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At least 865 records · Page 48Linked to original sources

PubMed1988

Is there any tubular secretion of protein?

Immunohistological investigations performed with the PAP method on tubular casts in the thick Henle loops and in the distal convoluted tubules led to the following results. 1) In control kidneys, casts consisting of sIgA and IgM occur, mostly isolated, in 30% and 20%, respectively, of cases. On the other hand IgG casts, likewise isolated, are only observed in 7% of cases. 2) In the case of mesangioproliferative glomerulonephritis of the IgA and non-IgA nephritis type, casts consisting of sIgA and IgM are observed more often than in control kidneys, especially when the serum creatinine concentration exceeds 1.3 mg%; i.e., the glomerular filtration is reduced. 3) In kidneys with inflammatory and non-inflammatory glomerular diseases which had led to nephrotic syndrome, casts consisting of sIgA and IgM are not observed more often than in kidneys with glomerulonephritides which had not been accompanied by nephrotic syndrome. 4) In kidneys with severe impairment of the excretory function (rapidly-progressive glomerulonephritis, primary malignant nephrosclerosis, acute renal failure) casts consisting of sIgA and IgM are observed more often than in controls but not more often than in IgA and non-IgA nephritides with increased serum creatinine concentration. 5) In kidneys which had become aglomerular as a result of scarring of the glomeruli, with atrophic proximal tubules and preserved epithelia of the ascending loop of Henle, casts consisting of sIgA and IgM as well as secretory component occur in a large quantity.(ABSTRACT TRUNCATED AT 250 WORDS)

Female↗

PubMed1986

Hypertension in black patients. Epidemiologic and pathophysiologic considerations.

In summary, the black patient with hypertension represents a challenge. This pathophysiologic state exists with much greater prevalence than in the nonblack population. The exact reasons for this are unknown, but because tribal blacks in Africa do not have hypertension, one might speculate that alterations in life-style, including increased stress and dietary alterations, play a large role. The black hypertensive patient also appears to differ from the white hypertensive patient in that he/she shows a tendency to volume expansion, low renin state, early nephrosclerosis, and lowered renal blood flow. Other parameters of the advanced hypertensive state, such as lowered cardiac output and increased total peripheral resistance, seem to be in common with the white patient with hypertension. The black patient is also unique in that he/she demonstrated less response to beta-adrenergic blocking agents and seems to require diuretic therapy under most circumstances. These considerations, as well as a discussion of appropriate therapy in black and white hypertensive patients, need to be considered in further detail.

Black or African American↗

PubMed1986

Does low protein diet halt the progression of renal insufficiency?

We evaluated 15 adult patients with a mean creatinine clearance of 18.35 ml/min and a mean age of 45.7 years. Four patients had glomerulonephritis, two interstitial nephritis and nine had nephrosclerosis. Paired controls were used. Experimental patients were instructed in a diet with 0.55 grams of protein/kilogram body weight/day; the control group was on an unrestricted diet. Protein intake was evaluated with dietary histories. Protein catabolic rates were calculated and were used for reinforcement. Nutritional status was evaluated with anthropometric measurements and laboratory testing. Progression of renal insufficiency was estimated using the reciprocal of the serum creatinine. The mean follow up was 14.9 months. During this period, three patients started dialysis, four had their creatinine clearance remain stable and six improved their renal function 20%. The rate of change of renal function in the treatment group was slower (p less than 0.05) than in the control group. Body weight, anthropometric measurements and chemical parameters did not change significantly. We conclude that a restricted protein diet stabilizes or improves renal function in most patients with end-stage renal failure without producing malnutrition.

Anthropometry↗

PubMed1987

Glomerular epithelial cell function and pathology following extreme ablation of renal mass.

