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At least 505 records · Page 28Linked to original sources

PubMed1997

Rapid-onset diabetic nephropathy in type II diabetes mellitus.

We report a case of rapidly progressive diabetic nephropathy, from little diabetic change on renal biopsy to severe, nodular, diabetic nephrosclerosis over 32 months. The patient was taking an angiotensin converting enzyme inhibitor and had a mean arterial pressure of 95 mm Hg over this time period. Her dietary protein intake was low, at least upon presentation. She had three additional mechanisms or potential mechanisms of injury: monoclonal kappa light chains; IgA immune deposits on the first, but not the second biopsy; and longstanding hypertension. Her renal histology was typical for diabetic nephropathy but was not characteristic of kappa light chain disease. We suggest that diabetic nephropathy may develop more rapidly than previously assumed, especially when additional mechanisms of injury, or additional promoters of mesangial matrix accumulation are present.

Aged↗

PubMed1997

Effects of quinapril hydrochloride in patients with essential hypertension and impaired renal function.

The short-term effects of administration of an angiotensin-converting enzyme (ACE) inhibitor, quinapril hydrochloride (quinapril) (5-10 mg/day), for 12 weeks on blood pressure and renal function were evaluated in 8 patients (60.5 +/- 7.3 years old, mean +/- SD) with mild to moderate essential hypertension and mild impairment of renal function due to nephrosclerosis. Systolic blood pressure and diastolic blood pressure were significantly reduced from 163.0 +/- 4.0 to 132.3 +/- 17.6 mmHg (p < 0.01) and from 98.3 +/- 4.6 to 81.5 +/- 6.4 mmHg (p < 0.001), respectively, before to after treatment. Both renal plasma flow (RPF) and glomerular filtration rate (GFR) were significantly increased in all patients, from 203.9 +/- 33.3 to 245.4 +/- 36.7 ml/min/1.73 m2 (p < 0.01), and from 43.4 +/- 6.4 to 53.5 +/- 4.6 ml/min/1.73 m2 (p < 0.05), respectively. Short-term quinapril administration was beneficial to renal function in patients with essential hypertension and impaired renal function.

Aged↗

PubMed1980

Serum uric acid in essential hypertension: an indicator of renal vascular involvement.

We measured glomerular filtration rate, renal and systemic hemodynamics, and intravascular volume in normotensive subjects and in borderline and established essential hypertensive patients classified according to serum uric acid level. Renal blood flow was lower and renal vascular and total peripheral resistances were increased in patients with high uric acid levels (p < 0.02). Serum uric acid concentration correlated inversely with renal blood flow/m2 body surface area (r = -0.45, p < 0.001) and directly with renal vascular (r = 0.41, p < 0.001) and total (r = 0.38, p < 0.001) resistance. Cardiac output, heart rate, and intravascular volume as well as glomerular filtration rate showed no uric-acid-department pattern. Mild asymptomatic hyperuricemia, therefore, was associated with decreased renal blood flow without affecting glomerular filtration rate. Increased renal vascular and total peripheral resistances reflecting renal and systemic hypertensive vascular disease paralleled the rising serum uric acid levels. These data suggest that heretofore unexplained hyperuricemia in patients with essential hypertension most likely reflects early renal vascular involvement, specially, nephrosclerosis.

Adult↗

PubMed1975

Renal microvasculature in chronic renal failure.

The renal microvasculature was examined stereoscopically after intraarterial injection of silicone rubber. Specimens studied were: 29 cases of normal kidney, 4 cases of sclerotic kidney, 10 cases of acute renal failure, and 10 cases of chronic renal failure from the final stage of chronic glomerulonephritis, malignant nephrosclerosis, diabetic nephropathy, and cortical necrosis. The following were common evidences for chronic renal failure: much reduction and wide deficiencies of filling in the cortex, increased filling of vasa recta, narrowing and spiralling of interlobular arteries and cortical afferent arterioles, appearance of giant glomeruli, rarefaction of the peritubular capillary plexus, and relative preservation of glomeruli in the juxtamedullary zone and vasa recta in the medulla may be the major pathway, after the interlobular arteries and afferent arterioles in the subcapsular cortex are destroyed, and these vascular architectural changes may be intimately related to the pathophysiology of chronic renal failure.

