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PubMed1984

Spontaneous hypertension and hypertensive renal disease in the fawn-hooded rat.

The fawn-hooded (FH) rat, a strain characterized by a platelet storage-pool disease, developed focal and segmental glomerulosclerosis at the age of 2-3 months (males) and approximately 6 months (females). Male animals died spontaneously at 11-13 months, and females at 15 months of age, both with overt malignant nephrosclerosis. During the first half year of life focal glomeruli showed depositions of IgG, IgA, IgM, C3 and fibrinogen in a segmental pattern and mainly in mesangial areas. Mesangial IgG and IgA were already demonstrable at the age of 5 weeks. On electron microscopy no electron-dense deposits suggestive of immune complexes were found. Mean arterial blood pressure in 5.5-month-old male FH rats was increased compared with that of matched Wistar rats. One-year-old FH rats had severe hypertension. The presumed relationship between the hypertension, the renal lesions and the blood platelet defect is discussed.

Animals↗

PubMed1978

[The bilateral nephrectomy in terminal renal disease (author's transl)].

45 cases of nephrectomy are reported. Mortality was 8.9%. Thirty-one had a drug-resistant, severe hypertension, three had infected kidneys, and in eleven cases nephrectomy was performed prior to transplantation. Although blood pressure improved in all patients, of the first group 24% died within one year after nephrectomy, which shows unsatisfactory prognosis of malignant nephrosclerosis. Only early nephrectomy can lead to better results. Routine nephrectomy before transplantation should be avoided. Indications for this group are discussed.

Adult↗

PubMed1982

An etiological study on renal adenomas: with some references to dysplastic tubular lesions and adenocarcinomas in autopsy and surgery cases.

An etiological study on renal adenomas with specific references to dysplastic tubular lesions and adenocarcinomas was made, concentrating on histopathological and statistical surveys. Seventy-two unilateral kidneys obtained at random in autopsy cases were examined macro- amd microscopically on the consecutive sliced sections. Adenomas were found frequently in the cortex of 15 cases (20.8%), and particularly dysplastic tubular lesions were considerably associated with adenomas and detected even more frequently in 26 cases (36.2%), whereas fibromas in the medulla of 8 cases (11.1%). Most of the adenomas (86.7%) were found in nephrosclerotic kidneys; i.e., in vascular nephrosclerosis (53.4%), chronic pyelonephritis (13.3%), and in end-stage kidneys. The morphological feature of adenoma cells were also confirmed in the dysplastic tubular epithelial cells. These data imply that long-term renovascular and/or renostromal damages may induce dysplastic tubular lesions and further act as important enhancing or promoting factors on adult renal oncogenesis from the cortical tubular epithelium.

Adenocarcinoma↗

PubMed1980

Urinalysis and clinical renal disease.

Urinalysis is a simple, efficient, and accurate guide in the diagnosis of renal disease. By determining a patient's history and obtaining a physical examination, the physician is very often able to diagnose a patient's renal lesion. Heavy proteinuria and a microscopic sediment containing red cells and red cell casts strongly suggest acute glomerulonephritis. The causes of this nephropathy are legion. On the other hand, mild proteinuria and a lack of microscopic findings suggest nephrosclerosis, interstitial nephritis, or acute tubular necrosis in the proper clinical setting. When glomerular disease produces nephrotic syndrome, the various types of glomerular disease can be diagnosed accurately without biopsy in a high percentage of cases.

Acute Kidney Injury↗

PubMed1995

[Long-term hemodialysis treatment using femoral vein puncture method (FV-method) as blood access in 12 patients].

It is well known that blood access is essential for long-term hemodialysis treatment. Arteriovenouos fistula (AVF) is the most widely used method. However, this method of access frequently fails (access failure) as a result of stenosis. We attempt simple femoral vein puncture (FV-method) instead of AVF in such patients and have experienced 12 patients who were undergoing hemodialysis treatment using the FV-method, three times a week for more than one year. We devised special needles (18- and 19-gauge) for the FV-method. Generally, we use a 19-gauge needle with 4 side holes. We discuss here the results of 12 patients consisting of 4 males and 8 females with a mean age of 57.9 years, a mean duration of dialysis of 10.0 years, and a mean duration of FV-method of 3.5 years. Their underlying diseases were chronic glomerulonephritis (9 patients), diabetic nephropathy (2 patients) and nephrosclerosis (1 patient). Before the use of the FV-method, AVFs were attempted a man of 3.8 times and an artificial graft, 4 times in 3 patients. Ten patients were outpatients and 2 were inpatients. As for the indications of the FV-method, 11 patients had access failure and another had suffered from heart failure resulting from an over flow of blood through AVF. KT/V, PCR and TACBUN were measured monthly and were within the normal range in almost all of the patients. Concerning complications of the FV-method, hematoma formation after detachment of the needle at the end of dialysis and pain at needle puncture were sometimes noted.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗

PubMed1995

[Renal arterial disease-induced tubulo-interstitial lesions].

