Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0033687 (proteinuria)
 24,015 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

During a retrospective study of 100 patients who underwent renal biopsy because of pregnancy complicated by hypertension, we found 19 patients whom proteinuria exceeded 5.0 Gm. per 24 hours and an additional eight patients in whom excretion ranged between 3.5 and 5 Gm. per day. Of these 27 patients, 23 had the kidney lesion of pre-eclampsia, and three of them had superimposed hypertensive changes in the vasculature. The remaining four had other renal diseases. We located and re-examined 10 of the 23 pre-eclamptic women, 12 to 104 (mean, 36) months after delivery. Serum creatinine levels were normal in all but one, who was discovered to have polycystic kidney disease. During the same time period, we located the records of six women who had heavy proteinuria during gestation but were normotensive. Thus, at our institution, pre-eclampsia is the most common cause of the nephrotic syndrome in pregnancy. The frequency of nephrotic proteinuria in pre-eclampsia appears higher than previously suspected, but, despite this fact, recovery was complete in most instances.
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PMID:Nephrotic proteinuria with pre-eclampsia. 92 Jul 65

This autosomal dominant disorder usually appears in middle life. The most common findings are proteinuria, abdominal pain and palpable kidneys, followed by hematuria, hypertension, pyuria, uremia and calculi. In 15% of patients, death is due to cerebral aneurysm. Family counseling and the detection of "at risk" family members are important elements of management. Statistically, half of the offspring of one affected parent will have the disease.
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PMID:Polycystic kidney disease. 93 Aug 6

Data on the outcome of pregnancy are based upon a prospective study of 14,833 single births to women whose blood pressures during the fifth and sixth months of gestation were recorded. With each 5 mm, Hg rise in the mean arterial pressure (MAP) there is a progressive increase in the perinatal mortality rate. At each MAP level, the stillbirth rates and neonatal mortality rates are higher in blacks than in whites. When middle-trimester MAP is 90 mm. Hg or more, there is a significant increase in (1) the stillbirth rate, (2) the frequency of proteinuria, hypertension, and diagnosed pre-eclampsia in the third trimester, and (3) the frequency of intrauterine fetal growth retardation. We believe that all of these events are due to an impaired uteroplacental circulation, with which elevated blood pressures are associated. Women who have an average MAP of 90 or more during the fifth and sixth months should be considered in a high-risk category.
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PMID:The impact of mean arterial pressure in the middle trimester upon the outcome of pregnancy. 93 99

The present studies were designed to characterize the extent and pathogenesis of the glomerular lesions which occur in the viable portion of the kidney following partial renal infarction in rats. Control rats with two normal kidneys had a mean blood pressure of 112 mm Hg, minimal proteinuria and no glomerular pathology on light (LM), electron (EM) or immunofluorescence microscopy (IFM). Rats with two-thirds infarction of one kidney (stage II) became hypertensive, although less than 4% of the glomeruli from either kidney were abnormal. Rats with two-thirds infarction of one kidney and contralateral nephrectomy (stage III) developed proteinuria and hypertension whether fed a normal, low or high Na+ diet. By light microscopy 37% of glomeruli were abnormal 28 days after partial infarction and contralateral nephrectomy and thereafter the percent of abnormal glomeruli increased. Detectable amounts of immunoglobulin and complement (C3) were present in kidneys of stage II or III rats but were always accompanied by more extensive albumin and fibrin deposits. Basement membrane deposits characteristic of immune complexes were not seen on EM. Administration of antihypertensive medication to stage III rats significantly lowered blood pressure and reduced the number of abnormal glomeruli on LM; however, IFM abnormalities remained prominent. Platelet thrombi seen by EM and abundant glomerular fibrin deposits seen on IFM suggested that coagulation mechanisms may be prominent in the pathogenesis of the renal lesion. Heparin-treated stage III rats had significantly lower blood urea nitrogen concentrations, blood pressures and proportion of abnormal glomeruli although glomerular deposition of serum proteins was still present on IFM. These observations suggest that this glomerulopathy is initiated by an unknown agent(s) which increased capillary permeability. This lesion progresses via thrombotic mechanisms which are prevented by heparin administration.
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PMID:Pathogenesis of the glomerulopathy associated with renal infarction in rats. 94 Feb 76

Glomerular disease is associated with a limited number of signs which are easily detected by routine clinical examination and urine tests. Haematuria, proteinuria, oedema, hypertension and renal impairment occur in various combinations including classical and predictable syndromes such as acute post streptococcal nephritis and the nephrotic syndrome in children. Apart from these classical syndromes clinico-pathological correlations in glomerular disease are poor. Early renal biopsy is required to determine the extent of the glomerular disease and the long term prognosis in most patients with prolonged proteinuria and haematuria.
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PMID:Glomerulonephritis in children and adults. 94 53

