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PubMed1996

Renal vascular lesions in the elderly: nephrosclerosis or atheromatous renal disease?

In white Europeans, renal size and function decline with age. This phenomenon has long been attributed to nephrosclerosis, i.e. primary vascular lesions associated with glomerular obsolescence, tubulointerstitial lesions and fibrosis. The part played by ageing and by pre-existing hypertension is still a matter of debate. Nephrosclerosis is a diagnosis of exclusion when no renal histology is available. As renal biopsy is rarely carried out in an elderly patient with atrophic kidneys, a long history of hypertension and only microalbuminuria or no proteinuria, the diagnosis of nephrosclerosis is generally overestimated. Even when renal histology is available, only subtle differences in vascular lesions have been claimed to distinguish those due to ageing from those due to hypertension. At any rate, meticulous control of blood pressure is certainly the most efficient means of protecting the renal vessels from further deterioration. Atheromatous renal disease has more recently been recognized as a major cause of progressive renal failure in the elderly. Renal artery stenoses due to atheromatous plaques might well be the cause of 10-15% of end-stage renal failure in whites aged > 50 and be the fourth cause of uraemia in this age group. Such stenoses are usually bilateral and developing. Present imaging methods, such as duplex ultrasound scanning and renal scintigraphy, are valuable means of diagnosis. Renal angioplasty can halt the the pace of renal insufficiency, or even durably improve it in nearly half of the cases. Finally, aorto-renal atheroma is a common and underestimated cause of cholesterol embolism. Minor, spontaneous forms thereof are indistinguishable from nephrosclerosis. Massive embolism entails a dismal prognosis, in terms of both renal function and patient survival. In conclusion, renal vascular lesions in the elderly remain a major concern. Improving non-invasive diagnostic procedures and applying preventative as well as curative measures should significantly reduce the incidence of end-stage renal disease is such patients.

Arteriosclerosis↗

PubMed2000

What is 'nephrosclerosis'? lessons from the US, Japan, and Mexico.

BACKGROUND: Selected features of 'nephrosclerosis' can be quantitated morphometrically in renal histology at autopsy. Specimens are available from Japan, Mexico, and the US (blacks and whites). METHODS: Autopsies of men and women aged 15-79 years provided renal samples for paraffin sectioning. These were assembled in New Orleans for objective evaluation after standardized staining with PAS-Alcian blue and interspersion with each other. Obsolescence of glomeruli, interstitial fibrosis, fibroplastic intimal thickenings of arteries, and arteriolar hyalinization, as operationally defined, were measured by objective morphometry. RESULTS: Obsolescence of glomeruli and interstitial fibrosis displayed the expected correlation with arterial intimal fibroplasia, but failed to confirm any direct association with arteriolar hyalinization. Some of the variation of 'nephrosclerosis', within and between populations, cannot be fully explained by microvascular defects. CONCLUSIONS: Arterial intimal fibroplasia appeared to promote 'nephrosclerosis', in the sense of fibrous replacement of atrophied nephrons, but arteriolar hyalinization did not. Hyaline deposits in arterioles may offer little or no threat to the integrity of the affected nephrons. 'Nephrosclerosis' appears to be multifactorial; it may be, in part, a consequence of fibroplasia in microscopic arteries causing ischaemic injury to scattered nephrons, but may also be a confluence of basically separate conditions, only some of which are known.

Adolescent↗

PubMed2004

Hypothesis: obesity and the insulin resistance syndrome play a major role in end-stage renal failure attributed to hypertension and labelled 'hypertensive nephrosclerosis'.

About a third of new cases of renal failure in USA are attributed to hypertension despite controversy about the frequency and pathology of so called hypertensive nephrosclerosis. In spite of good documentation that obesity causes renal failure and in spite of the global epidemic of obesity this diagnosis does not feature on most renal failure registries. New documentation that progressive renal failure in hypertension is linked to insulin resistance and analysis of NHANES III data which shows a strong positive significant dose-response relationship between insulin resistance and chronic kidney disease strengthen the view that so called hypertensive nephrosclerosis may be linked more closely to obesity and insulin resistance than to blood pressure. The pathology of the kidney in hypertension has changed. Studies 50 years ago did not show segmental glomerulosclerosis, which has recently been shown to be the key lesion in hypertensive nephrosclerosis. Recent documentation that this is a major mechanism of progression in hypertension together with the fact that similar segmental glomerulosclerosis is the key lesion in obesity and the metabolic syndrome suggests that these factors are more important than hypertension in renal failure attributed to hypertensive nephrosclerosis.