The role of the pathologic features and dysfunction of glomerular epithelial cells (GECs) in the pathogenesis of glomerular scarring was studied in the remnant kidney model (RK) (1 and 5/6 nephrectomy) in rats. Three weeks after surgery serum creatinine was greater in the RK than either sham-operation controls (SHAM) or spontaneously hypertensive rats (SHRs). Blood pressure was higher in the RK (181 +/- 26 mm Hg) than in SHAM (129 +/- 17, P less than 0.05) but not SHR (195 +/- 15, P less than 0.05). GEC endocytosis, assessed by protamine heparin aggregate (PHA) disappearance (10), was not different from that in SHAM. Glomerular damage was greater in RK (glomerular damage index, 30 +/- 18) than in SHAM animals (4 +/- 3, P less than 0.05) and SHR (0, P less than 0.05), and 2 of 11 RK animals had fibrinoid necrosis and thrombosis of arterioles and glomeruli. Segmental sclerosis occurred in only 1 RK animal (0.6% of glomeruli). Six weeks after surgery serum creatinine and urinary protein excretion remained higher in the RK than in the SHAM animals. Blood pressure was higher in RK (158 +/- 34 mm Hg) than in SHAM animals (144 +/- 24), but the difference was not significant. PHA disappeared from the glomerulus at a slower rate in RK than in SHAM animals (outside the 95% confidence limits of SHAM). Glomerular pathology was more widespread in RK than in SHAM animals (glomerular damage index, 73 +/- 62 versus 3 +/- 8, P less than 0.05), and 4 of 11 animals had acute hypertensive injury in arterioles and glomeruli. Segmental glomerular sclerosis was only seen in the animals with necrotic glomeruli. GEC dysfunction is not demonstrable until long after proteinuria and hypertension are established, and it only occurs in the context of severe, acute glomerular injury when the epithelial cells separate from the capillary wall and undergo severe degenerative changes and necrosis. The acute glomerular and vascular lesions in the RK model are morphologically similar to malignant nephrosclerosis in humans. Segmental glomerular sclerosis occurs only after proteinuria is well established in the context of severe glomerular injury, and it appears to represent, at least partially, progression of more proximate glomerular capillary injury.

Animals↗

PubMed1979

Postpartum hemolytic uremic syndrome: a study of three cases with a review of the literature.

Three cases of postpartum hemolytic uremic syndrome (HUS) are presented. Symptoms of acute renal failure, hypertension and microangiopathic hemolytic anemia with thrombocytopenia occurred 10, 17 and 24 days after delivery. Despite early heparin therapy in all cases, one patient went into terminal renal failure needing chronic hemodialysis, with persistent hypertension which became uncontrollable requiring bilateral nephrectomy 6 months later. The second patient had diuresis one month after starting hemodialysis, but 3 months later developed malignant hypertension. Slight improvement in renal function with persistent hypertension occurred after hemodialysis for 20 months. The third patient showed complete clinical recovery after 2 months. Pathological examination of renal tissue showed the typical lesions of thrombotic microangiopathy (TMA). However, striking differences were observed in the lesion seen in early and late specimens. Early lesions could be differenciated from infancy TMA because the medium-dize arteries were more severely involved. Late lesions were variable, ranging from minor changes in glomeruli and blood vessels, via ischemic and sclerotic lesions in glomeruli with arteriolosclerosis, to the vascular and glomerular lesions seen in malignant nephrosclerosis. There was a good correlation between the renal pathology and the clinical outcome of the patients. HUS with renal TMA as a cuase of postpartum renal failure has been reported in 49 patients with a fatal outcome in 61%. The pathogenesis of the syndrome probably involves a primary endothelial damage. This causes local renal intravascular coagulation in the presence of the usual postpartum hypercoagulable state. This is shown by the presence of fibrin-fibrinogen in glomeruli and vessels, increased plasma fibrin degradation products, thrombocytopenia and lowered levels of coagulation factors. There is little hematological or pathological evidence fo disseminated intravascular coagulation or an immune-complex disease. Hypocomplementemia seen frequently is probably due to local C3 activation via the alternative pathway.

Adult↗

PubMed1985

[Acute choriocapillaris occlusion in pregnancy and puerperium. Toxemias, thrombotic microangiopathies].

