diseases independently of their cholesterol-decreasing effects. OBJECTIVE: To clarify the effect of a statin on hypertensive nephrosclerosis. METHODS: We treated stroke-prone spontaneously hypertensive rats (spSHRs) chronically, starting at the age of 4 weeks, with cerivastatin (2 mg/kg per day by gavage) or vehicle. Physiological parameters, plasma chemistry and urine protein excretion were analysed. At 14 weeks of age, the rats had their kidneys removed for use in assays. RESULTS: Compared with vehicle treatment, statin treatment reduced proteinuria and renal injury independently of blood pressure and cholesterol concentrations in spSHRs. Although expression of adhesion molecules and infiltration of inflammatory cells were not different whether or not cerivastatin treatment was used, renal fibrosis was significantly reduced in statin-treated spSHRs. We also found that expression of transforming growth factor-beta1 in kidneys was significantly inhibited in statin-treated spSHRs. CONCLUSION: Cerivastatin prevents or retards hypertension-induced renal injury via inhibition of renal fibrosis and proteinuria. These results show the potential of statins as protective tools against proteinuric renal diseases, independent of their cholesterol-decreasing effects.

Animals↗

PubMed1978

Glomerular injury in malignant nephrosclerosis.

Electron microscopic analysis of subendothelial and mesangial alterations in the glomeruli was performed in 15 cases of malignant nephrosclerosis (MNS). 8 cases showed segmental or diffuse subendothelial accumulation of proteinaceous 'fibrinoid' material associated with thickening of glomerular basement membranes. 2 of these cases also showed similar deposits in the mesangium. When severe, this mesangial insudation resulted in almost complete replacement and destruction of the mesangial matrix. Endothelial injury with alteration of glomerular microcirculation and secondary intravascular coagulation is believed to play a role in the development of the glomerular lesions in MNS.

Basement Membrane↗

PubMed1985

Recovery of renal function in patients with accelerated malignant nephrosclerosis on maintenance dialysis with management of blood pressure by captopril.

Recovery of renal function to a self-sustaining level was observed in 4 patients with accelerated malignant hypertension who required chronic hemodialysis therapy. Excellent blood pressure control was achieved in all the patients on captopril therapy. Hemodialysis could be discontinued after 2-9 months of captopril therapy; on recovery of renal function levels of creatinine clearance became stable ranging from 28 to 56 ml/min within 5-15 months of captopril treatment, and remained at this level during 21-64 months of observation. The management of hypertension and the inhibition of the renin-angiotensin system afforded by chronic angiotensin-converting enzyme inhibition is very promising as a means of reversing the process of malignant nephrosclerosis.

Adolescent↗

PubMed1989

Long-term improvement in renal function after short-term strict blood pressure control in hypertensive nephrosclerosis.

Seventy-nine hypertensive nephrosclerosis patients entered a prospective randomized single-blind study to 1) establish the pattern of decay of renal function in this population and the variability therein and 2) to determine if strict diastolic blood pressure (DBP) control (less than or equal to 80 mm Hg) is more effective than conventional levels (90-95 mm Hg) in conserving renal function. Because of unexpected significant improvement in renal function in patients from both groups, which changed the perspectives on the course of this disease as described herein, this report is being published before completion of the trial. The selection criteria were 1) serum creatinine concentration of 1.6-7.0 mg/dl, 2) glomerular filtration rate of less than 70 ml/min/1.73 m2, and 3) absence of diseases (other than hypertension) known to destroy renal function. Renal function was assessed by glomerular filtration rate [( 125I]iothalamate clearance) and serum creatinine concentration. Before randomization, DBP was aggressively treated to reduce it to less than 80 mm Hg. Twenty-two subjects (14 in the strict DBP control group and eight in the conventional DBP control group) have been enrolled in the study for 36 months. In contrast to results from previous studies in humans and rats, renal function improved in both patient groups. Thus, irrevocable progression of renal damage after onset of renal failure from high blood pressure does not necessarily occur, and in fact, long-term improvement of renal function resulted from the effects of the study itself.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1978

Arteriolar nephrosclerosis in the Syrian hamster.

Syrian hamsters developed spontaneous renal lesions that resembled those of arteriolar nephrosclerosis in man, and differed from other spontaneously occurring or virus-induced renal diseases in other rodent species. Morphologic changes were mainly degenerative with little cellular exudation and were associated with histologic changes in the intrarenal vasculature. The renal lesions were progressive, often fatal and sometimes were complicated by glomerular amyloidosis with the nephrotic syndrome and uremia. Endstage kidneys often had fibrinoid necrosis of intrarenal arterioles and thus resembled lesions characteristic of the malignant phase of human essential hypertension. Fibrinoid necrosis of small arterioles was common in the uterus, ovaries or testes of affected animals; it was less frequent in mesenteric or coronary vessels. Cardiac thrombosis, often involving the left atrium or left atrioventricular valves, also was common. Changes occurred earlier and often were more severe in females than in males. This disease was a major cause of morbidity and mortality and hampered life-span studies.

Animals↗

PubMed1986

Prevention of nephrosclerosis and cardiac hypertrophy by captopril treatment of spontaneously hypertensive rats.

