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)

Different types of urinary protein excretion may be recognized by determination of the proteins molecular weight. Beside chromatography different electrophoretic procedures have been applied to urinary proteins to study the underlying renal disease. The various zone electrophoreses separate merely by surface charge, proteins however covered by sodium dodecyl sulfate (SDS) migrate according to their molecular radius. So by SDS-polyacrylamide electrophoresis (SDS-PAe) macromolecular proteinurias (Mr 60,000- greater than 300,000 daltons) due to glomerular damage may be distinguished from micromolecular forms (Mr 10,000-70,000 d) due to tubular dysfunction. By densitometric quantitation of the separated Ig and transferrin an index of the glomerular selectivity is obtained, i.e. the capacity of the glomerular system, to retain serum proteins of a Mr above 150,000 d. By this procedure proliferative and degenerative glomerulopathies may be distinguished from minimal change disease, focal glomerular sclerosis and early membranous nephropathy; serial determinations of this selectivity index in the latter two disease entities show a gradual deterioration of glomerular protein handling with time. A glomerular proteinuria of even "physiological" quantity has been proved as early sign of renal involvment in systemic diseases; it may be detected earlier as for example the retinopathy in juvenile diabetics. Micromolecular proteinurias also occur at least in two forms: the typical tubular proteinuria (MW 10,000-70,000 d) is associated with acute or chronic severe tubular dysfunction as in interstitial nephritis and acute kidney failure; rejection episodes of kidney transplants lead to transient tubular proteinurias, too. The second form of micromolecular proteinuria (Mr 40,000-70,000 d) has been found frequently in association with a glomerular in diabetic and hypertensive glomerulosclerosis. By measuring clearances of the microproteins, the proteinuria with this pattern could be established as form independant from glomerular and tubular proteinurias. The constancy of the two micromolecular proteinurias led to the hypothesis of at least two selective mechanism of tubular protein resorption. SDS-PAe additionally allows the differentiation of extrarenal proteinurias, as caused by overflow, paraproteins, postrenal Ig-secretion or bleeding etc. In comparing clinical and in part histological data of about 2,000 patients suffering from kidney diseases the analysis of urinary proteins by this method has been proved as valuable non-invasive tool for diagnosis and follow-up.
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PMID:Diagnostic significance of SDS-PAA-electrophoresis of urinary proteins: different forms of proteinuria and their correlation to renal diseases. 44 75

In an effort to determine the pattern of foot-process effacement or "fusion" in proteinuria, quantitative measurements were performed on human tissue from patients with urinary protein excretion exceeding 0.5 g/d. Serial electronmicrographs were analyzed and the results related to both quantitative urinary protein and underlying disease. Although foot-process effacement was widespread, it was never universal. Some portions of glomeruli were morphologically normal in every case. The proportion of effaced foot processes did not vary directly with the level of urinary protein. With the possible exception of focal glomerulosclerosis, the primary disease did not appear to influence the amount of effacement.
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PMID:Epithelial foot-process effacement in patients with proteinuria. 49 58

A 22-year-old black male presented with erythrocytosis and proteinuria. The erythrocytosis was characterized by increased red cell mass, normal arterial oxygen saturation, and normal hemoglobin electrophoresis and oxygen affinity. There was no splenomegaly, and the white blood cell count, platelet count, serum uric acid concentration, serum B12 levels and leukocyte alkaline phosphatase activity were normal. Tumors of the liver, lung, kidney and cerebellum, which have been associated with erythrocytosis, were not found. The only associated disease was biopsy proven focal glomerulosclerosis. Renal vein thrombosis was excluded by renal venography and arteriography. This case illustrates the rarely reported association of the nephrotic syndrome and erythrocytosis. Other nephrogenic causes of erythrocytosis are mentioned, including renal cysts, tumors, renal artery stenosis and transplantation. The role of the kidney in erythropoietin production and possible mechanisms of nephrogenic erythrocytosis are discussed.
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PMID:Focal glomerulosclerosis and erythrocytosis. 50 18

Isolated glomerulonephritis with mesangial IgA deposits was the most common single finding encountered in a large biopsy series in an Australian community and was found in 50 patients, 18% of those presenting for the investigation of primary glomerular disease. A uniform histopathological picture of mesangial enlargement, with or without focal and segmental features was present. A tendency to progression was suggested by the frequent presence of glomerulosclerosis, interstitial scarring and vascular hyalinization. Because of the uniform histological immunofluorescence and ultrastructural appearances, the term IgA nephropathy has been used for this condition. The clinical picture, however, was heterogenous. Presenting symptoms included macroscopic hematuria (34%), proteinuria (32%) acute nephritis (10%), nephrotic syndrome (6%), malignant hypertension (8%), acute renal failure (6%) and chronic renal failure (4%). There was a striking correlation of increased blood pressure and decreased renal function with increasing age. While the period of follow-up was too short to assess individual patient data, a gradual and progressive decrease in renal function over several decades is suspected in patients with this condition.
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PMID:IgA nephropathy: a syndrome of uniform morphology, diverse clinical features and uncertain prognosis. 58 77

Subtotal nephrectomy in the rat is followed by glomerular hypertrophy, glomerulosclerosis, and, ultimately, renal failure. To gain more insight into this sequence, we have made a morphometric study of the glomerular changes following subtotal nephrectomy in the rat during the period of functional compensation before glomerulosclerosis appears. We found a twofold increase in glomerular volume as compared with controls 2 weeks after operation (to approximately 2 X 10(6) cu mu) followed by a linear increase to approximately 5 X 10(6) cu mu at 21 weeks. The rate of increase in glomerular volume in controls did not significantly exceed that of body weight. The volume increase after subtotal nephrectomy is a true hypertrophy, since other morphometric parameters expressed per unit glomerular volume (surface and length densities) were approximately 80% of control values at 2 weeks and constant thereafter. Glomerular hypertrophy up to 21 weeks is accompanied by a stable BUN and a gradually increasing proteinuria. We conclude that glomerular hypertrophy in this system is a pathologic rather than a compensatory process and suggest that it may represent a counter-productive response to hemodynamic changes serving to increase the glomerular filtration rate.
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PMID:A stereologic study of glomerular hypertrophy in the subtotally nephrectomized rat. 61 92

