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PubMed2000

Monocyte chemoattractant protein-1 and macrophage infiltration in hypertensive kidney injury.

BACKGROUND: We investigated whether monocyte chemoattractant protein-1 (MCP-1) is expressed in hypertensive nephrosclerosis, and tested the effect of angiotensin II type 1 receptor blockade on MCP-1 expression and macrophage (MPhi) infiltration. METHODS: Rats with two-kidney, one-clip (2K1C) hypertension with and without treatment with the angiotensin II type 1 receptor antagonist valsartan (3 mg/kg/day) were studied. In these animals as well as in spontaneously hypertensive rats (SHR), stroke-prone SHR (SHR-SP), hypertensive mRen-2 transgenic rats (TGR), and respective control strains, MCP-1 expression in the kidney was investigated by Northern and Western blots and by immunohistochemistry. Glomerular and interstitial MPhis were counted. RESULTS: In the nonclipped kidney of 2K1C rats, MCP-1 expression was elevated at 14 and 28 days when significant MPhi infiltration was present. MCP-1 was localized to glomerular endothelial and epithelial cells, interstitial and tubular cells, MPhis, and vascular smooth muscle cells. A similar pattern of MCP-1 staining was present in TGR kidneys, whereas MCP-1 expression was not increased in SHR and SHR-SP. Valsartan reduced but did not normalize blood pressure, blocked the induction of MCP-1 protein in 2K1C kidneys, and decreased interstitial MPhi infiltration significantly. CONCLUSION: MCP-1 expression is increased in angiotensin II-dependent models of hypertensive nephrosclerosis and is temporally and spatially related to MPhi infiltration. The angiotensin II type 1 receptor mediates the induction of MCP-1.

Angiotensin Receptor Antagonists↗

PubMed1980

[Asymptomatic haematuria (author's transl)].

Mesangioproliferative glomerulonephritis of varying severity was found by renal biopsy in 86.2% among 130 patients with asymptomatic haematuria. 3.2% had benign nephrosclerosis, 3.2% had benign nephrosclerosis, 1.6% had interstitial nephritis and one patient showed a previously undiagnosed perimembranous glomerulonephritis. Normal renal parenchyma was observed in only 6.9% of cases. Iummunohistological findings were positive in 25.7% of investigated cases. The majority were IgA deposits combined with IgG and C3 complement. The intensity of haematuria is not correlated with the type and severity of histological changes. "Physiological" haematuria (erythrocytes less than 7/ml) which is usually considered normal must be re-evaluated as a consequence of these histological findings. After exclusion of urological or extrarenal disease only histological investigation of the kidneys will bring the final diagnosis. Repeated radiographical or urological investigations can thus be avoided. The risks of percutaneous renal biopsy under fluoroscopic or sonographic control are decidedly less than the information gained from histological evaluation. The different histological findings indicate that isolated haematuria should be considered only as a symptom and not as a uniform disease indicating focal nephritis.

Adolescent↗

PubMed2006

Elevated serum creatinine and a normal urinalysis: a short differential diagnosis in the etiology of renal failure.

OBJECTIVE: The diagnosis of renal failure with a normal urinalysis represents a short differential diagnosis that has not been characterized in the literature. This study was designed to identify the specific disease states that encompass this interesting renal condition. MATERIAL: The Regenstrief database, which is an electronic medical record containing inpatient laboratory and other clinical data for patients admitted to Wishard Memorial Hospital, was utilized to provide data for this study. METHODS: The database was culled to provide data for hospitalized patients admitted between March 1, 1992, and March 1, 2001, with the concurrent findings of a serum creatinine greater than or equal to 2 mg/dL, a normal urinalysis, and diagnoses of obstructive uropathy, multiple myeloma, prerenal azotemia, hypertensive nephrosclerosis, interstitial nephritis, renal vascular disease, hypokalemic nephropathy, and hypercalcemia, as identified by their corresponding ICD-9 codes. RESULTS: A search of the Regenstrief database yielded a total of 190,343 patient admissions. There were 515 patient admissions with renal failure and a concurrent normal urinalysis. The largest specific diagnostic categories within this group were hypertension and prerenal azotemia. CONCLUSIONS: An elevated serum creatinine and normal urinalysis present a short differential for the etiologies of renal failure and include such entities as hypertensive nephrosclerosis, prerenal azotemia, obstructive nephropathy, interstitial nephritis, renal vascular disease, and various electrolyte abnormalities. An awareness of these specific disease states may lead to an earlier diagnosis and more effective treatment of renal failure.

