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PubMed2001

Cytochrome c mediates apoptosis in hypertensive nephrosclerosis in Dahl/Rapp rats.

BACKGROUND: Renal damage from hypertension is the second most common cause of end-stage renal failure in the United States. The pathogenesis of this process is incompletely understood. The Dahl/Rapp salt-sensitive (S) rat is a model of low-renin hypertension, but these rats also develop renal lesions that are virtually identical to human hypertensive nephrosclerosis. METHODS: To explore apoptosis as a mechanism of progressive renal injury in S rats, age- and sex-matched S and Sprague-Dawley (SD) rats were placed on either 0.3 or 8.0% NaCl diets, which were continued for 21 days. RESULTS: At day 7, renal histology appeared relatively normal, but by day 21 on the high-salt diet, S rats displayed morphological evidence of severe renal injury that included glomerulosclerosis, arteriolosclerosis, and tubulointerstitial damage. Apoptosis was demonstrated in kidneys of hypertensive S rats by day 7. Cytoplasmic content of cytochrome c was increased in the kidney cortex of hypertensive S rats, and isolated mitochondria showed inappropriate release of cytochrome c sufficient to activate caspase-3 in vitro. Activation of caspase-9 and caspase-3 was observed only in kidney cortex from hypertensive S rats. CONCLUSIONS: Kidneys from hypertensive S rats display apoptosis related to mitochondrial release of cytochrome c and activation of caspase-9 and caspase-3. The findings support a primary role of cytochrome c release and apoptosis in the pathogenesis of hypertensive nephrosclerosis in S rats.

Animals↗

PubMed1978

[Are clotting disorders a pathogenetic factor in nephrosclerosis and hypertension? (author's transl)].

The clinical course of the haemolytic-uraemic syndrome in four patients suggests that hypertension may result from it. The morphological changes in the kidney are those of primary malignant nephrosclerosis. Hypercoagulability is thought to be an important pathogenetic factor in the development of the disease. But irreversible renal failure is not, contrary to typical primary malignant nephrosclerosis, an inevitable sequel. Abortive forms with predominant involvement of glomerular vessels have a more favourable prognosis than those forms with additional preglomerular vascular changes, in which a more or less marked impairment of renal function and hypertension persists. These forms are of particular interest because they indicate a renal pathogenetic mechanism of chronic hypertension. The described observations--taken together with those on the pathogenesis of hypertension caused by oral contraceptives--provide a pointer to the importance of clotting disorders in the initiation and development of some forms of hypertension.

Adult↗

PubMed1975

[Primary malignant nephrosclerosis (author's transl)].

Primary malignant nephrosclerosis shows a haemolytic-uraemic symptomatology and can be differentiated from secondary malignant nephrosclerosis on clinical and histological grounds. The disease was observed in 4 patients: a 25-year-old man and 3 women aged 19, 28 and 49 years. The disease is characterized by a fulminating course, malignant hypertension with progressive retinopathy, and development of progressive renal failure with subsequent irreversible anuria. In addition haemolytic anaemia or posthaemolytic states as well as consumption coagulopathy occur. In 2 cases schizozytes and in particular helmet-shaped forms could be demonstrated. On histology an obliterating necrotizing vascular change is seen which is limited to the kidneys as was demonstrated in one case by angiography. Therapeutic attempts included antibiotics, steroids, heparin, streptokinase, antihypertensive drugs, and haemodialysis. The 3 female patients died, the man survived after bilateral nephrectomy.

Acute Disease↗

PubMed2003

Clinical prognostic factors in biopsy-proven benign nephrosclerosis.