Adult↗

PubMedDate not supplied

Continuing follow-up of malignant hypertension.

The history of accelerated (malignant) hypertension is reviewed, and unsolved problems related to the disease are illustrated, including its relationship to malignant nephrosclerosis, as well as terminology, current frequency and treatment. Over the past 25 years, out of a series of 131 patients, 53 were classified as suffering from essential malignant hypertension, the only suitable model on which the effects of pharmacological treatment on the disease can correctly be evaluated. In 2000, there were 24 survivors in our series and the maximum follow-up was 290 months. Multiple daily B.P. self-measurements allowed us to establish that pharmacological treatment was only able to approximate, to a varying degree, the conventional threshold of 140/90. Yet, despite this incomplete control over blood pressure levels, renal function was maintained in those patients whose initial creatininemia levels had not been higher than 2 mg/L. The renal protection effect of treatment was preserved even in patients who relapsed intoaccelerated disease phase one or more times over the study period.

Adult↗

PubMedDate not supplied

[Nephropathy associated with arterial hypertension: genes and Barker's hypothesis].

For about three decades glomerular diseases have been the most intensively investigated research area in nephrology. The increasing proportion of patients with end-stage renal disease (ESRD) secondary to hypertension has now revived interest in hypertension. Prospective studies have firmly established that high blood pressure is associated with an increased risk of renal failure independent of other risk factors. Hypertension-related renal injury might be interpreted in a general context taking into account genes, intrauterine growth and environmental factors. Disturbed intrauterine growth (due to malnutrition or other factors) has a negative influence on the development of the cardiovascular system and favours the occurrence of hypertension, insulin resistance, hypercholesterolaemia and hyperuricaemia in adult life (Barker's hypothesis). Altered intrauterine growth has also been associated with a reduced number of nephrons at birth. Damage attributable to glomerular hyperperfusion in kidneys with a reduced number of nephrons is aggravated by vascular lesions in middle and small arterial vessels (secondary to hypertension, hyperlipidaemia and environmental risk factors such as smoking). The observation that subjects homozygous for the D allele of the ACE gene are predisposed to both cardiovascular complications and nephrosclerosis, suggests that genetic factors may interact with altered intrauterine growth in determining the risk of cardiovascular and renal diseases.

Alleles↗

PubMed2004

[Profibrotic effects of aldosterone].

Animal studies have shown that during high sodium intake aldosterone induces cardiac fibrosis and renal nephrosclerosis through activation of mineralocorticoid receptors. In the human heart mineralocorticoid receptors and activity of the enzyme 11beta-hydroxysteroid-dehydrogenase type 2, which is required for the activation of mineralocorticoid receptors by aldosterone, are both present. In clinical medicine the profibrotic effect of aldosterone has been related to diastolic dysfunction, arrhythmia and progression of cardiac and renal failure. The addition of an aldosterone receptor antagonist to optimal treatment in patients with heart failure causes a decrease in serum markers of collagen turnover and a decline in cardiac morbidity and mortality. These findings are a strong indication of a profibrotic effect of aldosterone in cardiac failure. Studies concerning the profibrotic effect of aldosterone in patients with primary hyperaldosteronism are contradictory and at the moment no data are available about a potential antifibrotic effect of aldosterone receptor antagonists in patients with impaired renal function.

Aldosterone↗

PubMed1992

Does essential hypertension cause end-stage renal disease?