Renal arterial disease-induced tubulo-interstitial lesions described in this chapter include benign arterio- and/or arteriolo-sclerotic and malignant nephrosclerosis, renal infarction and renal cortical necrosis. In these conditions renal glomeruli as well as tubules are always involved, and consequent loss of nephrons, or renal parenchyma results in interstitial fibrotic changes. The parenchymal lesions have a spectrum from slowly progressive atrophy and loss to necrosis of abrupt onset and disappearance of glomeruli and tubules. As for glomerular reactions to the ischemia, the intermediate type consisted of mesangial degeneration and epithelial cell proliferation described as "alterative glomerulitis" is noteworthy. Briefly, in renal arterial diseases, glomeruli are rather variably involved than tubules and loss of the parenchyma results in interstitial fibrosis.

Arteriosclerosis↗

PubMed1995

Renal damage in hypertension.

The kidney can be considered as both culprit and victim in the hypertensive process. Deranged renal function contributes to the development of arterial hypertension and of secondary vascular damage at the glomerular and arteriolar level and accounts for the development of progressive nephrosclerosis. The most common alteration of renal function observed in humans from the early stages of essential hypertension is the presence of renal vasoconstriction. This can be accompanied by hyperuricaemia and increased urinary excretion of enzymes such as N-acetyl-beta-glucosaminidase and proteins such as albumin and beta 2-microglobulin. Later, a progressive fall in glomerular filtration rate, sometimes accompanied by proteinuria, can be observed if high blood pressure persists.

Enzymes↗

PubMed1995

[New approaches to the treatment of nephritis].

The paper provides evidence and results of using new therapeutical treatment of glomerulonephritis, such as pulse-therapy with cyclophosphane, therapy with angiotension-converting enzyme (ACE) inhibitors or that with antihyperlipidemic agents. Based on much experience with pulse-therapy with cyclophosphane (over 100 patients with chronic glomerulonephritis (CGN) and lupus nephritis), it is concluded that this method is highly effective. Treating 57 patients with ACE inhibitors has shown that in CGN these drugs should be used only when taking into account their antihypertensive effect and capacity of lowering intraglomerular hypertension, as evidenced by the renal functional reserve, and diminishing proteinuria. The long-term (7-12 month) antihyperlipidemic therapy (diet and lovastatin) in 20 patients with CGN accompanied by the nephrotic syndrome caused a significant reduction in the concentration of serum cholesterol and proteinuria, a significant increase in serum albumin levels; remission of the nephrotic syndrome occurred in 9 patients; but better effects were observed in non-inflammatory nephropathies, such as membranous nephropathy, focal segmental glomerulosclerosis, and nephrosclerosis.

Animals↗

PubMedDate not supplied

Effects of MPC-1304, a novel calcium antagonist, on stroke-prone spontaneously hypertensive rats.

The effects of MPC-1304, a newly developed 1,4-dihydropyridine derivative, on blood pressure and hypertensive complications in stroke-prone spontaneously hypertensive rats fed a high-salt diet (0.8% NaCl), were investigated. The antihypertensive effectiveness of nicardipine was used for the purpose of comparison. MPC-1304 and nicardipine were added to the diet, in doses of 0.01% (0.01% MPC-1304 diet), 0.03% (0.03% MPC-1304 diet) and 0.1% (0.1% nicardipine diet), respectively, throughout the experimental period (8 to 30 weeks of age). This chronic ingestion of MPC-1304 and nicardipine inhibited the development of hypertension and reduced the concentration of blood urea nitrogen, creatinine, triglyceride and total cholesterol in serum. Treatment with MPC-1304 inhibited the incidence of cerebral stroke, cardiac fibrosis, proliferative and fibrinoid arteriolitis and malignant nephrosclerosis. There was no significant difference in the antihypertensive effectiveness between 0.01% MPC-1304 and 0.1% nicardipine diets. Thus, MPC-1304 had antihypertensive effects in stroke-prone spontaneously hypertensive rats.

Administration, Oral↗

PubMed1994

Diffuse renal disease. Diagnosis by ultrasound-guided cutting needle biopsy.