BACKGROUND: Hypertensive renal damage has become one of the most important causes of end-stage renal failure (ESRF) in Western countries. Affected patients rarely have a kidney biopsy and their diagnoses therefore remain uncertain. The objective of the present study was to examine patients suspected of renal glomerular disease, which at biopsy proved to have isolated benign nephrosclerosis. We wanted to study the effect of different clinical and laboratory variables at the time of biopsy on the short-term and long-term progression to ESRF and death. METHODS: We retrospectively examined 102 patients who were diagnosed by kidney biopsy in Norway between April 1988 and December 1990. All patients were followed by means of registries for approximately 13 years to describe renal and patient survival. RESULTS: The age of the patients at the time of biopsy was 55+/-15 years (range 15-88 years). Three years after the time of biopsy, 18% had developed ESRF and 24% had died; the corresponding numbers 13 years after biopsy were 32% and 47%. By Kaplan-Meier analyses, the following variables indicated short-term progression to ESRF: serum creatinine > or = 200 micro mol/l, systolic blood pressure > or = 160 mmHg and proteinuria > or = 1 g/24 h. In addition, patients with increased diastolic blood pressure, increased age and decreased serum albumin tended to develop ESRF more often. Long-term predictors of ESRF in Kaplan-Meier analyses were increased serum creatinine and urinary protein. Independent risk factors for progression to ESRF were increased serum creatinine and increased urinary protein. Independent risk factors for death were increased age and increased serum creatinine. CONCLUSIONS: Benign nephrosclerosis is a common condition that is associated with a high morbidity and mortality. Short-term predictors of ESRF differ from long-term predictors and this may reflect a pathophysiologically meaningful difference.

Adolescent↗

PubMed2006

Angiotensin II formation in the kidney and nephrosclerosis in Ren-2 hypertensive rats.

BACKGROUND: Ren-2 transgenic hypertensive rats develop malignant hypertensive nephrosclerosis despite low to normal plasma angiotensin II and suppressed renal renin. We tested the hypothesis that local angiotensin II formation occurs at sites of renal vascular and interstitial injury in this model. METHODS: Heterozygous Ren-2 transgenic rats were compared with normotensive Sprague-Dawley-Hannover control rats and Ren-2 transgenic rats treated with a very low dose of an angiotensin II type 1 (AT1) receptor antagonist, 1 mg/kg/day losartan, for 4 weeks. Blood pressure measurements, quantifications of urinary albumin, plasma and tissue angiotensin II as well as immunohistochemical analyses were performed. RESULTS: Systolic blood pressure was not affected by losartan during the study but intra-arterial recordings revealed a decrease of blood pressure. Losartan reduced albumin excretion, cell proliferation, macrophage influx, collagen I and collagen IV deposition. Plasma angiotensin II was decreased, while kidney tissue angiotensin II content was increased in Ren-2 transgenic rats compared with control rats. In Ren-2 transgenic rats, juxtaglomerular renin and angiotensin II staining were reduced, but there was a marked angiotensin II staining at foci of tubulo-interstitial fibrosis and at proliferative malignant vascular lesions. CONCLUSION: We conclude that local angiotensin II formation is increased in proliferative or fibrotic kidney lesions in the Ren-2 transgenic rat. Local angiotensin II formation may help to explain why the AT1 receptor antagonist prevents or ameliorates this transgenic model of malignant nephrosclerosis despite low to normal plasma angiotensin II and suppressed renal renin.

Angiotensin II↗

PubMed1996

Hydrochlorothiazide exacerbates nitric oxide-blockade nephrosclerosis with glomerular hypertension in spontaneously hypertensive rats.