Six cases of gravidic toxemia (4) and thrombotic thrombocytopenic purpura (Moschowitz's disease) in puerperium with choriocapillaris occlusion, were examined. At the acute stage, the vision is improved, ophthalmoscopy of the fundus revealed cystlike bullous exudative subretinal with retinal detachment, yellowish spots (of retinal pigment epithelium) and often minimal localized arteriolar narrowing. The evolution included retina application pigmentary disturbances and Elschnig's spots. Fluorescein angiography showed delayed filling of the capillaris and dye leakage in the subretinal space (first hypofluorescence and late hyperfluorescence). There are various stages of ischaemic involvement but in all cases visual symptoms may be due to central obstructive choroidopathy with delayed filling and occlusion. The retinal detachment in toxemia or Moschowitz disease in pregnancy in secondary to microcirculatory choroidal damage (short ciliary vessels essentially) with rupture of blood retinal barrier. Other constatations are made in disseminated intravascular coagulation, periarteritis nodosa, accelerated nephrosclerosis, hemolytic uremic syndrome in puerperium, and these suggested possible relationship between the various conditions.

Choroid↗

PubMed1979

[Causes of death in lymphogranulomatosis].

The results of 97 autopsy cases of lymphogranulomatosis showed the causes of death to be either progression of the disease (78 cases), complications of treatment (12) or other diseases (7). The immediate causes of death in the progression of the disease were toxicity (29%), pulmonary insufficiency (22%), pulmonary-cardial insufficiency (12%), hepatic insufficiency (21%), peritonitis (3.4%), sepsis (5.8%), uremia (3.4%), posthemorrhagic anemia (1.7%), cerebral edema (1.7%). The immediate causes of death in complications of therapy were secondary infection (5 cases), posthemorrhagic anemia (3), pulmonary insufficiency (3), cerebral edema (1). In 7 observations death was not due to lymphogranulomatosis: in 2 cases it was caused by disseminated hematogenic tuberculosis, in 2 pneumonia (with cured lymphogranulomatosis, in 1 myocardial infarction, in 1 uremia (aterosclerotic nephrosclerosis) and 1 patient died accidentally.

Adult↗

PubMed1979

[A case of multiple fusiform aneurysms presenting homonymous hemianopsia (author's transl)].

Fusiform Aneurysms are encountered in elderly persons with advanced arteriosclerosis. When they are enlarged to compress the neighboring structures, they may resemble tumors symptomatically. Especially when situated in close relation to the optic nerve or chiasmatic region, pituitary tumor is likely to be suspected. This is a case of 62 year old female with a giant fusiform aneurysm of the right internal carotid artery extending to the middle cerebral artery which caused left homonymous hemianopsia and a large aneurysm in the cavernous portion of the left internal carotid artery with fusiform extension of the distal portion of the carotid artery which presented left blepharoptosis, dilated pupil and total ophthalmoplegia. The basilar artery and the right meningohypophyseal artery showed fusiform dilatation as well. Systemic atherosclerotic change, abdominal aortic aneurysm, nephrosclerosis were also accompanied. The computed tomography demonstrated the aneurysms distinctly. Left oculomotor palsy disappeared after six months with residue of left homonymous hemianopsia. Surgical intervention was not attempted, because of the widely distributed constitutional aneurysms in the whole body.

Carotid Artery, Internal↗

PubMed1979

The pathology of end-stage renal disease in hemodialysis patients.

The pattern of the renal disease and the pathological changes were studied in the kidneys of 80 autopsied patients who were maintained on hemodialysis for periods of up to seven years. Chronic pyelonephritis was most frequently encountered (25%); next in frequency were chronic glomerulonephritis (17.5%) and nephrosclerosis (17.5%). Moderate to severe intrarenal vascular changes were seen; intimal changes were most prominent. Statistically significant differences were observed in the distribution of the initimal lesions in intrarenal vessels of different calibres. Deposits of oxalate crystals, usually in the renal tubules, were encountered in all kidneys except four. Twenty-four patients (30%) showed acquired cystic kidney disease; renal calcification was observed in 61 others. The pathogenesis of these lesions in hemodialysis kidneys and their clinical significance are discussed.