Creatinine↗

PubMed2006

Transient improvement of hypertension-induced chronic renal failure with mycophenolate mofetil treatment.

A young female with essential hypertension developed progressive azotemia; renal biopsy showed hypertensive nephrosclerosis with considerable tubulointerstitial disease and cellular infiltration. The addition of mycophenolate mofetil (MMF) to her antihypertensive treatment resulted in a dramatic improvement of renal function during the following three months. When the patient discontinued MMF treatment, end-stage renal failure rapidly developed. This patient represents the first report of the beneficial use of MMF in non-immune chronic renal disease and demonstrates that significant functional improvement may be obtained with the addition of MMF to the treatment of hypertensive nephrosclerosis for patients in whom there is significant tubulointerstitial inflammatory infiltration.

Adult↗

PubMed1989

Pseudo renal artery stenosis (PRAS) syndrome.

During the course of a long-term, prospective, randomized study in 77 hypertensive nephrosclerosis patients, five patients developed evidence suggestive of renal artery stenosis. However, arteriography demonstrated patent renal arteries. The evidence suggestive of renal artery stenosis was: (1) converting-enzyme inhibitor (CEI)-induced renal dysfunction including marked and reversible increases in serum creatinine and urea concentrations, (2) minoxidil-induced hyperreninemia despite beta-adrenoceptor blockade and volume expansion, and (3) minoxidil-induced salt and water retention with diuretic resistant edema. Thus, the renal dysfunction induced by CEI in these patients with patent renal arteries is similar to the alterations occurring in patients having bilateral renal artery stenosis. The diuretic resistant edema and the beta-adrenoceptor blocker resistant high renin release are also functional alterations of renal artery stenosis. We suspect that the long-standing and usually severe hypertension in these patients has caused sufficient arteriolar hypertrophy or sclerosis to interfere with renal blood flow and to induce these functional lesions of renal artery stenosis. With widespread use of the new CEI agents in patients with renal disease, this syndrome suggestive of renal artery stenosis may be encountered in as many as 10% of hypertensive nephrosclerosis patients during long-term treatment with converting-enzyme inhibitors.

Angiography↗

PubMed1982

Analysis of interracial variation in kidney transplant and patient survival.

Negro recipients appear to have essentially the same graft and patient survival rates as Caucasian recipients after accounting for the center effect. Cadaver kidneys from Negro donors yielded very slightly lower survival rates than kidneys from Caucasian donors after correction for the center effect. It appears that centers with poor results may have influenced the conclusions from earlier data regarding Negro donors. Transplants into Oriental recipients either from related donors or from Caucasian cadaver donors result in transplant outcomes that are comparable to the outcomes in Caucasian recipients. Most interesting is the comparable survival rate from Caucasian donors into either Caucasian recipients or Oriental recipients, despite a considerable difference in histocompatibility antigen frequencies between these races. Both Caucasian and Negro patients with nephrosclerosis have graft and patient survival rates that are comparable to patients of the same race without nephrosclerosis. The transfusion effect is noted in both Caucasian and Negro recipients. Comparable proportions receive similar numbers of transfusions in each race.

Black People↗

PubMed2001

Oxidative stress and renal dysfunction in salt-sensitive hypertension.

Hypertension is a risk factor for the development of end-stage renal disease. The mechanisms underlying hypertensive nephropathy are poorly understood. There is evidence, however, that in hypertension there is an accumulation of partially reduced oxygen and its derivatives, known collectively as reactive oxygen species, which may contribute to progressive renal dysfunction. In the present study, we assess the contribution of oxidative stress in the development of salt-dependent hypertensive nephrosclerosis. Going beyond previous end point studies, which inferred renal function either indirectly or only qualitatively, we have determined oxidative stress concurrently with direct and quantitative measurements of renal function (via inulin and p-aminohippuric acid clearances). Moreover, in this time-dependent study, the measurements have been taken under low- as well as high-salt diets. As was expected from previous studies, in the Dahl salt-sensitive rat, a high-salt diet (8% NaCl) resulted in the development of hypertension, in a decreased glomerular filtration rate, and in a decreased renal plasma flow as compared with the normotensive control, the Dahl salt-resistant rat. In addition, however, we found clear evidence for the accumulation of reactive oxygen species in renal tissue homogenates of Dahl salt-sensitive rats on the high-salt diet. Our time-dependent protocol also indicated that renal oxidative stress follows, in time, the development of hypertension. We also found that after 2 weeks of increased salt loading, Dahl salt-sensitive rats excreted less cyclic guanosine monophosphate and NO(x) than Dahl salt-resistant rats on the same diet. It is known that urinary cyclic guanosine monophosphate and NO(x) represent the activity and stable derivatives of renal NO., respectively, and that they closely correlate with renal vascular resistance. Therefore, our results suggest that, in the Dahl salt-sensitive rat, increased oxidative stress is associated with salt-dependent hypertensive nephrosclerosis and that decreased NO. bioavailability may represent a common factor responsible for the vascular and glomerular dysfunction.