OBJECTIVE: To determine whether a diuretic can also reverse the clinical, systemic, renal and glomerular haemodynamic and pathological changes caused by nephrosclerosis. METHODS: Three groups of 20-week-old spontaneously hypertensive rats (SHR) were investigated: control male SHR; a similar group, administered 50 mg/l NG-nitro-L-arginine methyl ester (L-NAME) for 3 weeks; and SHR treated similarly with L-NAME but also with 80 mg/kg per day hydrochlorothiazide (HCTZ) by gavage for 3 weeks. RESULTS: The mean arterial pressure, cardiac output, effective renal plasma flow and glomerular filtration rate decreased as urinary volume increased in the SHR treated with HCTZ and L-NAME. A micropuncture study demonstrated increased glomerular capillary pressure (PG, 56 +/- 1 versus 68 +/- 3 mmHg) associated with increased efferent (2.1 +/- 0.2 versus 2.9 +/- 0.3 u) but no change in afferent arteriolar resistances compared with the SHR group treated with L-NAME only. In addition, HCTZ administration increased the juxtamedullary glomerular injury score (47 +/- 13 versus 114 +/- 29) associated with elevated urinary protein excretion (35 +/- 1 versus 53 +/- 13 mg/100 g body weight per 24 h) The afferent arteriolar injury score was not changed. The PG elevation was related not only to severe glomerulosclerosis but also to increased fibronectin and alpha-smooth muscle actin deposition. CONCLUSION: HCTZ administration exacerbated the changes in renal and micropuncture dynamics, proteinuria and histopathological nephrosclerosis produced by L-NAME in SHR.

Animals↗

PubMed1995

Effects of novel, nonpeptide vasopressin antagonists on progressive nephrosclerosis in rats.

Effects of novel, nonpeptide vasopressin V1 and V2 receptor antagonists on partially nephrectomized and salt-loaded spontaneously hypertensive rats (SHR), which develop severe hypertension and progressive nephrosclerosis, were investigated. SHR were 5/6-nephrectomized and fed a high salt diet. The rats were divided into four groups: group 1 was an untreated control, group 2 received the V1 antagonist OPC-21268, group 3 received the V2 antagonist OPC-31260, and group 4 received both the V1 and V2 antagonists. The V1 antagonist alone or combined with the V2 antagonist significantly decreased the increase in blood pressure (BP) of groups 2 and 4 rats, but the V2 antagonist alone did not reduce the increase in BP of the group 3 rats. The V2 antagonist alone or combined with the V1 antagonist induced a significant diuresis of rats in groups 3 and 4. The increase in urinary protein excretion and the progression of renal hyaline arteriolosclerosis were attenuated by the V1 antagonist with or without the V2 antagonist in rats in groups 2 and 4, but not by the V2 antagonist alone in rats in group 3. This implies that the progressive nephrosclerosis in SHR with partial renoablation and salt-loading was associated with V1 agonism.

Animals↗

PubMed2004

Imidapril improves L-NAME-exacerbated nephrosclerosis with TGF-beta 1 inhibition in spontaneously hypertensive rats.

OBJECTIVE: This study was designed to investigate whether chronic angiotensin-converting enzyme (ACE) inhibition prevents hypertensive glomerular injury and inhibits increases in the mRNA levels and immunohistological expression of the apoptosis inducer caspase-3, and transforming growth factor (TGF)-beta 1 during prolonged nitric oxide synthase (NOS) inhibition with N-nitro-L-arginine methyl ester (L-NAME) in spontaneously hypertensive rats (SHR). METHODS AND RESULTS: For 3 weeks, we studied three groups of 20-week-old male SHR: a control group, a l-NAME group, and a group treated with L-NAME and the ACE inhibitor imidapril. L-NAME rats developed severe hypertensive nephrosclerosis with significantly elevated blood pressure, markedly increased urinary protein excretion and serum creatinine levels, and more severe glomerulosclerosis and tubulo-interstitial changes. Levels of TGF-beta 1 mRNA in the renal tissue was also significantly increased in L-NAME rats compared with control SHR. Addition of imidapril significantly lowered blood pressure, inhibited nephrosclerosis and attenuated the mRNA level of TGF-beta 1 in comparison with L-NAME/SHR. Histologically, the glomerular cell apoptosis labeling index, terminal doxynucleotidil transferase-mediated dUTP nick-end labeling of fragmented DNA (TUNEL) and active caspase-3, and TGF-beta 1 positive areas were also reduced by imidapril. CONCLUSION: These data suggest that imidapril prevents glomerular and arteriolar damages and renal functions, through inhibiting both TGF-beta 1 production and apoptosis induction.

