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)

To study some of the aspects of albumin homeostasis and proteinuria in PNS, the hepatic production of albumin is analyzed using semiquantitative immunofluorescent techniques, in biopsy specimens from nine subjects, free of hepatic or renal disease and nine patients with PNS, where renal biopsies were also made. Tissue sections 0.5 millimicron thick were cut. The hepatic synthesis of albumin, interpreted by the number of cells with specific fluorescence, was much higher in patients with PNS (p less than 0.001), and kept inverse relationship with serum albumin concentrations. Numberless droplets containing albumin were observed in the renal tissue indicating intense resorption and catabolism in the luminal and basal portions of the proximal convoluted tubules. Our findings indicate that, in PNS, albumin synthesis is substantially increased and hypoalbuminemia is caused by exaggerated renal excretion and catabolism.
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PMID:Hepatic synthesis and albumin distribution in the primary nephrotic syndrome (PNS). as demonstrated by immunofluoresce. 70 87

Proteinuria was studied in 110 females - 28 pregnant with nephropathy of pregnancy with primary late toxicosis and 82 with past history of the disease with a residual proteinuria after childbirth. Selective type proteinuria was more often found both in pregnant women and in those with a past history of nephropathy. The relative share of the pregnant with non-selective proteinuria is considerably greater. After childbirth, in parallel with the decrease of proteinuria quantity, the non-selective one turns to selective in the majority of the cases. The quantity of the excreted proteins, in the urine, of patients with confirmed glomerular lesions, shows no tendency to decrease. The absence of dynamics in proteinuria quantity and its non-selectivity provides grounds to suspect a deeper lesion of the renal filter, retaining the involution of the morbid process and a tendency to its chronification.
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PMID:[Proteinuria in the nephropathy of pregnancy and posttoxicosis renal lesion]. 71 74

Urine specific gravity, osmolality, and the incidence of proteinuria were assessed in 18 caged cats. The values for these parameters were increased when dry, as compared to moist, cat food was fed. Failure to recognize these characteristics of feline urine could lead to erroneous interpretations of laboratory data since elevation of these values, particularly protein, has been associated with renal disease.
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PMID:Effects of diet on feline urine. 72 17

In order to evaluate a possible relation between cigarette smoking and prevalence of diabetic microangiopathy, a series of 180 consecutive patients suffering from insulin-dependent juvenile-onset diabetes mellitus with different durations of disease (60 patients each with diabetes for 10 to 19 years, 20 to 29 years, and 30 to 39 years, respectively) were examined for clinical signs of retinopathy, nephropathy, and peripheral neuropathy. The results were compared with the patients' previous and actual smoking habits. Cigarette smoking was defined as daily smoking of at least ten cigarettes for one year or more. Smoking habits of the total diabetic sample were not significantly different from those of a nondiabetic control sample. However, a decline in the number of cigarette smokers and a rising number of ex-smokers were noted with increasing duration of diabetes. In comparing smokers and nonsmokers, no difference was found in the prevalence of peripheral neuropathy, background retinopathy, and proliferative retinopathy. However, the prevalence of nephropathy (persistent proteinuria) was significantly higher (p less than 0.05) among these patients who were or had been cigarette smokers. Thus, cigarette smoking might be considered a risk factor for the development of diabetic nephropathy.
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PMID:Cigarette smoking and prevalence of microangiopathy in juvenile-onset insulin-dependent diabetes mellitus. 72 38

Chronic atrophic pyelonephritis is associated with vesicoureteric reflux in infancy. Reflux disappears during childhood in 50% of cases. It is more commonly detected in infants (49%) and children (26%) with infection than in adults (4.4%). Severe reflux may persist in adults and is usually (94%) associated with scarring. Patients with end-stage renal failure due to pyelonephritis are much younger than patients with end-stage renal failure due to other causes. The incidence of reflux according to sex is equal in infancy, but after infancy both pyelonephritic scarring and reflux are far more common in females. Infection is the likely cause of progressive scarring in females. Hypertension is associated with chronic atrophic pyelonephritis. Proteinuria is the worst prognostic feature in patients with reflux nephropathy and pyelonephritic scarring. Intrarenal reflux determines the site of scarring. The role of surgical correction of vesicoureteric reflux remains uncertain, but meticulous control of infection appears to prevent progressive scarring.
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PMID:Reflux nephropathy and chronic atrophic pyelonephritis: a review. 73 56