Animals↗

PubMed1996

ACE inhibition prevents and reverses L-NAME-exacerbated nephrosclerosis in spontaneously hypertensive rats.

Chronic nitric oxide inhibition exacerbates hypertension and nephrosclerosis in spontaneously hypertensive rats (SHRs). In this study, we determined whether angiotensin-converting enzyme (ACE) inhibition could prevent or reverse the systemic, renal, and glomerular hemodynamic alterations and the pathological changes of nephrosclerosis. Four groups of 20-week-old SHRs were studied: group 1, untreated controls; group 2, treated with N omega-nitro-L-arginine methyl ester (L-NAME, 50 mg/L for 3 weeks); group 3, L-NAME cotreated with quinapril (3 mg.kg-1.d-1 for 3 weeks); and group 4, L-NAME for 3 weeks followed by quinapril for 3 weeks (same doses). The results of this study demonstrated that both cotreatment (group 3) and posttreatment (group 4) with quinapril reduced mean arterial pressure (186 +/- 9 and 192 +/- 9 mm Hg, respectively, compared with group 2 SHRs, 221 +/- 5 mm Hg) and total peripheral resistance index associated with significant reductions in afferent and efferent arteriolar resistances; nephrosclerosis pathological scores; and urinary protein excretion (all at least P < .01). ACE inhibition also significantly increased stroke index, single-nephron glomerular filtration rate, and ultrafiltration coefficient compared with the L-NAME SHRs. Most notable were the findings that cotreatment with quinapril completely prevented the renal glomerular hemodynamic alterations with reduced glomerular capillary hydrostatic pressure and efferent arteriolar resistance compared with both the untreated and the L-NAME-treated SHRs (all at least P < .01). Posttreatment with quinapril also reversed the glomerular injury (subcapsular, -83%; juxtamedullary, -56%) and arteriolar (-87%) injury scores obtained from renal biopsy specimens (P < .005 and P < .0001, respectively). These changes were associated with decreased periarteriolar fibronectin and increased afferent arteriolar alpha-smooth muscle actin deposition (immunohistochemistry). These data, therefore, demonstrate that ACE inhibition not only prevents but also reverses L-NAME-exacerbated severe nephrosclerosis in SHRs, as indicated by improved systemic, renal, and glomerular hemodynamic changes, proteinuria, and histological alterations.

Analysis of Variance↗

PubMed2001

Temporary treatment of prepubescent rats with angiotensin inhibitors suppresses the development of hypertensive nephrosclerosis.

Hypertensive nephrosclerosis is a leading cause of end-stage renal disease; therefore, strategies to prevent the development of renal disease require close study. Here it is demonstrated that transient treatment of prepubescent rats with angiotensin inhibitors attenuated their susceptibility to the development of hypertensive nephrosclerosis after maturation. Stroke-prone spontaneously hypertensive Izumo strain rats were divided into four groups, treated with vehicle, the angiotensin-converting enzyme inhibitor (ACEI) delapril (40 mg/kg per d), the angiotensin receptor antagonist (AT1R-Ant) candesartan cilexetil (1 mg/kg per d), or the vasodilator hydralazine (25 mg/kg per d) from weaning to puberty (3 to 10 wk of age), and then monitored without treatment for 6 mo. BP in the ACEI- and AT1R-Ant-treated groups remained significantly decreased, compared with the untreated and hydralazine-treated groups. Moreover, marked proteinuria and nephrosclerosis developed in the untreated and hydralazine-treated groups at 30 wk but were suppressed in the ACEI- and AT1R-Ant-treated groups. Of interest, plasma renin activity, plasma angiotensin II concentrations, and renal renin mRNA levels were reduced by >50% in the ACEI- and AT1R-Ant-treated rats, suggesting that the treatments may have attenuated the development of nephrosclerosis by overcoming the susceptibility of stroke-prone spontaneously hypertensive rats to overactivation of the renin-angiotensin system.