Three hundred and forty-six nulliparous women with pregnancy-induced hypertension prior to term were monitored in a high-risk pregnancy unit while awaiting fetal maturity. Management included ambulation as desired, regular hospital diet without salf restriction, blood pressure measured 4 times daily, weight and urine protein determined 3 times each week, creatinine clearance determined weekly, and serial sonography to monitor fetal growth. Sedation and antihypertensive agents were not prescribed. Delivery was delayed until term unless hypertension persisted or recurred following an initial salutary response. Factors other than hypertension that contributed to the decision to effect delivery were 1) rapid weight gain, 2) decreasing creatinine clearance, 3) appearance of significant proteinuria, 4) suspected fetal growth retardation, and 5) the development of severe headache or scotomata. With this method of management the perinatal mortality rate was 9/1000. Only 5 infants developed the respiratory distress syndrome and all survived. There were 26 women who left the unit against medical advice. Severe hypertension subsequently developed in 7 of these women and 4 of their fetuses were stillborn. The perinatal mortality rate among this group of patients was 154/1000. It is concluded that the nulliparous patient with pregnancy-induced hypertension prior to term can be safely managed by hospitalization and close observation as a viable alternative to prompt delivery.
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PMID:Management of pregnancy-induced hypertension in the nullipara. 94 68

No differences were found at the 30th week of pregnancy in total body water, serum sodium, potassium, chloride and osmolality, plasma volume, total protein concentration, intravascular protein mass, serum albumin concentration, intravascular albumin mass, and urinary estriol and pregnanediol in 94 primigravidae who remained normotensive, 35 who developed mild preeclampsia, and 23 who developed severe preeclampsia (i.e. hypertension and significant proteinuria in the third trimester). In twin pregnancies no differences were found between 13 primigravidae who remained normotensive and nine who subsequently developed proteinuria and hypertension.
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PMID:Changes preceding the development of preeclamptic toxemia. 95 65

A retrospective analysis of 235 patients at the National Institutes of Health who met at least five criteria for systemic lupus erythematosus (SLE) indicated that 45% were hypertensive. Approximately two thirds of these hypertensive patients had creatinine clearances of more than 60 ml/min and nonnephrotic range proteinuria. Only 16% of normotensive patients had creatinine clearances of less than 60 ml/m9n. A subgroup of 36 patients with SLE and with biopsy-proved diffuse renal disease were studied. For these patients, the presence of hypertension could not be correlated with the degree of proteinuria or hematuria, with the level of serum complement, or with the presence of casts, focal necrosis, crescent formation, or interstitial inflammation. Hypertensive patients had a median age of 24.5 years; the majority had creatinine clearances of more than 60 ml/min. In SLE, hypertension is not necessarily associated with advanced renal disease, and high blood pressure may occur relatively early in the course of the disease.
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PMID:Hypertension and renal disease in systemic lupus erythematosus. 96 43

Indentations of the glomerular basement membrane were observed by light microscopy in ultrathin Epon-embedded serial sections from the renal biopsies of patients who had membranous glomerulonephritis, minimal change glomerulonephrits, acute or resolving exudative glomerulonephritis and focal glomerulonephrits, interstitial nephritis, amyloidosis, rheumatoid arthritis, or ankylosing spondylitis. In patients with membranous glomerulonephritis, acute or resolving exudative glomerulonephritis, amyloidosis, or rheumatoid arthritis, the occurrence of indentations in the glomerular basement membrane differed significantly from that in controls. The presence of indentations did not correlate with proteinuria, hematuria, leukocyturia, arterial hypertension, or with the nephrotic syndrome or its treatment with steroids. Examination of alternate serial sections by light and be electron microscopy showed that the indentations that were light microscopically visible corresponded to craters on the epithelial surface of the glomerular basement membrane seen in the electron microscope. These craters contained protruding portions of the epithelial cells, extracellular electron-lucent material or electron-dense amorphous or striated membranous material. They were often surrounded by spikelike protrusions of the lamina densa. These indentations might represent solitary remnants of former subepithelial deposits.
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PMID:Indentations of the glomerular basement membrane in renal diseases. A light and electron microscopic study on ultrathin serial sections. 97 63

A total of 99 patients with pre-eclampsia and proteinuria were managed conservatively between 30 and 37 weeks of gestation, based on serial urinary estriol, liquor amnii, and renal function studies. The over-all perinatal wastage was 14 per cent, but was 35 per cent in association with subnormal estriol excretion and oligohydramnios (less than 250 ml.). In severe pre-eclampsia (blood pressure greater than 170/110 mm. Hg with proteinuria greater than 5 Gm. per liter) the incidence of subnormal estriol was 73 per cent and, becuase of this and the associated maternal hazards, conservative treatment had little place. However, in less severe pre-eclampsia with proteinuria early in the third trimester, this prospective study, based on serial placental and renal function tests, showed that frequently the pregnancy could be prolonged and fetal losses due to prematurity avoided. It should be stressed that such conservative treatment should not be continued when there are strong clinical contraindications. Irrespective of the severity of the prior pre-eclampsia, it was unusual for patients to show residual hypertension, proteinuria, or abnormal pyelography at their postnatal examination. Postpartum renal biopsy showed either normal histology or regression of the classical glomerular lesion in 77 per cent of cases.
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PMID:Placental function and renal tract studies in pre-eclampsia with proteinuria and long-term maternal consequences. 98 68


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