We have made a blind retrospective analysis of 334 renal biopsies, each containing more than 10 glomeruli, from adults and children with glomerulonephritis, in order to assess the clinicopathological significance of segmental lesions. These were defined as endocapillary proliferation and/or sclerosis involving capillary loops, and a less than half the glomerular tufts. On optical microscopy of paraffin-embedded material, 57 biopsies containing segmental lesions were independently classified by two observes as "focal proliferative glomerulonephritis" or "focal segmental glomerulosclerosis". These results were then reviewed with immunofluorescence, electron microscopic and clinical data and an "executive" diagnosis reached. Scarred focal proliferative glomerulonephritis could not be reliably distinguished from focal segmental glomerulosclerosis by optical microscopy alone. Some cases of focal proliferative glomerulonephritis are not associated with systemic disease and may have negative immunofluorescence findings, and we were unable to distinguish scarring in these patients from the lesion of focal segmental glomerulosclerosis with any of the tools at our disposal. Some patients with scarred focal proliferative glomerulonephritis showed profuse proteinuria, a nephrotic syndrome and progression to renal insufficiency. These cases cannot therefore be differentiated from focal segmental glomerulosclerosis by their clinical features. It would seem that the morphological lesion of focal segmental glomerulosclerosis should be regarded as focal segmental glomerular scarring from a variety of insults, rather than a distinct disease entity.
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PMID:Focal segmental sclerosis or scarred focal proliferative glomerulonephritis? 66 23

70 cases of focal glomerulosclerosis (FGS) followed for periods ranging from 1 to 24 years are reported. 39 patients had a nephrotic syndrome. 31 patients had asymptomatic proteinuria. 97 renal biopsies were performed. At least one biopsy specimen from every patient showed focal and segmental involvement of glomeruli, but no lesions were observed on the first biopsy in 6 patients. 26 of the 35 patients with a nephrotic syndrome were treated with steroids alone and/or chemotherapy and/or indomethacin. Resistance to treatment was encountered in 21 patients. Complete remission was observed in 6 cases, despite persistence or accentuation of histological lesions on serial biopsies in 3 cases. Actuarial renal survival rate at 10 years was 45% in the group with a nephrotic syndrome versus 91% in patients with proteinuria. FGS with a persistent nephrotic syndrome represents the 'malignant' form of the disease. Recurrence of the disease was observed after transplantation in 2 cases and was absent in 1.
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PMID:Focal glomerulosclerosis: natural history and treatment. A report of 70 cases. 67 92

We have examined the nature of focal glomerular sclerosis (FGS) in fawn-hooded (FH) rats. The fawn-hooded rat develops pathologic features similar to those observed in steroid-resistant focal glomerular sclerosis, ie, by light microscopy some of the glomeruli appear normal but others show areas of solidification confined to one or two lobules of the tuft. The pathogenesis of this disease is not well known and there is a great need for an animal model. In the FH animal, a marked difference in the development of the lesion was noted between male and female rats. Fifty percent of 4-month-old males had proteinuria in excess of 10 mg/day (none of the females had significant proteinuria), while all 12-month-old males had proteinuria in excess of 45 mg/day (female 12-month-old FH rats had mean proteinuria of 7 mg/day). At 6 months of age continuing through 12 months of age, male FH rats had mesangial deposits of IgG, IgM, and, occasionally, C3, demonstrable by immunofluorescence, whether or not FGS was present. Subepithelial electron-dense deposits were never seen by electron microscopy either at 6 of 12 months. Six-month-old animals frequently did not exhibit FGS. Instead, the glomerular epithelial cells, exhibited fusion of foot processes, vacuolization, and, in some areas, focal loss of the epithelial covering on the glomerular basement membrane (GBM). Six-month-old males with proteinuria exhibited focal loss of negative charge from all layers of the filtration barrier. The GBM from sclerotic glomeruli of 12-month-old rats was commonly denuded of epithelium. None of the animals in this study was uremic. FH rats demonstrated FGS associated with progressive glomerular epithelial cell injury.
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PMID:Focal glomerular sclerosis in the fawn-hooded rat. 68 52

We describe 11 patients whose renal biopsies showed minimal changes with focal segmental glomerulosclerosis. These patients, in contrast to the majority of patients with similar renal histology, went into renal failure within 2 1/2 years of clinical onset. All were young, severely nephrotic, most hypertensive, with microscopic hematuria, non-selective proteinuria and extreme hypercholesterolemia. Treatment with corticosteroids and cytotoxic drugs was without effect in any patient. Despite rapid decline in renal function, profuse proteinuria and a nephrotic syndrome persisted into terminal uremia and continued even after dialysis had begun. Seven patients were given nine allografts; four grafts failed because of immediate vascular complications, and a persistant nephrotic syndrome was evident in two of the five surviving grafts. This did not, however, lead to graft failure. Two patients died on dialysis because of myocardial problems. These patients with rapid decline in renal function constitute a distinct clinical subgroup amongst those with focal and segmental glomerulosclerosis; it is possible that they have a different primarily vascular pathogenesis in contrast to other patients with similar renal biopsy appearances.
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PMID:Focal segmental glomerulosclerosis with rapid decline in renal function ("malignant FSGS"). 69

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


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