The relationship between hypertension and cardiovascular damage was assessed in three groups of spontaneously hypertensive rats (SHR): 1. stroke prone SHR (SHR-SP) treated orally with an angiotensin I converting enzyme inhibitor (captopril) (100-400 mg/L in the drinking water) from 6 to 35 weeks of age, 2. SHR-SP maintained on tap water until 30 weeks of age, 3. stroke resistant SHR (SHR-SR) maintained on tap water. The controls were Wister Kyoto rats (WKY) maintained on tap water. Captopril-treated SHR-SP showed blood pressure lower than that of untreated SHR-SP, similar to SHR-SR. The ratio of heart weight to body weight was 0.55% in SHR-SP, 0.39% in captopril-treated SHR-SP, 0.46% in SHR-SR, and 0.39% in WKY. The kidneys of SHR-SP showed glomerular sclerosis, glomerular fibrosis, tubular casts, interstitial cell infiltration and vascular wall thickening or hyperplasia of the small arteries and arterioles. The severe glomerular sclerosis was mostly distributed in the inner and middle portions of cortex. Immunohistological study showed IgG, C3 and fibrinogen in the glomeruli and arterioles in SHR-SP. In captopril-treated SHR-SP, similar to SHR-SR, only minor histological changes were seen and there was no deposition of IgG, C3 or fibrinogen. No changes were seen in WKY. Thus, it was concluded that nephrosclerosis and cardiac hypertrophy in SHR-SP are prevented by captopril. The role of the renin-angiotensin and kallikrein-kinin systems in organ pathogenesis in SHR-SP is discussed.

Animals↗

PubMed1982

Dexamethasone suppressible hyperaldosteronism in a child with nephrosclerosis.

A 9 year old Mexican boy presented with severe hypertension, hypokalaemia and features suggesting acute glomerulonephritis. Nephrosclerosis was present on renal biopsy. Aldosterone levels were unresponsive to variations in dietary salt intake and plasma renin activity was suppressed. Following oral dexamethasone therapy (2 mg/day), plasma aldosterone decreased to undetectable levels, serum potassium normalized and plasma renin activity gradually increased. Dexamethasone also restored the normal responsiveness of the renin-aldosterone system to postural stimuli. The patient exhibited a marked response to a single dose of ACTH with a rise in plasma aldosterone. Long-term blood pressure control and normal potassium levels have been achieved with oral prednisone therapy (5 mg/day) for a period of one year. This case of dexamethasone suppressible hyperaldosteronism (DSH) illustrates that the degree of hypertension in this syndrome may produce severe renal microvascular lesions. DSH should be considered in all children who present with low renin hypertension.

Adrenocorticotropic Hormone↗

PubMed2001

Benign nephrosclerosis: incidence, morphology and prognosis.

AIMS: Study of benign nephrosclerosis (BNS) is often mixed up with IgA nephritis (IgAN) associated with hypertension or thin basement membrane disease (TBMD). Here we examined the clinicopathological features, incidences and prognosis of decompensated BNS. MATERIALS AND METHODS: BNS was identified in 590 (8.3%) adult cases among 7,108 renal biopsies of a mean age of 56.5 years (male: female ratio = 2.5:1). The post-biopsy follow-up period ranged from 3 to 22 years (10.1 +/- 4.6 years). RESULTS: Patients with progressive BNS were more likely to develop end-stage renal disease within 5 years of biopsy. Poor prognostic factors included poor or no control of arterial blood pressure by anti-hypertensive drugs, global glomerulosclerosis (GS) (> or = 41%) at biopsy, presence of collapsed glomeruli and/or segmented or semi-global GS. Tubulointerstitial damage, glomerular hypertrophy and loop dilatation were secondary to GS. Gender, duration of HT and onset of HT to biopsy were not significant factors. CONCLUSION: GS in BNS is due to ischemia induced by luminal narrowing or obstruction of preglomerular vessels, and glomerular HT due to loss of autoregulation in preglomerular vessels (irregularly shaped atrophic or segmented medial smooth muscle cells, with expansion of extracellular matrix with or without fibrous intimal thickening). GS resulted in luminal dilatation. Both pathological changes affecting the glomerulus may occur in the same kidney and different nephron units.

Female↗

PubMedDate not supplied

Mechanisms in nephrosclerosis and hypertension-beyond hemodynamics.

These studies support that global glomerulosclerosis is a key lesion in human hypertensive nephrosclerosis, and cannot be simply explained by worse vascular sclerosis caused by higher blood pressure. Possible pathogenetic mechanisms include genetic susceptibility, accelerated aging and a primary microvascular disease. The potential importance of the renin angiotensin system in glomerular sclerosis is underscored by the effectiveness of therapies that aim to inhibit its manifold actions, including induction of plasminogen activator inhibitor-1 (PAI-1). Further, regression of existing glomerulosclerosis, including age-related renal and vascular sclerosis, can be achieved in various experimental settings by high dose angiotensin inhibiton, and is linked to inhibition of PAI-1. Ongoing studies will establish which of these provocative findings from animal models are relevant to human diseases, and may lead to optimal therapies to forestall progression and perhaps even induce regression of sclerosis.

Animals↗

PubMed1987

[Interrelation of changes in the epithelium of kidney tubules and interstitium in nephrosclerosis based on morphometric and histochemical data].

Kidneys from 90 individuals who had died from atherosclerosis, hypertensive disease, or chronic glomerulonephritis were examined following early autopsies. The nephron epithelium and the endothelium of peritubular capillaries were studied for activities and distribution patterns of NADPH2 dehydrogenase, lactate dehydrogenase, succinate dehydrogenase, and acid and alkaline phosphatases, for relative capillary and connective tissue volumes, and for lymphocyte, monocyte, and plasma cell numbers. A mathematical analysis of the histochemical and morphometric data provided information on the nature of changes in the renal microcirculatory bed and on the roles of free stromal cells in various forms of nephrosclerosis as well as on the zonal distribution of the parameters studied. Intercellular and vascular-cellular links were found to be weakest in the most advanced stage of chronic glomerulonephritis involving reduction of peritubular capillaries. In cardiovascular disorders, the morphofunctional characteristics of the microcirculatory bed and of its volume showed reciprocal changes, probably of a compensatory character.

Alkaline Phosphatase↗