The results of ultrasound (US)-guided renal parenchymal cutting needle biopsies in 101 consecutive patients were reviewed. The biopsies were done with the automated Biopty device mounted with a 2.0-mm needle. One or 2 needle passes yielded sufficient material for histologic analysis in 94% (95/101). Three or more passes were required in 6% (6/101) to obtain an adequate specimen. Mesangioproliferative glomerulonephritis, IgA-nephropathy, nephrosclerosis, diabetic nephropathy, secondary amyloidosis, lupus nephritis, minimal change glomerulonephritis and interstitial nephritis accounted for 79% of the final histologic diagnoses. The high quality and quantity of the tissue specimens yielded a definitive histologic diagnosis in renal parenchymal diseases of unknown etiology. Four major complications occurred, but no deaths or loss of kidney function were recorded. US proved useful as a guide to suitable biopsy site and in the detection of clinically significant complications. Prebiopsy screening of coagulation variables did not seem to prevent complications. Special attention should be paid to post-biopsy clinical observation.

Adolescent↗

PubMed1977

The significance of vesicoureteric reflux in non-pyelonephritic patients supported by long term hemodialysis.

Vesicoureteric reflux was found unexpectedly during routine investigations before renal transplantation in 12 patients with chronic glomerulonephritis and in one with hypertensive nephrosclerosis. They had all received long term hemodialysis treatment for nine to 106 months (mean 47 months) at the time of micturating cystourethrography (MCU). Four of the patients had previously had a normal MCU indicating that reflux developed after onset of end stage renal failure. The cause of reflux is obscure. It was not related directly to defunctioning of the urinary tract as several patients had daily urine volumes in excess of 300 ml. Infection, another potential cause, was uncommon in patients with reflux. Histology of the excised ureters showed abnormality in most cases with loss of the normal mucosal folds and submucosal cellular infiltrate and fibrosis. These changes are also unexplained. In this group of patients nephroureterectomy for reflux in anticipation of renal transplantation was associated with considerable morbidity. A minimal estimate of the incidence of reflux in chronic glomerulonephritis was 11%. We suggest that in this group and in patients with renal diseases other than chronic pyelonephritis reflux alone does not constitute sufficient indication for nephroureterectomy before transplantation to warrant the risks of major surgery.

Adolescent↗

PubMedDate not supplied

Prevalence of renal disease in elderly hypertensive patients with cardiovascular problems.

Renal vascular damage caused by arterial hypertension participates in the alterations to systemic vascular function and structure. Nephrosclerosis seems to run in parallel with systemic atherosclerosis, which accounts for the increased cardiovascular morbidity and mortality seen in hypertensive patients. Parameters indicating the existence of an alteration in renal function (increased serum creatinine, proteinuria and microalbuminuria) are independent predictors for an increased cardiovascular morbidity and mortality. Hence, parameters of renal function have to be considered in any stratification of cardiovascular risk in hypertensive patients.

Aged↗

PubMed1997

[Chronic renal insufficiency in Côte d'Ivoire: study of 800 hospital cases].

We report a retrospective study of 800 cases of chronic renal failure (CRF) admitted in the Internal Medical Department at Teaching Hospital of Treichville in Abidjan from January 1990 to December 1990 for precising the etiological, radiological, biological, clinical and epidemiological aspects of this entity in our practice. Kidney renal failure represents 5.8% of the whole patients hospitalised at the same period. 61% of patients were less 45 years old with a weak or mild socio-economic status (92%). In clinical field, 84% of our patients had a variety signs and symptoms which referred to a late uremic state in 41% of cases. Chronic glomerulonephritis (49.1%) and nephrosclerosis (25.4%) were the two main revealed causes. In therapeutical field, 95% of our patients did not receive any treatment in dialysis. Only 5% of patients could be treated by dialysis. The analysis of the results has permitted us to describe clinical particularities of CRF in black African patient.

Adolescent↗

PubMed1998

Prostatic atrophy: an autopsy study of a histologic mimic of adenocarcinoma.