Angiotensin II↗

PubMed2002

Proteinuria in patients with arterial/arteriolar nephrosclerosis.

UNLABELLED: Controversy exists regarding the level of proteinuria in patients with nephrosclerosis. MATERIAL AND METHODS: We retrospectively examined the clinical parameters of 67 patients with the histologic diagnosis of nephrosclerosis defined as arteriolar hyalinization and/or arterial intimal fibrosis in the absence of other findings in an adequate renal biopsy. Biopsies were performed for clinical indications and were submitted to Cedars-Sinai Pathology Department from January 1994 to March 1999. RESULTS: The mean age and blood pressure (+/- SD) was 60 +/- 17 years, and 139 +/- 19/80 +/- 12 mmHg. Mean serum creatinine was 2.3 +/- 1.3 mg/dl and 24-hour urinary protein excretion was 0.94 +/- 0.73 g, 66% had < or = 1 g/day, 25% had > 1 but < or = 2 g/day, 6% had > 2 g but < 3 g/day and 1 patient had nephrotic range proteinuria. Twelve patients had no history of hypertension. They had a mean blood pressure of 121 +/- 8/76 +/- 8. Their mean serum creatinine was 1.5 +/- 0.6 mg/dl and their mean 24-hour urinary protein excretion was 0.78 +/- 0.43 g. CONCLUSIONS: Our data do not confirm that of Innes et al. [1993] who reported proteinuria > 1.5 g/day in 40% and nephrotic syndrome in 22% of patients with nephrosclerosis; systemic hypertension may not be a prerequisite for the development of nephrosclerosis.

Adult↗

PubMed2005

The MTHFR 677TT and 677CT/1298AC genotypes in Cypriot patients may be predisposing to hypertensive nephrosclerosis and chronic renal failure.

AIM: The homozygous 677TT mutation of the MTHFR gene has been linked to deep vein thrombosis and to arterial atherosclerotic events of the coronary, carotid and peripheral arteries. Its putative association with renal arteriosclerosis and chronic renal failure (CRF) in the presence of hypertensive nephrosclerosis is yet to be investigated. METHODS: Two hundred and twenty-one Greek-Cypriot patients with CRF from one single renal unit in Cyprus were divided into 6 diagnostic categories: 49 due to chronic glomerulonephritis (22.2%), 43 due to diabetes mellitus (19.4%), 26 due to autosomal dominant polycystic kidney disease (11.8%), 30 due to essential hypertension leading to nephrosclerosis (13.6%), including 4 patients with primary malignant hypertension, 32 with other rarer causes of CRF (14.5%) and 41 of uncertain etiology (18.5%). These 221 CRF patients had their MTHFR C677T and A1298C genotypes analyzed by the polymerase chain reaction and agarose gel electrophoresis after restriction enzyme digestion. The frequency of the homozygous states 677TT and 1298CC and the double heterozygous 677CT/1298AC were compared to those of 210 unrelated normal local controls. RESULTS: A statistically significant increase in the frequency of the 677TT genotype compared to controls was only found in the hypertensive nephrosclerosis CRF sub-group of patients. The prevalence rate of the 677TT genotype was 46.7% (controls 17.6%, P=0.0007). Combined together the homozygous 677TT and the double heterozygous 677CT/1298AC genotypes were found in 86.7% of the hypertensive nephrosclerotic CRF patients, compared to 46.6% in normal controls (P=0.0001). CONCLUSIONS: The findings support the hypothesis that Caucasian patients with essential hypertension, homozygous for 677TT or doubly heterozygous for 677CT/1298AC genotypes, are predisposed to develop hypertensive nephrosclerosis and CRF.

Adolescent↗

PubMed2006

[Clinical and pathological characteristics in patients with clinically presumed hypertensive nephrosclerosis].

