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)

Placental growth retardation caused 84 fetal and neonatal deaths per 100,000 births. Its frequency increased as mothers' diastolic blood pressure levels increased, an effect augmented by proteinuria. The perinatal deaths also increased with advancing maternal age, anemia, and poverty. Maternal weight gains were low in the involved pregnancies, and the fetuses and neonates who died had a pattern of growth retardation characteristic of fetal undernutrition. Microscopic abnormalities in the decidua and placenta were characteristic of inadequate perfusion of the placenta from the uterus. They included fibrinoid changes in the arteries and arterioles of the decidua, villous cytotrophoblastic hyperplasia, and an obliterative endarteritis in fetal stem arteries of the placenta.
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PMID:Causes and consequences of placental growth retardation. 62 66

Severe renal failure associated with proteinuria occurred in a 21-year patient, who had massive rheumatic aortic regurgitation. There was no sign of congestive heart failure or extra-cellular dehydration. Subacute bacterial endocarditis was ruled out by appropriate laboratory investigations. Prosthetic aortic valve replacement resulted in normalization of the renal function and marked reduction of proteinuria. Renal histology showed severe sclerotic endarteritis involving predominantly the large arteries, and membrano-proliferative-like glomerulopathy without immune deposits. The role of the massive aortic regurgitation in the production of renal failure and histologic alterations is suggested.
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PMID:Reversible renal failure secondary to severe compensated aortic regurgitation. 65 89

A clinicopathologic study of 41 biopsy specimens from renal grafts transplanted at least ten years earlier showed normal findings or only mild tubulointerstitial lesions in 63% of cases. Results confirmed the good prognostic value of renal graft biopsy performed ten years after transplantation. A very close correlation was demonstrated between histologic evidence of chronic rejection (interstitial fibrosis, tubular atrophy, and fibrous endarteritis) and long-term graft outcome. Severity of interstitial fibrosis was apparently a more reliable indicator of prognosis than severity of fibrous endarteritis. Among 16 patients with a history of acute rejection, none had residual parenchymatous lesions. In contrast, among patients with major tubulointerstitial and/or vascular lesions, most had previously experienced one or several episodes of acute rejection. Evidence of allograft glomerulopathy was seen in approximately one case in four (11 patients). Among these patients, only eight had proteinuria and only four lost their graft. Among the four patients who developed recurrent membranoproliferative glomerulonephritis (type I in three cases and type II in one case), three lost the deposits previously detected by immunofluorescence, probably as a result of immunosuppressive therapy.
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PMID:[Long term results in 70 pediatric renal transplants after more than 10 years. Histological study]. 192 9

Renal biopsies were carried out in 29 patients with scleroderma to study the early vascular lesions and their eventual clinical significance. Haemolytic acute renal failure was present in 9 patients. The biopsies showed early vascular lesions on interlobar arteries. The main biological change was proliferative or fibrous endarteritis. Mucoid infiltration was found in 3 biopsies. The arterioles were spared or only slightly affected without major fibrinoid necrosis. These lesions were therefore distinct from those of malignant hypertension. However, at autopsy of 2 of these cases, the vascular lesions were undistinguishable from those of malignant hypertension. The biopsies in 13 out of 14 patients with scleroderma without obvious renal involvement (9 cases) or with moderate proteinuria and/or hypertension without renal failure (5 cases) showed interlobar endarteritis with associated mucoid infiltration in 3 patients. This lesion was isolated but sometimes extensive even in young patients without hypertension. One patient died within one year, of disseminated colonic carcinoma, and 4 of cardio-respiratory failure due to scleroderma without hypertension, renal failure or proteinuria. Eight of the 9 remaining patients were traced 6 to 16 years after biopsy. Two were moderately hypertensive but none had renal failure. Cutaneous and internal organ scleroderma had regressed in the majority and proteinuria had disappeared in 3 cases.
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PMID:[Renal involvement in scleroderma]. 652 54