Prostatic atrophy (PA) is one of the most frequent mimics of prostatic adenocarcinoma. It occurs almost exclusively in the peripheral zone of the gland and gained importance with the increasing use of needle biopsies for the detection of prostatic carcinoma The etiopathogenesis is unknown, and there is controversy related to the potential of PA as a precancerous lesion. The frequency increases with age. Compressions caused by hyperplastic nodules, inflammation, hormones, nutritional deficiency, or systemic or local ischemia, are all possible factors in the pathogenesis of PA. The peripheral zone of the prostate was step-sectioned and totally embedded from the bodies of 100 consecutively autopsied men more than 40 years of age. The fragments were microscopically studied for presence of PA, latent (histologic) carcinoma, high-grade prostatic intraepithelial neoplasia, local arteriosclerosis, and prostatitis. The prostates were macroscopically examined for the presence of nodular prostatic hyperplasia. The autopsy reports provided information concerning the presence of generalized atherosclerosis and benign or malignant nephrosclerosis. PA was seen in 85 of the 100 prostates examined and histologically was subtyped into simple, hyperplastic, and sclerotic atrophy. In 65 (76.47%) of 85 cases, the histologic subtypes were combined. In 33 (50.76%) of these 65 cases, the three subtypes were seen concomitantly, favoring the hypothesis that they represent a morphologic continuum of only one lesion. Fibrosis of the stroma may or may not be present in simple and hyperplastic atrophy. Hyperplastic atrophy associated with fibrosis of the stroma is the histologic subtype that most frequently mimics adenocarcinoma Sclerotic atrophy always presents fibrosis of the stroma. PA increases with age, and, in our study, ischemia caused by local intense arteriosclerosis seems to be a potential factor for its etiopathogenesis. Because there was no relation to latent (histologic) carcinoma or high-grade prostatic intraepithelial neoplasia, PA is probably not a premalignant lesion.

Adenocarcinoma↗

PubMed1998

Rapid progression to end-stage renal disease in young hypertensive African Americans with proteinuria.

Hypertensive nephrosclerosis (HN) remains the most common cause of end-stage renal disease (ESRD) in blacks. This study examined whether renal histology corresponds with clinical hypertension in proteinuric blacks. Nondiabetic hypertensive blacks who satisfied inclusion criteria were enrolled in this study. Four male patients, each with a family history of hypertension and mean age 41 years, consented to kidney biopsy. Their mean arterial pressure was 116.5 mm Hg, mean urine protein excretion was 7.7 +/- 3.5 g/day. All patients progressed to ESRD within a mean duration of 14 months; the mean rate of decline in glomerular filtration rate was 53 mL/min/y, with an ESRD incidence of 80%/y. The histologic findings were consistent with previously described features of HN. Prominent glomerulosclerosis involved 30% to 75% of the glomeruli and extensive arteriolosclerosis/arteriosclerosis, tubular atrophy, and interstitial fibrosis. There was no evidence of immune complex disease by either immunofluorescence, electron microscopy, or serologic studies. The mean arterial pressure showed a strong but nonsignificant correlation with progression to ESRD (r = 0.8) and arteriosclerosis/arteriolosclerosis (r = 0.8). Glomerular sclerosis correlated with the reciprocal of serum creatinine (r = 0.6), interstitial fibrosis (r = 0.8), and arteriosclerosis/arteriolosclerosis (r = 0.3). Urine protein excretion correlated weakly with progression to ESRD (r = 0.4). These results indicate a poor correlation between clinical findings and histologic features on renal biopsy in young hypertensive African Americans. Hypertension remains a major cause of ESRD among African Americans, and progression to ESRD may be rapid in patients with marked proteinuria. Early and aggressive intervention is warranted.

Adult↗

PubMed2002

Effect of blood pressure lowering and antihypertensive drug class on progression of hypertensive kidney disease: results from the AASK trial.

CONTEXT: Hypertension is a leading cause of end-stage renal disease (ESRD) in the United States, with no known treatment to prevent progressive declines leading to ESRD. OBJECTIVE: To compare the effects of 2 levels of blood pressure (BP) control and 3 antihypertensive drug classes on glomerular filtration rate (GFR) decline in hypertension. DESIGN: Randomized 3 x 2 factorial trial with enrollment from February 1995 to September 1998. SETTING AND PARTICIPANTS: A total of 1094 African Americans aged 18 to 70 years with hypertensive renal disease (GFR, 20-65 mL/min per 1.73 m(2)) were recruited from 21 clinical centers throughout the United States and followed up for 3 to 6.4 years. INTERVENTIONS: Participants were randomly assigned to 1 of 2 mean arterial pressure goals, 102 to 107 mm Hg (usual; n = 554) or 92 mm Hg or less (lower; n = 540), and to initial treatment with either a beta-blocker (metoprolol 50-200 mg/d; n = 441), an angiotensin-converting enzyme inhibitor (ramipril 2.5-10 mg/d; n = 436) or a dihydropyridine calcium channel blocker, (amlodipine 5-10 mg/d; n = 217). Open-label agents were added to achieve the assigned BP goals. MAIN OUTCOME MEASURES: Rate of change in GFR (GFR slope); clinical composite outcome of reduction in GFR by 50% or more (or > or =25 mL/min per 1.73 m2) from baseline, ESRD, or death. Three primary treatment comparisons were specified: lower vs usual BP goal; ramipril vs metoprolol; and amlodipine vs metoprolol. RESULTS: Achieved BP averaged (SD) 128/78 (12/8) mm Hg in the lower BP group and 141/85 (12/7) mm Hg in the usual BP group. The mean (SE) GFR slope from baseline through 4 years did not differ significantly between the lower BP group (-2.21 [0.17] mL/min per 1.73 m2 per year) and the usual BP group (-1.95 [0.17] mL/min per 1.73 m2 per year; P =.24), and the lower BP goal did not significantly reduce the rate of the clinical composite outcome (risk reduction for lower BP group = 2%; 95% confidence interval [CI], -22% to 21%; P =.85). None of the drug group comparisons showed consistent significant differences in the GFR slope. However, compared with the metoprolol and amlodipine groups, the ramipril group manifested risk reductions in the clinical composite outcome of 22% (95% CI, 1%-38%; P =.04) and 38% (95% CI, 14%-56%; P =.004), respectively. There was no significant difference in the clinical composite outcome between the amlodipine and metoprolol groups. CONCLUSIONS: No additional benefit of slowing progression of hypertensive nephrosclerosis was observed with the lower BP goal. Angiotensin-converting enzyme inhibitors appear to be more effective than beta-blockers or dihydropyridine calcium channel blockers in slowing GFR decline.