The number of patients developing end-stage renal disease (ESRD) as a consequence of hypertension is increasing and accounts for 25% of new cases of ESRD in the United States. However, the diagnosis of hypertensive ESRD is one of exclusion and no pathologic data corroborate this classification. Undoubtedly, these patients suffer from a variety of diseases, including accelerated hypertension and atherosclerotic disease of the large arteries. Also included are patients with an undiagnosed primary renal disease. The prevalence of these conditions in the hypertensive population is unknown. It is also proposed that mild to moderate hypertension can lead to ESRD. In support of this view, early investigators noted that nephrosclerosis was correlated with hypertension and/or left ventricular hypertrophy. More recently, in the Hypertension Detection and Follow-up Program, renal function was found to decline in some patients despite treatment. Data from the Baltimore Longitudinal Study of Aging indicate that the rate at which creatinine clearance declines with aging is correlated with blood pressure. A recent retrospective study reported that serum creatinine increased significantly in approximately 15% of treated hypertensive patients. However, in none of these studies was the presence of intrinsic renal disease definitively excluded. Furthermore, although an increase in serum creatinine or decline in clearance has been reported, progression to end-stage renal disease has not been documented. Therefore, additional studies are necessary to determine the frequency with which essential hypertension leads to end-stage renal disease.

Humans↗

PubMed2005

Life-threatening hyperkalemia during a combined therapy with the angiotensin receptor blocker candesartan and spironolactone.

We describe a hypertensive nephrosclerosis patient presenting with severe hyperkalemia due to a combination therapy of the angiotensin receptor blocker (ARB) candesartan and spironolactone despite mildly decreased renal function. Recently, ARBs are replacing the ACE inhibitors. The combined therapy with ARB and spironolactone will eventually become the standard regimen. The strict attention and close monitoring of serum potassium should be mandatory in combination therapy to prevent hyperkalemia. Assessment of trans-tubular potassium gradient (TTKG) and fractional excretion of potassium (FEK) before starting the therapy would help in identifying the patients at higher risk of developing hyperkalemia. Co-administration of thiazide or loop diuretics is recommended to reduce the risk of hyperkalemia.

Angiotensin II Type 1 Receptor Blockers↗

PubMed2005

[The course of chronic glomerulonephritis in chronic opisthorchiasis].

AIM: To characterize clinical, functional and morphological features of chronic glomerulonephritis (CGN) running with chronic opisthorchiasis (CO) and to justify dehelminthization. MATERIAL AND METHODS: Clinical, functional and morphological examinations of the kidneys, immunological characteristics were studied in 100 patients with primary CGN and CO (group 1), 30 patients with CGN free of CO (group 2) and 40 patients with long-term CO. RESULTS: CGN in CO runs with frequent rise of creatinine, glomerular filtration and canal reabsorption fall. Pathogenetic therapy with addition of pulse cyclophosphamide in a dose 10 mg/kg and conduction of dehelminthization a year later lead to long-term remission and inhibition of nephrosclerosis development. CONCLUSION: Clinicofunctional and morphological characteristics of the kidneys in mixed pathology necessitate addition of immunosuppressor cyclophosphamide in a dose 10 mg/kg and dehelminthization in combined treatment of patients with glomerulonephritis and opisthorchiasis.

Chronic Disease↗

PubMed1990

Renal protection in essential hypertension: how do angiotensin-converting enzyme inhibitors compare with calcium antagonists?

By interrupting the integrity of the systemic and renal renin-angiotensin system, angiotensin-converting enzyme inhibitors have been shown, experimentally, to preferentially reduce postglomerular capillary arteriolar resistance, to reduce glomerular capillary pressure, and to increase the ultrafiltration coefficient. Under normal physiological conditions, angiotensin-converting enzyme inhibitors have little effect on glomerular filtration rate; however, they increase effective renal plasma flow at renal perfusion pressures within the normal autoregulatory range and renal vascular resistance is decreased. In contrast, calcium antagonists have been shown, experimentally, to preferentially reduce preglomerular capillary arteriolar resistance. Their effects on angiotensin II and postglomerular capillary arteriolar resistance (hence, glomerular capillary pressure and the ultrafiltration coefficient) are controversial. Under normal physiological conditions, calcium antagonists increase both glomerular filtration rate and effective renal plasma flow at renal perfusion pressures within the normal autoregulatory range and renal vascular resistance is decreased. In patients with essential hypertension, studies have demonstrated that angiotensin-converting enzyme inhibitors (as predicted) sustain glomerular filtration rate, increase effective renal plasma flow, and decrease renal vascular resistance. However, essential hypertensive patients with impaired glomerular filtration rate may demonstrate marked improvement in both glomerular filtration rate and effective renal plasma flow. Calcium antagonists (as predicted) may increase both glomerular filtration rate and effective renal plasma flow (at high renal perfusion pressures) and may decrease renal vascular resistance. Calcium antagonists may also improve both glomerular filtration rate and effective renal plasma flow in patients with impaired glomerular filtration rate. Long-term clinical trials comparing the renal effects of angiotensin-converting enzyme inhibitors with those of calcium antagonists in essential hypertensive patients have not been reported. It remains to be determined if the potentially different effects of these two classes of antihypertensive drugs on the renal microcirculation do or do not translate into different renal protective advantages to patients at risk for the development and/or progression of hypertensive nephrosclerosis.