Animals↗

PubMed1978

Renal lesions in chronic pancreatitis.

Many patients with chronic pancreatitis (CP), even in the absence of intrinsic renal disease, are found to have abnormal urine, with persistent proteinuria, cylindruria, microhematuria and leukocyturia. The kidneys of 12 necropsy cases with CP showed mild to moderate arterial and arteriolar nephrosclerosis and no other significant changes. Renal biopsies were performed in 10 patients with CP without evidence of systemic disease or intrinsic renal disease, but with persistent urinary abnormalities. By light microscopy, mild arterial and arteriolar nephrosclerosis was present in 5 instances. In 1 patient, evidence of the reparative phase of acute tubular necrosis was noted. In 5 biopsies, electron microscopy revealed minimal to mild increase in mesangial matrix. Mild thickening of the glomerular basement membrane (GBM) was found in three instances but there was no clear-cut evidence of diabetic glomerulosclerosis. The presence of subendothelial electron-lucent material in 3 cases suggests the possibility of previous subclinical episodes of intravascular coagulation. The most consistent finding was the presence of lipid material in the cytoplasm of glomerular and tubular cells. The renal lesions associated with CP are mild, nonspecific and nonprogressive. Various pathogenetic factors can be invoked to account for their presence and for the urinary abnormalities found in patients with CP.

Adolescent↗

PubMed1979

The role of the interstitium of the renal cortex in renal disease.

Morphometrical investigations (point-counting method) showed that in different inflammatory (endocapillary -- acute -- GN, mesangioproliferative GN, membranoproliferative GN) glomerulonephritides and in non-inflammatory glomerular diseases (perireticular amyloidosis), there are statistically significant correlation between serum creatine concentrations at the time of biopsy and the enlargement of the cortical interstitium by fibrosis. Similar results were obtained in investigating different grades of benign nephrosclerosis with transition into secondary malignant nephrosclerosis conditioned by hypertension and in chronic diffuse sclerosing interstitial nephritides of different etiologies. As hypothesis, we assume that a narrowing of the postglomerular vessel network by interstitial fibrosis take place. This could lead to an increase resistance of the renal cortical blood flow. In spite of an elevated effective filtration pressure, the slowing of the glomerular blood flow may lead to the reduction of GRF and to an increase of the serum creatinine concentration. Additionally, in the case of interstitial fibrosis the tubules look atrophied. This could be the consequence of the reduced GFR as a sign of inactivity. On the other hand, tubular atrophy could result from malnutrition in the case of interstitial fibrosis. The resorptive capacity of these atrophied-looking tubules could be lowered and the GFR could be diminished by the so-called Thurau mechanism.

Amyloidosis↗

PubMed1995

Transforming growth factor-beta 1 expression and phenotypic modulation in the kidney of hypertensive rats.

