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)

Between 1962 and 1970, 36 children with acute biopsy-proven poststreptococcal glomerulonephritis (PSGN) entered a prospective long-term follow-up study. The initial biopsies were scored into four histological grades using criteria based on endocapillary proliferation, leucocyte infiltration, epithelial "hump" and crescent formation; 5 patients had grade-1 (least severe), 14 grade-2, 15 grade-3 and 2 grade-4 biopsies. Two children died from rapidly progressive glomerulonephritis; both had grade-4 biopsies. Early repeat biopsy in 12 patients showed improvement in all but one patient who progressed from grade 2 to type 2 mesangiocapillary glomerulonephritis (MCGN). The initial biopsy grade correlated significantly with heavy proteinuria (chi2 = 9.73, P less than 0.01) but not with hypertension, haematuria or renal functional impairment. Follow-up observations were made after mean periods of 9.5 years (range 5.4-12.4 years; 32 subjects) and 19.0 years (range 14.6-22 years; 30 subjects). None of the survivors had an abnormal plasma creatinine. Only one patient (grade-3 biopsy), a female with a subsequent history of recurrent pyelonephritis, was hypertensive. Isolated microscopic haematuria persisted in 1 grade-2 and 2 grade-3 subjects. One grade-2 subject had proteinuria secondary to MCGN and one grade-3 subject had mild proteinuria and borderline hypertension. Although 20% of subjects had urinary abnormalities, we conclude that the long-term outcome of PSGN in children is excellent.
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PMID:Poststreptococcal glomerulonephritis in children: clinicopathological correlations and long-term prognosis. 315 45

The aim of the present study was to identify factors predicting later hypertension following a hypertensive pregnancy. In the years 1969-1973, 261 out of a total of 17 000 pregnancies were complicated by pre-eclampsia or hypertension in pregnancy. In a follow-up study seven to 12 years later, 238 (91.2%) of these women were investigated. It was discovered that 26.4% of the women had hypertension and 10.1% had borderline hypertension compared with 2 and 6.5% respectively in a group of matched control subjects. A stepwise regression analysis was performed in order to evaluate the association between nine different variables and blood pressure at follow-up. We found that systolic blood pressure in early pregnancy was the single most important factor predicting systolic blood pressure at follow-up (r2 = 0.28). When highest recorded blood pressure before delivery and age were entered into the statistical model, r2 was increased to 0.35 (P less than 0.0001). Unlike previous studies, parity and proteinuria did not add to the predictive power of the analysis. Late hypertension was found in more than 25% of women seven to 12 years after a hypertensive pregnancy. The most important factor associated with later hypertension was blood pressure before pregnancy.
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PMID:Prediction of later hypertension following a hypertensive pregnancy. 659 6

A now 33-year-old woman first had psychomotor seizures at the age of 3 years. At 9 years tuberous sclerosis (Bourneville-Pringle disease) was diagnosed, on the basis of sebaceous adenoma, white spots of the skin and periventricular cerebral calcifications. Later she developed hyperostoses of the cranium and two periungual fibromas. When aged 23 years she was first noted to have borderline hypertension (145/95 mmHg) and signs of renal insufficiency which, over the subsequent 10 years, gradually worsened: computed tomography and magnetic resonance imaging demonstrated angiolipomas and cysts. Haemodialysis became necessary when serum creatinine level had risen to 9.0 mg/dl, creatinine clearance to 8 ml/min, with proteinuria of 2660 mg/24 h and metabolic acidosis (pH 7.17, base excess -8.1 mmol). She had no mental retardation nor other neurological deficits and is scheduled to have renal transplantation. There were no hamartomas in other organs.
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PMID:[Terminal kidney insufficiency in tuberous sclerosis]. 775 11

The kidneys play an important role in the development of cardiovascular risk factors. It is well known that heavy proteinuria can induce hyperlipidemia, the uric acid is elevated in some renal deficiencies and that hypertension develops in most end stage renal diseases. In prehypertensive states, specially in subjects with a family history of hypertension, some hemodynamic changes take place, characterized by an increase in renal vasoconstriction with a reduction in renal plasma flow and an elevation of sodium reabsorption. The mechanisms for these alterations are not well understood, but an increase in intracytosolic calcium in vascular smooth muscle cells, a reduction in vasodilatory substances such as nitric oxide and an increased sympathetic nervous activity have been proposed. In normotensive subjects with two hypertensive parents a reduction in sodium diet, an increase in protein intake or in arginine diet could prevent established essential hypertension from developing. In borderline hypertension an early therapy with low doses of calcium antagonists, ACE inhibition or diuretics could be indicated.
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PMID:Can the kidney prevent cardiovascular diseases? 874 38

Patients with hypertension (78 men, 113 women aged 20-73 years) were stratified according to risk of development of cardiovascular complications. In low and moderate risk patients (n=31) with borderline hypertension, dyslipidemia and pronounced obesity mainly non-drug measures were employed directed at lowering of excess body mass. Medium risk patients (n=25) with isolated hypertension group were treated with angiotensin converting enzyme inhibitors and phenylalkylamine calcium antagonists. High risk patients (n=55) with metabolic syndrome received same antihypertensive drugs as medium risk patients. In very high risk patients (n=79) with diabetes, excessive body mass, dyslipidemia and proteinuria complex therapy consisting of antihypertensive and hypoglycemic drugs and non-drug interventions was used. This risk stratification based management of patients with hypertension on turned out to be highly effective and resulted not only in normalization of blood pressure but also in improvement of carbohydrate and lipid metabolism, lowering of resistance to insulin and excessive body mass, and improvement of renal function.
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PMID:[Stratification of patients with hypertension and selection of antihypertensive therapy]. 1249 81

Preeclampsia is a prevalent and potentially devastating disorder of pregnancy. Characterized by a sudden spike in blood pressure and urinary protein levels, it is associated with significant obstetric complications. BPH/5 is an inbred mouse model of preeclampsia with borderline hypertension before pregnancy. BPH/5 mice develop hypertension, proteinuria, and endothelial dysfunction during late gestation (after E14.5). We hypothesized that BPH/5 mice might exhibit early feto-placental abnormalities before the onset of maternal disease. All placental cell lineages were present in BPH/5 mice. However, the fetal and placental weights were reduced, with abnormalities in all the placental zones observed starting early in gestation (E9.5-E12.5). The fractional area occupied by the junctional zone was significantly reduced at all gestational timepoints. Markedly fewer CDKN1C-stained trophoblasts were seen invading the proximal decidual zone, and this was accompanied by reductions in Cdkn1c gene expression. Trophoblast giant cell morphology and cytokeratin staining were not altered, although the mRNA levels of several giant cell-specific markers were significantly downregulated. The labyrinth layer displayed decreased branching morphogenesis of endothelial cells, with electron microscopy evidence of attenuated trophoblast layers. The maternal decidual arteries showed increased wall-to-lumen ratios with persistence of actin-positive smooth muscle cells. These changes translated into dramatically increased vascular resistance in the uterine arteries, as measured by pulse-wave Doppler. Collectively, these results support the hypothesis that defects at the maternal-fetal interface are primary causal events in preeclampsia, and further suggest the BPH/5 model is important for investigations of the underlying pathogenic mechanisms in preeclampsia.
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PMID:Severe feto-placental abnormalities precede the onset of hypertension and proteinuria in a mouse model of preeclampsia. 1695 25