Angiotensin-Converting Enzyme Inhibitors↗

PubMed1990

Scleroderma renal crisis in progressive systemic sclerosis: a case report.

We report a case of progressive systemic sclerosis with scleroderma renal crisis 10 years after onset. The patient (female) had progressive renal dysfunction, hypertension which was difficult to control, and massive gastrointestinal bleeding. An angiotensin converting enzyme inhibitor (enalapril) could not control her hypertension. Only intravenous nicardipine had a slight effect on her hypertension. Hemodialysis and plasma exchange, did not reverse the renal crisis, and the patient died. Microscopic examination of her kidney showed thickening of the capillary walls and mild nephrosclerosis.

Acute Kidney Injury↗

PubMedDate not supplied

The pathological basis of endstage renal disease in Nigerians: experience from Benin City.

A prospective study involving 1,980 patients aimed at defining the pathological basis of endstage (chronic) renal failure in Nigerians was carried out over a six-year period in Benin City, Nigeria. Using information derived from intravenous pyelography, ultrasonography, renal biopsies and autopsies, it was found that 43% of cases of chronic renal failure were due to hypertensive nephrosclerosis, 33% due to obstructive uropathy and 18% due to chronic glomerulonephritis. Chronic atrophic pyelonephritis was a rare finding. The frequency and severity of essential hypertension in Nigerians and their propensity to go into renal failure are similar to what obtains in American blacks. In a society which cannot afford regular dialysis and transplant facilities, there is need for early detection and adequate treatment of essential hypertension.

Adolescent↗

PubMed1989

Evidence for the failure of the Laplace law as a sole explanation for wall thickening of arteries in hypertensive and aging normotensive kidneys.

Nephrosclerosis, the morbid condition of the kidney that accompanies essential hypertension, is characterized by thickening of the walls of cortical arteries. According to the law of Laplace, the tension in the wall of an artery should be proportional to the product of pressure (P) times diameter (D). Thus, if wall thickness (T) is governed by wall tension, then it should be proportional to the same product: T = kPD, where k is a proportionality constant. A comparison of immersion-fixed kidneys in normotensives aged 75 to 90 years with those aged 19 to 34 years showed the magnitude of k to increase with age. The increase was 41% in vessels that were relatively close to the heart (outer diameter, 150 to 300 microns) and 30% at the more remote level (outer diameter, 80 to 140 microns). In perfusion-fixed specimens, k also increased with age, being 77% and 35% greater, respectively, for the comparison between normotensives in the two age groups. Normotensives were defined to be those with mean blood pressure less than 115 mm Hg. A similar result was found by defining normotension to be systolic pressure less than 140 mm Hg. Wall thickness was not proportional to pressure in hypertensive compared with normotensive subjects, but rather to a quadratic function that combined age and blood pressure taken together. The law of Laplace did not fully encompass the data that relate the thickening of renal arterial walls to hypertension or to aging in the absence of hypertension. The thickening with age is structurally a metaplasia that exchanges fibrotic intima in the elderly for muscular media in the young. The result was reproduced in perfusion- as well as immersion-fixed specimens and is therefore not distorted by postmortem collapse. The results favor the conclusion that arterial wall thickening in hypertensive and aging normotensive kidneys is sclerosis and not adaptive hypertrophy.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1987

Spontaneous hypertension and its sequelae in woolly monkeys (Lagothrix lagotricha).