We have previously reported that renal mRNA levels for transforming growth factor-beta 1, fibronectin, and collagens were increased in 32-week-old stroke-prone spontaneously hypertensive rats (SHRSP) with severe nephrosclerosis. To elucidate the mechanism of hypertension-induced nephrosclerosis, we examined gene expression and localization of transforming growth factor-beta 1 and cellular phenotype in the kidney of 25-week-old SHRSP with moderate renal damage. Renal mRNA was measured by Northern blot analysis. The localization of transforming growth factor-beta 1 and cellular phenotype was determined by immunohistochemistry. In the kidney of 25-week-old SHRSP, renal transforming growth factor-beta 1 mRNA was elevated compared with Wistar-Kyoto rats (WKY), whereas renal collagen mRNAs of SHRSP were not increased. Immunoreactive transforming growth factor-beta 1 in SHRSP was mainly localized in glomerular cells. Furthermore, alpha-smooth muscle actin and desmin were significantly expressed in SHRSP glomerular cells, in contrast to negligible expression of these proteins in WKY. alpha-Smooth muscle actin staining was also observed in interstitial cells, and vimentin, another phenotypic marker, was expressed in atrophic tubular cells of SHRSP, despite no staining of these proteins in WKY. Furthermore, all these phenotypic changes in SHRSP were associated with increased cell proliferation, as shown by the increased number of proliferating cell nuclear antigen-positive cells. Treatment of SHRSP with cilazapril and nifedipine (from the age of 13 to 25 weeks) prevented the increase in transforming growth factor-beta 1 expression and the cellular phenotypic modulation and was accompanied by a reduction of urinary albumin excretion and inhibition of cell proliferation.(ABSTRACT TRUNCATED AT 250 WORDS)

Actins↗

PubMed1976

Protective effect of digitoxin in adrenal-compression hypertension.

Bilateral compression of the adrenal glands combined in mononephrectomy and followed by the imposition of a high NaC1 intake resulted in severe hypertension in all rats so treated. It was accompanied by enlargement of the heart, kidneys, and adrenal glands, atrophy of the thymus, and the occurrence of severe nephrosclerosis. Digitoxin treatment delayed the onset, reduced the incidence, and ameliorated the magnitude of the hypertensive response in such animals; it also reduced the degree of cardiac hypertrophy and the severity of nephrosclerosis and completely prevented enlargement of the adrenals and kidneys and atrophy of the thymus.

Adrenal Glands↗

PubMed1978

Renal vasculature in essential hypertension: racial differences.

In an attempt to explain the greater morbidity from essential hypertension in the black as compared with the white race, we evaluated the intrarenal vasculature of 27 patients with hypertension (19 white and 8 black). All patients had mild-to-moderate hypertension (mean arterial pressure, 110 to 125 mm Hg), normal renal function, and minimal target-organ damage. All patients had selective renal angiograms, which were evaluated for arterial nephrosclerosis. Additionally, renal blood flow was estimated by the clearance of para-aminohippurate. Patient age, blood pressure, and plasma renin activity did not differ between the two races. Black hypertensives had significantly (P less 0.01) more severe nephrosclerosis than the white patients. Renal blood flow was lower (P less than 0.05) in black patients (390 +/- 35 ml/min - m2 body surface area) than white patients (473 +/- 19 ml/min - m2 body surface area). These findings may help to explain racial differences in morbidity and mortality from essential hypertension.

Adult↗

PubMed2002

[Arterial hypertension and renal vascular disease: nephroangiosclerosis].

Nephroangiosclerosis and nephrosclerosis are terms used to define the renal disease induced by essential hypertension. The predominant histologic changes occur in the preglomerular microvasculature. Epidemiological data about the risk of hypertensive patients from developing renal failure offer conflicting results. Nevertheless, renal vascular disease, including nephroangiosclerosis and/or ischemic nephropathy, appears to be an important cause of end-stage renal disease. Presumably, nephrosclerosis is the renal expression of systemic atherosclerosis: male sex, age > 55-60 years, black race, high serum cholesterol and/or uric acid levels, and coronary heart disease, peripheral artery disease, and/or cerebrovascular disease are common associations with the renal alteration. Treatment strategy should include an intensive blood pressure control, probably below 130/80 mmHg, together with antiplatelet and lipid-lowering agents when necessary. Although specific studies are lacking, ACE inhibitors and angiotensin II antagonists may offer additional benefits in slowing the renal disease progression.

Humans↗

PubMed2002

[Prevention of hypertensive renal damage by prepubertal treatment with ARB].

Epidemiological data have suggested that the incidence of hypertensive nephrosclerosis is increasing despite the development of newer drug treatments. Recently, we studied the effects of temporary treatment of prepubescent rats with angiotensin receptor blocker (ARB) on the development of hypertensive nephrosclerosis in later life. Studies were performed using stroke-prone spontaneously hypertensive rats(SHRSP) and Dahl salt-sensitive rats(Dahl-S). In the case of SHRSP, treatment with ARB or angiotensin converting enzyme inhibitor(ACEI) from weaning to puberty(3 to 10 weeks) resulted in a continued reduction of blood pressure, and attenuation of proteinuria and renal histological changes at 30 weeks. In the case of Dahl-S, the prepubertal treatment with ARB caused a partial, but statistically significant reduction in proteinuria and renal damage. These results may be relevant for understanding the mechanisms of development of hypertension and hypertensive renal damage in these animal models.