Adult↗

PubMed1979

Sclerosing glomerulonephritis and malignant hypertension in a patient with congenital renal dysplasia: A case report.

A patient with a single functioning kidney presented with the nephrotic syndrome. On the basis of highly selective proteinuria, a diagnosis was made of lipoid nephrosis. Steroid therapy over a 2-year period did not control the disease. The patient eventually developed end-stage renal failure and malignant hypertension. Nephrectomy was performed to control the hypertension. Histological examination showed congenital dysplasia in one kidney and sclerosing glomerulonephritis, malignant nephrosclerosis, as well as dysplastic changes in the other.

Child↗

PubMed1984

Enalapril treatment in a patient with impaired renal function and intolerance to captopril.

In a 36-year-old woman with malignant hypertension and moderate renal insufficiency from nephrosclerosis normotension was not achieved by the combination of a beta-blocker, a vasodilator, and a loop-diuretic. The angiotensin-converting enzyme (ACE) inhibitor captopril was then added to the therapy. The blood pressure control was good. However, due to adverse reactions, captopril had to be withdrawn. Later on, the patient was successfully treated with enalapril, another ACE inhibitor, without the relapse of any adverse reactions.

Adult↗

PubMed1978

Is low-renin hypertension an overdiagnosed syndrome?

The controversy surrounding low-renin hypertension ranges from the concept that it carries a favorable prognosis to the therory that it a form of nephrosclerosis. At least a part of the debate may result from the use of different methods of classifying patients with this condition. The study presented here clearly shows that age and sex have an important influence on plasma renin activity. Women had lower values than age-matched men, and studies in normal volunteers showed that plasma renin activity decreases with age. Other factors also affect renin profiling. Diabetes is associated with renin suppression, and blacks have lower values of plasma renin activity than whites. In addition, use of anti-inflammatory drugs such as aspirin significantly lowers renin levels. Since some of these variables have not been considered in published studies to date, it would seem that the true incidence of low-renin hypertension among hypertensives is lower than the accepted figure of 25%.

Adult↗

PubMed1981

Cutaneous malakoplakia.

A case of cutaneous malakoplakia is reported. The patient is a 53-year-old white woman on immunosuppressive therapy 6 years after renal transplantation for end-stage nephrosclerosis. She developed yellow-pink papular lesions in her natal cleft which, on histopathologic examination, showed typical features of malakoplakia, namely, a diffuse dermal infiltrate of histiocytes (von Hansemann cells) which contained calcified Michaelis-Gutmann bodies with a concentric ring appearance. Gram-negative bacteria were also identified in some of the histiocytes. The Michaelis-Gutmann bodies stained positively with the PAS-diastase, mucicarmine, and Grocott stains and thus resembled fungal spores from which they must be differentiated. Electron microscopy showed that the Michaelis-Gutmann bodies developed within phagolysosomes of the histiocytes. Malakoplakia appears to be caused by an acquired defect in the intracellular digestion of phagocytized bacteria.

Escherichia coli↗

PubMed1984

Proteinuria following transplantation. Correlation with histopathology and outcome.

A review of 693 renal transplant recipients revealed 77 (11%) in whom persistent, heavy proteinuria (greater than 2 g/24 hr) developed. Renal histology was available in all 77 patients. Twenty-one patients had received kidneys from living-related donors, the remaining 56 from cadaveric donors. The cause of proteinuria in these 77 patients was as follows: transplant glomerulopathy (30), allograft glomerulonephritis (22), chronic rejection (21), renal vein thrombosis (2), diabetic glomerulosclerosis (1), and hypertensive nephrosclerosis (1). Of the 22 patients who developed glomerulonephritis in the transplanted kidney, 6 had recurrent disease (3--membranous glomerulopathy, 2--focal sclerosis and hyalinosis, 1--membranoproliferative glomerulonephritis); 6 developed de novo glomerulonephritis; and in 10 the type of glomerulonephritis could not be classified as recurrent or as de novo because of lack of characterization of the original kidney disease. Renal vein thrombosis occurred in association with other lesions in an additional 5 cases (3--chronic rejection; 2--membranous glomerulopathy). In follow-up only 23.4% (18 of 77) of the patients maintained prolonged graft function; the majority of grafts being lost within one year of the development of persistent, heavy proteinuria. Of the 18 patients who retained their grafts, 8 had glomerulonephritis, 5 transplant glomerulopathy, and 5 chronic rejection. This study confirms the poor prognosis that has been reported with the development of nephrotic-range proteinuria in renal allograft recipients.