OBJECTIVE: To investigate the clinical and pathological characteristics of patients with clinically presumed hypertensive nephrosclerosis (HN). METHODS: Clinical data and renal biopsy results were obtained in 63 patients diagnosed clinically as HN (primary hypertension plus renal injury). RESULTS: HN was confirmed by biopsy in 47 out of 63 patients (74.6%, 12 malignant nephrosclerosis and 35 benign nephrosclerosis). Primary nephritis (PN) was diagnosed by biopsy in 10 patients (7 IgA nephropathy, 2 mesangial proliferative nephritis, 1 chronic interstitial nephritis) and focal and segmental glomerulosclerosis (FSGS) in 6 patients. Blood pressure, body mass index, GFR and blood lipids were similar among groups. HN patients were related to higher age, more frequent family history of hypertension, longer hypertension duration, higher left ventricular mass index, lower serum creatinine and lower incidence of microscopic hematuria. Most patients with malignant nephrosclerosis and FSGS patients showed grades III and IV retinopathy. CONCLUSION: Our results show that HN was misdiagnosed in nearly 25% patients in this cohort. Since the clinical features are similar between HN, PN and FSGS, renal biopsy is needed to establish the diagnosis of HN.

Adult↗

PubMed1988

Blood pressure, nephrosclerosis, and age autopsy findings from the Honolulu Heart Program.

The aspect of nephrosclerosis reflected by fibrous intimal thickening of small arteries (arteriosclerosis) was measured by a newly introduced morphometric procedure in 154 autopsies of Japanese-American men in Honolulu. These men were subjects of the Honolulu Heart Program and had previously been assessed for blood pressure and other clinical characteristics in a prospective study. In periodic acid-Schiff (PAS)-stained sections of renal cortex, measurements were made of interlobular artery diameters and intimal thicknesses. Vessels of outer diameter 80 to 130 microns and 160 to 300 microns were examined separately and are called the "remote" and "close" levels of the interlobular arteries, respectively, defined in relation to the heart. Nephrosclerosis thus quantified, together with age, could be used to predict the levels of blood pressure (BP) to be found in retrospective review of past records. The mathematical function obtained in a former study to make these predictions was found to predict the observed levels of blood pressure to an acceptable degree in the groupings that involved 92% of the subjects. Verification of that formerly obtained predictive function is now claimed. Correlation coefficients relating BP to close and remote measures were about of equal magnitude (r = 0.34 and 0.40, respectively). Subjects with cardiovascular-renal causes of death differed in both nephrosclerosis and blood pressure from subjects whose cause of death was unrelated to cardiovascular-renal diseases; the two factors taken together each contributed significantly to the cause of death difference. Correlations between nephrosclerosis and aortic atherosclerosis were stronger than could be explained solely by a linkage to observed values of blood pressure.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗

PubMed1986

Proteinuria in benign nephrosclerosis.

Benign nephrosclerosis seldom is associated with significant proteinuria or reduced renal function. This study demonstrated that, despite the finding of benign nephrosclerosis on a renal biopsy specimen, concomitant proteinuria is predictive of a poor prognosis. Twelve patients, ranging in age from 24 to 59 years, with hypertension, proteinuria (greater than 1 g/d), and findings of benign nephrosclerosis on renal biopsy specimens were studied retrospectively. In three of these patients, the hypertension and proteinuria were diagnosed during pregnancy. Follow-up was possible in 11 patients. Nine patients became nephrotic in the course of their disease. Two patients had endstage renal disease and required maintenance dialysis treatment. Seven patients had decreased renal function as shown by the increase in serum creatinine levels. Thus, the combination of hypertension, proteinuria (greater than 1 g/d), and benign nephrosclerosis may be indicative of a progressive condition with a high percentage of patients having renal failure.

Adult↗

PubMed1986

[Nosological characteristics of the morphogenesis of nephrosclerosis].

Morphology of nephrosclerosis at its early stage is characterized by nosologic specificity. Morphogenetic mechanisms of glomerulosclerosis vary greatly and depend on the specific feature of the disease pathogenesis, underlying nephrosclerosis. Stromal sclerosis of renal cortex stroma is associated with the increase in collagen-synthesizing function of interstitial fibroblasts. At the late stages of nephrosclerosis all renal tissue structures are equally affected with sclerosis, resulting in loss of nosologic specificity of the process. Arterial hypertension favours the progression of nephrosclerosis.

Adult↗

PubMed1985

[Morphological characteristics of nephrosclerosis of different etiologies].