Animals↗

PubMed2000

Induction of apoptosis during development of hypertensive nephrosclerosis.

BACKGROUND: As the biology of programmed cell death, or apoptosis, is clarified, a role for this process in the pathophysiology of organ dysfunction and fibrosis has been hypothesized. Hypertensive nephrosclerosis represents an important cause of end-stage renal disease. One model of the progressive, noninflammatory, sclerotic renal lesion of hypertension is the Dahl/Rapp salt-sensitive rat, which was examined in this study. METHODS: Male, Dahl/Rapp salt-sensitive (SS) and Sprague-Dawley rats were placed on either 0.3 or 8.0% NaCl diets for three weeks. Blood pressure was determined, and the kidneys were harvested for histochemical analysis and to obtain total RNA for RNase protection assays and total protein for Western blotting. RESULTS: An increase in apoptosis in the glomerular and tubular compartments was observed only in kidneys of SS rats on the high-salt diet. These findings occurred at a time when renal function was markedly impaired and irreversible changes in renal morphology developed. Temporally associated with this increase in apoptosis was augmented expression of pro-apoptotic molecules that included Fas, Bax, and Bcl-XS. CONCLUSIONS: The inappropriate shift in expression of proteins that facilitate apoptosis in the nephron, along with ongoing cell death that manifested at a time when renal function was deteriorating, supported an important role for this process in development of hypertensive nephrosclerosis.

Animals↗

PubMed2004

Proteinuria and hypertensive nephrosclerosis in African Americans.

Proteinuria is a known risk factor for both renal disease progression and cardiovascular morbidity and mortality in hypertensive populations. African Americans are among the highest risk groups for development of renal disease in the setting of hypertension and suffer a disproportionate burden of end-stage renal disease attributed to hypertension. Population-based studies indicate that African Americans have higher rates of albuminuria compared to non-African Americans in part due to higher rates of hypertension and diabetes in African Americans as compared to non-Hispanic whites for example. The African American Study of Kidney Disease and Hypertension (AASK) Trial was a prospective long-term clinical trial that examined the effect of aggressive blood pressure lowering versus usual blood pressure lowering in three different classes of antihypertensives on renal outcomes in approximately 1200 African Americans with hypertensive nephrosclerosis. Two thirds of trial participants had < 300 mg protein, and one third had > or = 300 mg of protein in a 24-hour urine specimen at baseline. Those with > 300 mg protein excretion compared to those with < 300 mg protein excretion at baseline had more rapid decline in renal function and ESRD events. Moreover, lower levels of proteinuria than previously thought may be important for identifying those at higher risk for kidney disease progression. The AASK cohort study, a follow-up to the trial, is now underway. The longer term follow-up will provide new insights into proteinuria and other risk factors for progression of kidney disease in hypertensive nephrosclerosis.

Black or African American↗

PubMed1998

ET(A) receptor antagonist ameliorates nephrosclerosis and left ventricular hypertrophy induced in rat by prolonged inhibition of nitric oxide synthesis.