Graft Survival↗

PubMed1982

Uterine, placental, renal biopsies, and fibrin deposits in toxemia of pregnancy.

Histopathologic lesions of toxemia of pregnancy found in 46 first trimester-induced abortions and 82 women with kidney biopsies are reviewed and discussed. Decidual arteriolar vasospasm and degeneration, syncytial trophoblastic degeneration, and chorionic villous fibrin deposits characterize the early toxemic changes of the uterus and placenta. Pure toxemic glomerular, arteriolar, tubular, and juxtaglomerular alterations were present in about 40% of the kidney biopsies. Others had arteriolar nephrosclerosis, chronic glomerulonephritis or both. Two women had renovascular hypertension. Excessive vascular permeability predisposed to fibrinogen leakage and fibrin deposits. The mechanisms of preclinical toxemia of pregnancy and clinical preeclampsia are considered in view of these biopsy observations.

Female↗

PubMed1981

Secondary hyperparathyroidism manifesting as acute pancreatitis and status epilepticus.

A 36-year-old with end-stage renal disease secondary to hypertensive nephrosclerosis had a two-day history of epigastric pain and nausea. Soon after admission, multiple grand mal seizures uncontrolled by intravenous phenytoin sodium and diazepam developed. His calcium level was 14 mg/dL and his amylase level was 2,230 mg/dL; lumbar puncture was normal. Hemodialysis lowered his calcium level to 10.7 mg/dL but failed to control his seizures. Secondary hyperparathyroidism was thought to be the cause of his malignant hypercalcemia, and an emergency subtotal parathyroidectomy was performed. Postoperatively, his grand mal seizures resolved. Confusion and aphasia also developed, but they resolved over the ensuing three weeks. Microscopic examination of the parathyroid glands revealed diffuse chief cell hyperplasia. Preoperative parathormone level was 2,196 pg/dL (normal, less than 450 pg/dL). A review of the literature has failed to reveal a similar case.

Acute Disease↗

PubMed1980

[Morphogenesis of chronic pyelonephritis (electron microscopic study)].

Examinations of 51 rabbits and 86 patients with chronic pyelonephritis showed the morphogenesis of chronic pyelonephritis to be due to the effect of certain factors. One of them is the capillary-parenchymatous block resulting from the outgrowth of the connective tissue between the tubules and peritubular capillaries. Glomerular sclerosis occurs both periglomerularly (growth of the connective tissue into the capsule) and intraglomerularly (tropocollagen synthesis by mesangiaal cells). Nephrosclerosis combines diffuse sclerosis (the consequence of increasing hypoxia) and focal sclerosis (the consequence of renal tissue destruction during pyelonephritis attacks) which determine the features of regenerative hypertrophy of nephrons and the pattern of pyelonephritic shrinking of the kidney.

Adult↗

PubMed1980

[Pyelonephritis in various types of obstructive uropathies in children].

Kidney biopsies were examined in 73 children with some forms of obstructive uropathies: vesico-renal reflux and obstructive megaurether. In 59 patients (80%), chronic pyelonephritis was detected. The predominant morphological form of chronic pyelonephritis in patients with obstructive uropathies is a mixed form with a combination of tubulo-stromal-vascular changes. In most patients chronic pyelonephritis was extensive up to the development of nephrosclerosis, in 22% it developed against the background of renal dysplasia. The nature and intensity of pyelonephritis was shown to depend on the severity of congenital pathology of the urinary tracts and the age of the patients.

Adolescent↗