Morphology of nephrosclerosis at the early stage of its development is characterized by its nosological specificity which is determined by qualitative alterations and by the degree of renal structural components involvement into the sclerotic process. Complex morphometric assessment allows one to reveal and make it objective the morphological differences between nosological variants of nephrosclerosis. All the structural renal components equally undergo sclerosis at the late stages of nephrosclerosis and this leads to the leveling off the nosological specificity in the majority of cases. Arterial hypertension in chronic glomerulonephritis and chronic pyelonephritis favours the progressing of the nephrosclerosis and leveling off its nosological differences.

Adult↗

PubMed1993

Clinical features of benign hypertensive nephrosclerosis at time of renal biopsy.

Although hypertension accounts for approximately 15-20% of end-stage renal disease and renal impairment occurs in 15% of patients with essential hypertension, there are few data available on the clinical features of patients with benign hypertensive nephrosclerosis, the histological consequence of hypertension on the kidney. To determine its prevalence on renal biopsy and its clinical features (including proteinuria and renal function), we used the U.K. MRC Glomerulonephritis Registry of 7339 biopsies from 20 centres to define all patients with benign hypertensive nephrosclerosis. In patients with no co-existing disease, 185 biopsies were classified solely as benign hypertensive nephrosclerosis (2.5%). Sixty-nine percent of patients were male and 72% aged over 50 years. Sixty-four percent had diastolic blood pressure above 90 mmHg and severe hypertension (diastolic > 120 mmHg) was present in 9%. Protein excretion of > 1.5 g/day was noted in 40%, with 22% excreting > 3 g/day. Eighteen percent had serum albumin values under 30 g/l. Eighty-one percent had serum creatinine > 120 mumol/l; in 51% this was > 250 mumol/l. There was significant correlation between serum creatinine and systolic blood pressure at time of biopsy (p = 0.01) and between serum creatinine and serum albumin (p = 0.001). Benign hypertensive nephrosclerosis accounts for 2.5% of all registered biopsies. Significant proteinuria is a common finding and proteinuria within the nephrotic range does occur. Systolic blood pressure appears to influence serum creatinine levels. Hypertensive nephropathy should be considered in all patients with heavy proteinuria and renal impairment.

Adult↗

PubMed1993

[Nephrosclerosis: current status].

Nephrosclerosis is the most typical and widespread renal manifestation of hypertension and can be judged as the pathological hallmark of essential hypertension. Nephrosclerosis is an important and frequent cause of progressive renal disease, however, information in the literature on the risk of developing renal failure in the course of essential hypertension is sparse. Traditionally, nephrosclerosis was thought to result from glomerular ischemia. Alternatively, glomerular sclerosis in hypertension may result from glomerular hyperperfusion or hypertension. Studies in experimental models of renal disease have identified a promising intervention with either Ca antagonists or angiotensin-converting enzyme inhibitors. Application of these therapies to patients with nephrosclerosis should await the results of careful clinical trials.

Angiotensin-Converting Enzyme Inhibitors↗

PubMed1975

The glomerular mesangium in hypertension: a morphometrical comparison of nephrosclerosis with mesangioproliferative glomerulonephritis on renal biopsies.

Glomerular changes were morphometrically studied in renal biopsies of 27 cases of nephrosclerosis showing clinically benign or malignant hypertension and of 15 cases of mild mesangioproliferative glomerulonephritis with hypertension. In nephrosclerosis, there was a mild increase in mesangial matrix without cell proliferation. The degree of the mesangial changes varied little despite a large variation in blood pressure and showed no significant difference between benign and malignant hypertension. In mild mesangioproliferative nephritis with hypertension, mesangial matrix, as well as the number of mesangial cells, showed an increase of varying degree. A quantitative assessment of the mesangium was proved effective in differentiating the glomerular changes in nephrosclerosis from those in mesangioproliferative nephritis with hypertension.

Adult↗

PubMed1976

Primary malignant nephrosclerosis.

1. As proposed by Schürmann & MacMahon (1933), we suggest that two types of malignant nephrosclerosis exist. 2. In the type called primary malignant nephrosclerosis, renal vascular lesions precede hypertension. 3. In the second type, called secondary malignant nephrosclerosis, renal vascular lesions are considered to be the consequence of malignant hypertension.