We investigated the ability of the ETA receptor antagonist T-0115 and the angiotensin-converting enzyme (ACE) inhibitor imidapril hydrochloride to prevent hypertensive complications induced in rats by chronic inhibition of nitric oxide (NO). Male Wistar rats were given distilled water (control), NG-nitro-L-arginine methyl ester (L-NAME) 500 mg/l, or L-NAME plus imidapril 10 mg/l in the drinking water. In rats treated with L-NAME 500 mg/l plus T-0115, T-0115 was given in the food at a dose of 0.2 mg/g food or 0.6 mg/g food. We then collected 24-h urine samples at 2, 4, and 6 wk, obtained blood samples at 6 wk, and histologically examined the kidney and heart. L-NAME markedly reduced the levels of NO metabolites in serum and urine while increasing the tail-cuff blood pressure, the urinary albumin level (1.90+/-0.65 vs. 0.05+/-0.02 mg/d/100 g in control), and the area of the left ventricular wall (83.3+/-3.0 vs. 69.8+/-1.8 mm2 in control). The plasma renin activity was significantly higher in rats treated with L-NAME than in the control rats. The concomitant administration of T-0115 0.6 mg/g food with L-NAME ameliorated the tail-cuff pressure and the albuminuria (0.56+/-0.23 mg/d/100 g), although to a lesser extent than the changes seen with imidapril 10 mg/l. T-0115 0.6 mg/g food prevented left ventricular hypertrophy as effectively as imidapril 10 mg/l (70.8+/-1.8 with T-0115 vs. 68.3+/-2.7 mm2 with imidapril). Chronic inhibition of NO synthesis produced left ventricular hypertrophy and nephrosclerosis. Our results demonstrate that inhibition of the renin-angiotensin system morely effectively prevents nephrosclerosis than does the blockade of ETA receptors in a model of hypertension induced by chronic NO blockade. However, inhibition of the ET-1 pathway appeared to be as effective as ACE inhibitors in preventing left ventricular hypertrophy in this model.

Albuminuria↗

PubMed1999

Effects of angiotensin inhibitors on renal injury and angiotensin receptor expression in early hypertensive nephrosclerosis.

Angiotensin converting enzyme inhibitors (ACEI) are known to inhibit the progression of established renal failure. The aim of this study was to compare the efficacy of an ACEI and an AT1 receptor antagonist (AT1R-Ant) in preventing the development of renal disease, at an early stage of hypertensive nephrosclerosis. SHRSP/Izm rats (n = 61) were treated from 10 wk until 22 wk with the ACEI delapril (40 mg/kg/d) or the AT1R-Ant candesartan cilexetil (1 mg/kg/d). Proteinuria, and structural/ultrastructural changes were assessed at 14 and 22 wk. Treatment with either agent resulted in reductions in blood pressure and cardiovascular hypertrophy. Neither proteinuria nor major renal histological changes were evident at 14 wk. At 22 wk, however, proteinuria accompanied by nephrosclerotic changes was seen in the untreated SHRSP/Izm. Treatment with either ACEI or AT1R-Ant resulted in similar reductions in proteinuria (untreated, 32.2 +/- 7.4; delapril-treated, 5.5 +/- 1.2; candesartan-treated, 3.9 +/- 0.3 mg/100 g/d). Prominent sclerosis of small-to-medium sized renal arteries was seen in the untreated SHRSP/Izm at 22 wk, but was similarly attenuated by the ACEI and AT1R-Ant. The glomerular ultrastructure was comparable between the two groups. No significant changes in renal AT1a or AT1b receptor subtype mRNA expression were seen throughout the course of the study. In contrast, a decrease in AT2 receptor mRNA was seen in the drug-treated groups at 14 wk but not at 22 wk. These results suggest that both ACEI and AT1R-Ant have similar efficacy in attenuating the onset of renal injury in early hypertensive nephrosclerosis, and that treatment with either agent is associated with a transient decrease in AT2 receptor mRNA expression.

Angiotensin Receptor Antagonists↗

PubMed2001

Cilnidipine is as effective as benazepril for control of blood pressure and proteinuria in hypertensive patients with benign nephrosclerosis.