Adrenergic beta-Antagonists↗

PubMed1990

Micronodular transformation (nodular regenerative hyperplasia) of the liver: a report of 64 cases among 2,500 autopsies and a new classification of benign hepatocellular nodules.

Nodular regenerative hyperplasia is defined by hepatocellular nodules distributed throughout the liver in the absence of fibrous septa between the nodules. Most reports have been single cases so that the prevalence and clinical significance of nodular regenerative hyperplasia is uncertain. In this study, the hepatic histology of 2,500 consecutive autopsies was reviewed. A spectrum of nodular transformation was found with nodular regenerative hyperplasia present in 2.6% of autopsy livers and qualitatively similar but lesser degrees of nodular transformation in a further 10.2%. Nodular transformation was also seen in 47% of livers with cirrhosis and 69% with incomplete cirrhosis. Obliteration of many small portal veins was seen in all cases with nodular regenerative hyperplasia, but only 4.7% of these had evidence of portal hypertension. The prevalence of various clinical states was compared in nodular regenerative hyperplasia and in controls. The results confirm, extend and quantify the spectrum of associated diseases. Nodular regenerative hyperplasia occurs in 5.6% of individuals over age 80 and with increased frequency in patients with systemic arteritis, polymyalgia rheumatica, massive tumor infiltration and mineral oil deposition. Nodular regenerative hyperplasia appears to be the hepatic analogue of arterial and arteriolar nephrosclerosis. A new classification of nodular transformation is proposed that encompasses the spectrum of lesions described here and the previously defined entities of focal nodular hyperplasia, partial nodular transformation and "cirrhosis telangiectasia hepatis." The major conclusion is that nodular regenerative hyperplasia is a secondary and nonspecific tissue adaptation to heterogeneous distribution of blood flow and does not represent a specific entity.

Aged↗

PubMed1987

Immunohistochemical demonstration of vitronectin in association with elastin and amyloid deposits in human kidney.

The multifunctional glycoprotein vitronectin, also called serum spreading factor and S-protein of complement, is a potent inducer of cell adhesion and spreading in vitro, and also has a regulatory function in the complement and coagulation pathways. It is present both in plasma and tissue. Recently, vitronectin immunoreactivity was demonstrated in the elastic fibres of normal human skin. Normal and amyloid kidney tissue was investigated for vitronectin immunoreactivity using polyclonal and monoclonal antibodies in an avidin-biotin-peroxidase complex technique and in an alkaline phosphatase anti-alkaline phosphatase complex technique. Vitronectin was found in the elastic layers of normal vessel walls, and in glomerular sclerotic lesions in cases of benign nephrosclerosis, but not in normal glomeruli. Strong specific vitronectin immunoreactivity was found in the amyloid deposits in kidneys from cases with amyloid A type amyloidosis, and in cases with amyloid light chain type amyloidosis. Structures immunostainable with anti-amyloid A antiserum were invariably immunostainable with anti-vitronectin. An antiserum against serum amyloid P component stained the same structures as did the anti-vitronectin antibodies, and in addition stained normal glomerular basement membranes. In conclusion, vitronectin immunoreactivity was demonstrated in elastic tissue, in amyloid deposits and in sclerotic lesions in human kidney.

Amyloid↗