Arteriolar nephrosclerosis was observed at necropsy in 26 of 38 woolly monkeys (Lagothrix lagotricha). This lesion is the earliest histologic change associated with hypertension in humans. Seventeen of the monkeys had died of congestive heart failure, renal failure or acute cardiovascular accident, complications similar to those seen in human hypertension. All monkeys known to be over 4 years of age were affected. Direct blood pressure measurements in nine otherwise healthy woolly monkeys revealed systolic pressures of 194 +/- 20 mmHg. Our physiologic, clinical and pathologic studies suggest that woolly monkeys develop hypertension spontaneously and could be a useful model for the study of human hypertension.

Animals↗

PubMed1986

Spontaneous hypertension in the fawn-hooded rat: a cardiovascular disease model.

The fawn-hooded (FH) rat develops hypertension spontaneously. Systolic blood pressure is already elevated at 5 weeks of age, increases with age, and the final range is 180-240 mmHg at the age of 1 year. Concomitantly with the rise in blood pressure proteinuria occurs and increases with age. Fawn-hooded rats reaching the accelerated phase of the hypertension are characterized by blood pressure values exceeding 220 mmHg, heavy proteinuria and increased heart, kidney, liver, adrenal and spleen weights. Those prone to malignant hypertensive disease show a period of increased water turnover for several weeks after weaning; during this period, they do not show the pronounced decrease in water intake upon fasting for 24 h as observed in FH rats of the same age prone to a milder form of hypertension, i.e. diuresis and drinking continue even when no food is consumed. The major cause of death for FH rats is malignant nephrosclerosis with the nephrotic syndrome and/or cardiac failure with chronic pulmonary congestion. Some animals die of bleeding from mesenteric vessels with periarteritis nodosa. In FH rats with malignant hypertension, heart, kidney, liver and spleen weights are significantly increased compared with FH rats of the same age with mild hypertension. Histopathology shows myocardial fibrosis and myocardial infarctions. Generalized arteriolosclerosis is common, sometimes accompanied with local fibrinoid degeneration and (peri)arteritis. Some major arteries show intimal proliferation. It is concluded that the FH rat provides an interesting model for the study of hypertension and its consequences.

Animals↗

PubMed1979

[Symptomatic arterial hypertension in lupus nephropathy].

Sixty six patients with lupus nephropathy with hypertonic syndrome are examined. In patients with latent (inactive) lupus glomerulonephritis hypertonic syndrome developed 3--8 months after the initiation of the corticosteroid treatment, advancing with fluctuations, in some of the patients the arterial pressure being normalized after the discontinuation of that treatment. In patients with chronic active lupus glomerulonephritis without nephrotic syndrome, the hypertension develops before the initiation of the corticosteroid treatment, fluctuating at the beginning, and gradually assumes a stable character 3--5 months after the beginning of such treatment, sometimes with a malignant course and rapid development of renal insufficiency. The hypertonic syndrome advances most severely and malignantly in chronic lupus glomerulonephritis with nephrotic syndrome and is resistant to the active antihypertensive treatment. In 18, out of 25, such patients, the hypertonic syndrome is manifested in parallel with nephropathy before the inclusion of the cortocosteroid treatment. The grave and malignant course of the hypertonic syndrome is associated with the peculiarities of the clinical form and histomorphological type of that lupus nephropathy. In the patients with nephrosclerosis, the hypertonic syndrome is with a gradually progressing evolution, in parallel with the progress of the renal insufficiency.

Adolescent↗

PubMed1979

Kidney tumors induced in rats by the antischistosomal drug niridazole.

An increased incidence of kidney tumors was found in MRC rats fed the antischistosomal drug niridazole at four dose levels in the diet. Histologically, the adenomas and adenocarcinomas were solid papillary, clear cell, and tubular types, with the latter type predominating. Seven mesenchymal tumors were found among the 107 renal epithelial neoplasms. Severe nephrosclerosis occurred in both treated and control rats and has been suggested as important in renal carcinogenesis. Niridazole is considered a potent inducer of epithelial kidney tumors.

Adenocarcinoma↗