To investigate the beneficial effects of cilnidipine, a calcium channel blocker that shows high selectivity for N-type receptors, on the progression of chronic renal insufficiency, we compared the efficacy of cilnidipine to that of benazepril, an angiotensin-converting enzyme (ACE) inhibitor with known renal protective effects, in a one-year trial evaluating hypertensive control, serum creatinine, and albuminuria in a cohort of patients. Given the seeming importance of the etiology of chronic renal insufficiency in determining drug efficacy, we limited our study to 20 patients with a single common condition, benign nephrosclerosis. The average age of the patients was 62+/-4 years old. The changes in systolic and diastolic blood pressure over the course of the study year revealed a similar reduction with cilnidipine and benazepril. Both cilnidipine and benazepril induced similar reductions in systolic and diastolic blood pressure over the course of the study year. The baseline levels of serum creatinine were 1.40+/-0.2 mg/dl and urinary excretion of albumin was 168+/-10 mg daily. The levels of serum creatinine were not significantly changed throughout the study in either group, although the levels of urinary excretion of albumin were significantly decreased in both groups. There were no significant differences in either of these values between the two groups. In conclusion, both cilnidipine and benazepril equally and effectively reduced blood pressure and albuminuria in hypertensive patients with benign nephrosclerosis in a one-year trial.

Albuminuria↗

PubMed1978

An accelerated hypertension with neither malignant nephrosclerosis nor elevation of plasma renin activity.

A case of accelerated hypertension, which was unique in a resistance to an angiotensin antagonist, and a lack of the elevation of plasma renin activity (PRA) is reported. Non-elevated PRA was coincided with non-malignant nephrosclerosis in renal histology. The acceleration was attributed to the neurological cause i.e., cerebral hemorrhage in the right hypothalamus which extended to the ventricle and subarachnoid space. The case therefore clinically seemed malignant-like, but it was not malignant hypertension in the sense of Volhard's classical definition. This does not conflict with the usefulness of the determination of PRA in the diagnosis of malignant hypertension with nephrosclerosis.

Aged↗

PubMed1978

Pathology of malignant nephrosclerosis with special reference to the difference between histologic manifestations of pure and exacerbated forms.

Fourteen autopsied cases of malignant nephrosclerosis were classified into 6 of pure form in which syndrome of malignant hypertension developed from the beginning of the disease, and 8 of exacerbated form with appearance of the syndrome in the course of essential hypertension. Pathohistological study of these cases elucidated the differences in histologic manifestations between pure and exacerbated forms of malignant nephrosclerosis as to which little had been known as yet. In the pure form arterioles and small arteries characteristically demonstrated acute or recent lesions such as fibrinoid necrosis and hemorrhage into intima, and intimal cellular hyperplasia of somewhat longer duration, whereas in the exacerbated form coexistence of vascular lesions of various intensities and durations, acute (fibrinoid necrosis and hemorrhage), intermediate (intimal cellular hyperplasia) to chronic (sclerosis and lamellar elastosis), and superposition of more recent vascular lesions on more advanced or older ones were noted. Superposition of vascular alterations was interpreted to be not necessarily specific for exacerbated form but histologic manifestation of recurrence which is liable to be the case more frequently in exacerbated form than in pure form in the longer course of essential hypertension or of malignant hypertension. Some other related problems were also considered and discussed.

Adult↗

PubMed1991

Reversible renal insufficiency due to angiotensin converting enzyme inhibitors in hypertensive nephrosclerosis.