Many patients with chronic pancreatitis (CP), even in the absence of intrinsic renal disease, are found to have abnormal urine, with persistent proteinuria, cylindruria, microhematuria and leukocyturia. The kidneys of 12 necropsy cases with CP showed mild to moderate arterial and arteriolar nephrosclerosis and no other significant changes. Renal biopsies were performed in 10 patients with CP without evidence of systemic disease or intrinsic renal disease, but with persistent urinary abnormalities. By light microscopy, mild arterial and arteriolar nephrosclerosis was present in 5 instances. In 1 patient, evidence of the reparative phase of acute tubular necrosis was noted. In 5 biopsies, electron microscopy revealed minimal to mild increase in mesangial matrix. Mild thickening of the glomerular basement membrane (GBM) was found in three instances but there was no clear-cut evidence of diabetic glomerulosclerosis. The presence of subendothelial electron-lucent material in 3 cases suggests the possibility of previous subclinical episodes of intravascular coagulation. The most consistent finding was the presence of lipid material in the cytoplasm of glomerular and tubular cells. The renal lesions associated with CP are mild, nonspecific and nonprogressive. Various pathogenetic factors can be invoked to account for their presence and for the urinary abnormalities found in patients with CP.
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PMID:Renal lesions in chronic pancreatitis. 74 Jan 5

A 16-year-old male (S.F.) and his 21-year-old sister (D.H.) from a large family of Italian and Swedish descent had virtually identical lipoprotein pattern and complete absence of LCAT activity. Both had typical corneal opacities and mild anemia with target cells. S.F., but not D.H., presented with proteinuria, which has increased over three years of follow-up. His kidney biopsy revealed lipid deposits in the glomerular basement membrane. Ten relatives in 4 generations had normal LCAT activity and/or lipoprotein pattern. The patients and their relatives had haptoglobin type 2. Factors that might influence the different clinical presentation in our patients (previous renal disease, diet, abnormal lipoproteins), prognosis, and treatment (diet, enzyme replacement, cholestyramine) are discussed.
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PMID:Familial LCAT deficiency. Report of two patients from a Canadian family of Italian and Swedish descent. 74 43

HgCl2 chronically injected in the Brown-Norway rat induced a biphasic renal disease. The first stage was characterized by anti-glomerular basement membrane antibodies. The second stage by the appearance of immune complexe type deposits in the glomerular tufts and in the small renal arteries. These immune complexes were constituted of a basement membrane component and anti-basement membrane antibodies. Other immune complexes were perhaps involved. In most of the rats, a proteinuria and a nephrotic syndrome appeared, as a consequence of this immune disease. No abnormalities were observed in Lewis rats, suggesting a role for a genetic control of this immune response.
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PMID:Immune type glomerulonephritis induced by HgCl2 in the Brown Norway rat. 74 85

We have studied sodium retention during volume expansion in rats with autologous immune complex nephropathy (AICN), a model of nephrotic syndrome (NS) in which GFR after volume expansion was not different from that in adjuvant-injected controls (C). AICN rats developed heavy proteinuria (298 +/- 27 vs. less than 10 mg/day), hypoalbuminemia (2.14 +/- 0.15 vs. 3.08 +/- 0.12 g/100 ml) and hypercholesterolemia (181 +/- 22 vs. 58 +/- 4 mg/100 ml). After saline, there were no significant differences in blood pressure (119 +/- 2 vs. 114 +/- 2 mm Hg), renal plasma flow (4.9 +/- 0.41 vs. 4.1 +/- 0.28 ml/min), inulin clearance (1.37 +/- 0.06 vs. 1.55 +/- 0.10 ml/min), or SNGFR (47 +/- 2 vs. 53 +/- 4 nl/min). Sodium excretion, however, was significantly lower in NS rats (4.7 +/- 1.1 vs. 9.2 +/- 1.2 muEq/min). Proximal sodium reabsorption was decreased in NS rats (35 +/- 2 vs. 41 +/- 2%, 2.5 +/- 0.2 vs. 3.3 +/- 0.2 nEq/min). Sodium delivery into the loop, however, was equal in NS and C, since the slightly lower filtered load in NS rats offset the depression in proximal reabsorption. Sodium reabsorption by the loop and by the distal convoluted tubules were equal in NS and C. Thus, sodium delivered into the cortical collecting ducts was the same in both groups (0.33 +/- 0.17 vs. 0.34 +/- 0.07 nEq/min; 4.5 +/- 0.6% of filtered sodium vs. 4.4 +/- 0.3%). The percent of filtered sodium excreted in the urine, however, was significantly lower in the NS rats, 2.18 +/- 0.48% vs. 4.0 +/- 0.58%. We conclude that antinatriuresis in this model of NS is determined beyond the superficial late distal convoluted tubule. The inability to excrete the sodium load during volume expansion is due to either enhanced reabsorption by the collecting duct or to abnormal function in deep nephrons.
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PMID:Renal sodium retention during volume expansion in experimental nephrotic syndrome. 75 Jun 93

Antireflux surgery was performed in five patients with vesicoureteral reflux at a time when renal insufficiency was present. Notable proteinuria was present in four of the patients, and a kidney biopsy specimen showed glomerular lesions in one. Despite the eradication of reflux and of infection, all five patients continued to have progressive renal insufficiency culminating in renal failure. Vesicoureteral reflux nephropathy may include a glomerulopathy leading to progressive glomerular sclerosis. Antireflux surgery would not alter this ongoing process and therefore would not halt progressive renal failure.
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PMID:Irreversible renal failure following vesicoureteral reflux. 75 14


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