Angiotensin Receptor Antagonists↗

PubMedDate not supplied

[X-ray control of the kidneys and their development in the long-term period after surgical correction of hydronephrosis in children].

After surgical correction of hydronephrosis, the development of the kidneys was studied in 40 patients (44 hydronephroses) operated on at the age of 8 months to 12 years. Postoperative follow-ups lasted at least 10 and 25 years. X-ray planimetric studies made it possible to quantitatively characterize the growth of the kidney, the increase or decrease in its parenchymal area, the appearance or progression of prior nephrosclerosis. X-ray studies could yield an objective assessment of the trend in renal development. By supplementing the data of excretory urography, radiological techniques and ultrasonography provided additional data on the kidney and its parenchyma. Analysis of the results of the X-ray planimetric studies have indicated that 28 patients (32 kidneys) had a uniform increase in the areas of the kidney and its parenchyma by 50-100%; in 9 patients, the parenchyma increased by 2.5-4 times, the area of the kidney became only 50-100% larger. There was progression of nephrosclerosis with a 3-10% decrease in the area of parenchyma along with a 24-80% growth of the organ only in 3 cases after a quite satisfactory growth in the organ. These data show it necessary to perform long-term follow-ups of patients under the control of X-ray study as the most objective radiation diagnostic technique.

Adolescent↗

PubMed2005

[Pathogenesis of renal failure in hypertension. The role of genetic factors, low weight at birth and endothelial dysfunction].

Nephrosclerosis is usually diagnosed in patients with essential hypertension with no or mild proteinuria and no urinary abnormalities. Microalbuminuria is considered to be a marker of high risk for progressive renal disease in patients with diabetes mellitus but there is still no solid evidences that this alteration entails an adverse renal prognosis in essential hypertension. Independently of hypertension, nephrosclerosis is associated with endothelial dysfunction and evidence is accruing that genetic factors and a low number of nephrons at birth are important determinants of this disease.

Endothelium, Vascular↗

PubMed1992

Cardiovascular causes of death at Tshepong Hospital in 1 year, 1989-1990. A necropsy study.

Cardiovascular disease is the third most common cause of death in Tshepong Hospital in the western Transvaal, and the most common cause of death in patients older than 35 years. A prospective study was undertaken which included limited necropsies in 90 of the 167 cardiovascular disease deaths over 1 year. A reliable mortality pattern for cardiovascular deaths is described. Additionally, attention is paid to co-existing conditions. Conditions relating to cardiovascular disease, such as hypertension, benign hypertensive nephrosclerosis, atherosclerosis and obesity, were also evaluated. Cerebrovascular conditions were found in 32% of cardiovascular deaths. Intracerebral haemorrhage was found in 50% and cerebral infarction in 29% of cases. Fifty-seven per cent of cardiovascular deaths were due to cardiac conditions, the most common being pulmonary hypertension (31%), dilated cardiomyopathy and chronic rheumatic valvular disease (17% each) and hypertensive heart disease (14%). Forty-nine per cent of subjects were hypertensive, while 40% exhibited benign nephrosclerosis and only 3% of the examined vessels had signs of severe atherosclerosis. Tuberculosis was present in 13% of cases. The clinical diagnosis was the same as the final necropsy diagnosis in 38% of cases. These results emphasise the importance of performing necropsies to obtain reliable mortality statistics.

Adolescent↗

PubMed1988

Late somatic effects in mice after total lymphoid irradiation.

Late somatic effects of total lymphoid irradiation have been investigated in BC3F1 mice. A total X-ray dose of 34 Gy was distributed in 17 daily fractions. The cumulative mortality curve is shifted in time because all the irradiated mice died earlier than the unirradiated controls. There was a 24% shortening of life span. A marked increase of solid tumor incidence, mostly due to skin cancers, was observed (66% vs 30%). In contrast, the incidence of malignant lymphomas was greatly reduced in irradiated mice (6% vs 49%). Furthermore, nephrosclerosis was a common finding in the irradiated group (38% vs 8%). Death-rate analysis revealed an association between life shortening and the presence of solid tumors and nephrosclerosis at death.

Animals↗