OBJECTIVE: To review the incidence of reversible renal insufficiency in patients with hypertensive nephrosclerosis undergoing antihypertensive therapy. DESIGN: Retrospective analysis of 73 patients in a long-term blood pressure control study that compared the effects of an angiotensin converting enzyme (ACE) inhibitor plus conventional antihypertensive agents compared with placebo plus antihypertensive agents. SETTING: Hospital-based outpatient treatment center. INTERVENTIONS: Patients were divided into group 1, which received enalapril plus conventional antihypertensives, and group 2, which received placebo plus conventional antihypertensives. MEASUREMENTS: Blood pressure and serum creatinine levels were measured, and imaging studies of the main renal arteries were done. MAIN RESULTS: In group 1, eight of 42 patients (19%, 95% CI, 9% to 34%) developed reversible renal insufficiency, defined as an unexpected increase in serum creatinine of 88 mumol/L or higher. Six episodes of reversible renal insufficiency occurred during July and August when temperatures were 32.2 degrees C to 37.8 degrees C (90 degrees F to 100 degrees F). Renal artery stenosis was excluded by renal arteriogram or ultrasonic duplex scanning. All eight group-1 patients had a significant decrease in mean arterial pressure below their baseline level during reversible renal insufficiency (mean change, -28 +/- 10 mm Hg, P less than 0.001). The increase in the serum creatinine level was inversely correlated with the decrease in the mean arterial pressure (r = -0.68, P less than 0.01). Reversible renal insufficiency was successfully managed by withdrawing or reducing enalapril as well as other antihypertensive agents. Subsequently, enalapril was tolerated by seven of the eight patients without recurrence of renal insufficiency. In contrast, none of 31 (CI, 0% to 11%) patients in group 2 developed reversible renal insufficiency despite the fact that both the incidence of decreases in mean arterial pressure in 6 of 31 patients (19%) and the magnitude of the decreases in mean arterial pressure (mean change, -33 +/- 16 mm Hg) were similar to those observed in group 1. CONCLUSIONS: Reversible renal insufficiency in hypertensive nephrosclerosis associated with ACE inhibitor therapy correlates with relative hypotension, is not dependent on renal artery stenosis, and can usually be managed by dose reduction.

Aged↗

PubMed2002

[Effect of astragalus-angelica mixture on osteopontin expression in rats with chronic nephrosclerosis].

OBJECTIVE: To observe the effect of Astragalus-Angelica Mixture (AAM) on osteopontin (OPN) expression in rats with chronic nephrosclerosis. METHODS: Chronic nephrosclerosis model rats induced by repeated intraperitoneal injection of puromycin were randomly divided into the model group, AAM group and Irbesartan (an antagonist of angiotensin) group. The experimental course lasted 12 weeks. Blood and urine samples were examined by biochemical method. Kidney tissue was taken for pathological stain and immunohistochemical method and was applied to examine OPN expression, mononuclear macrophage, laminin in extracellular matrix and decorin expressions. RESULTS: AAM showed the effects of decreasing urinary protein and improving renal function similar to that of Irbesartan. It also could alleviate the pathological damage of kidney tissue, especially in decreasing renal tubular mesenchymal damage index. The accumulation of decorin and laminin in the mesenchymal extracellular matrix significantly decreased. Renal tubular OPN expression and mesenchymal infiltration of mononuclear macrophage decreased significantly and in a positive correlated manner (r = 0.885, P < 0.01). CONCLUSION: AAM has similar renal protective action to that of Irbesartan, this action may be related to the inhibition of up-regulated OPN expression.

Angelica sinensis↗

PubMed1991

Blood pressure and nephrosclerosis in black and white men and women aged 25 to 54.

Kidney samples obtained at autopsy were evaluated for nephrosclerosis by quantitatively measuring the severity of intimal fibroplasia in the interlobular arteries and counting the number of hyalinized arterioles. Most cases were obtained from the coroner and had violent causes of death; subjects with cardiovascular diseases were excluded. Blood pressures in Health Survey data were obtained from published sources. Measures of nephrosclerosis in 365 black and white men and women in age groups 25 to 34, 35 to 44, and 45 to 54 yr were examined by three-way Analysis of Variance (ANOVA). Blacks exceeded whites in fibroplasia at all ages and in both sexes; this excess was paralleled by mean blood pressure in all comparisons. White women were not different from white men in fibroplasia; black women significantly exceeded black men at all ages. Women had lower blood pressures than men when matched for age, race, and fibroplasia; the average magnitude of this difference was 5.5 mm Hg. Since women are known to have as much hypertensive disease as men after age 50 yr, it seems possible that the arterial fibroplasia seen in young women may represent progression toward the hypertensive state, even through blood pressure does not reveal the equality of the sexes in this respect until after menopause. Hence, in women arterial fibroplasia is seen to precede a later rise in blood pressure. Arteriolar hyalinization was greater in men than in women but did not differ significantly between races. Hyalinization did not consistently follow blood pressure in comparisons between subgroups of subjects.

Adult↗