Basement Membrane↗

PubMed2002

Hypertensive nephrosclerosis in African Americans versus Caucasians.

BACKGROUND: Extensive global glomerulosclerosis (GS) has been reported in African Americans with hypertension and renal insufficiency, far exceeding that in Caucasians. To assess and compare severity and phenotype of injury in biopsied African Americans and Caucasians who morphologically had hypertensive nephrosclerosis, we performed a retrospective biopsy study. METHODS: All renal biopsies with a histological diagnosis of hypertensive nephrosclerosis from the last 11 years were identified from our clinical files. Lesions of global and segmental sclerosis, interstitial fibrosis and vascular sclerosis were semiquantitatively analyzed as percent involved, or on a 0 to 3 scale, respectively. The phenotypes of global glomerulosclerosis also were categorized as either the solidified (that is, the entire tuft is solidified) or the obsolescent type (that is, Bowman's space is occupied by collagenous material and the tuft is retracted). RESULTS: Sixty-two patients (19 African Americans, 43 Caucasians) were included in the study. At biopsy, African Americans were younger than Caucasians with higher serum creatinine, but no difference in proteinuria or mean arterial pressure (MAP). African Americans had a marked increase in the solidified form of GS (25 +/- 6 in African Americans vs. 8 +/- 2% in Caucasians, P < 0.01). This extensive solidification of glomeruli was associated with segmental sclerosis in African Americans (38 +/- 10%), contrasting low prevalence of solidified GS in Caucasians with segmental sclerosis (10 +/- 3%, P < 0.05) and in African Americans without segmental sclerosis (10 +/- 4%, P < 0.05). African Americans with segmental sclerosis were younger and clinically expressed a more severe renal disease than Caucasians with this lesion. Interstitial fibrosis was greater in African Americans than in Caucasians (54 +/- 6 vs. 33 +/- 3%, P < 0.01) and correlated with proteinuria and serum creatinine levels, especially in African Americans, and also with GS. Vascular sclerosis was worse in African Americans than in Caucasians (0.96 +/- 0.04 vs. 0.77 +/- 0.08 score, P < 0.05) and did not correlate with GS. By modeling, neither MAP nor age was useful in predicting any morphological lesions and proteinuria accounted only minimally for the variability of GS. CONCLUSIONS: Blood pressure levels and proteinuria did not account for morphological lesions, suggesting other factors (such as genetic factors, microvascular disease) may play a role. The phenotype of GS differs in biopsied African Americans versus Caucasians with hypertensive nephrosclerosis, with a marked increase in the solidified form of GS in African Americans. The association of extensive solidified GS with segmental sclerosis lesions in African Americans, but not in Caucasians, suggests different mechanisms may contribute to the development and progression of sclerosis in these two patient groups.

Adult↗

PubMed2002

Myeloperoxidase-antineutrophil cytoplasmic antibody-associated glomerulonephritis superimposed on biopsy-proven diabetic nephrosclerosis.

We present a case of myeloperoxidase-antineutrophil cytoplasmic antibody (MPO-ANCA)-associated glomerulonephritis with diabetic nephrosclerosis, diagnosed by serial renal biopsies within a short period. A 78-year-old man with renal insufficiency, who had been diagnosed with diabetic nephrosclerosis by renal biopsy 9 months earlier, was admitted to the hospital for dyspnea and rapid deterioration of renal function. The titer of serum MPO-ANCA was high, and the second renal biopsy confirmed the presence of necrotizing glomerulonephritis with crescents. Methylprednisolone pulse therapy followed by oral administration of prednisolone led to resolution of respiratory symptoms and reversal of MPO-ANCA. Renal function did not improve, however, necessitating hemodialysis. A review of the literature showed several cases of necrotizing glomerulonephritis superimposed on diabetic nephropathy but only a few reported cases of MPO-ANCA glomerulonephritis associated with diabetic nephrosclerosis. Diabetic patients who show rapid deterioration of renal function should undergo renal biopsy to determine the concomitant presence, if any, of other glomerular diseases and to prevent life-threatening systemic involvement.

Aged↗