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)

In vitro concentrative transport to tritiated p-aminohippuric acid (3H-PAH) was evaluated in renal biopsy specimens from human subjects by section freeze-dry autoradiography. Renal cortical tissue obtained by percutaneous needle biopsy (23 of 27 tissue specimens) was incubated in vitro using a modified renal cortical slice technic. Following incubation in medium containing 3H-PAH, the biopsy fragment was snap-frozen, and section freeze-dry autoradiographs were prepared. The autoradiographs demonstrated cellular accumulation of 3H-PAH by proximal tubules of human kidney in vitro and suggest that PAH transport is uphill across the luminal as well as the antiluminal membrane. The number of proximal tubules which accumulate 3H-PAH in vitro diminishes as renal failure progresses. Cellular accumulation of PAH, however, was not impaired by heavy proteinuria, and appeared not to be related to the underlying glomerular histologic diagnosis. The frequency of proximal tubules showing 3H-PAH uptake in the cortex varied directly with the glomerular filtration rate and inversely with the degree of interstitial involvement. Proximal tubules which maintain the ability to accumulate 3H-PAH are clustered in fewer regions of the cortex in patients with reduced glomerular filtration rates. This observation is consistent with the view that residual renal function is renal failure arises from a few relatively normal nephrons rather than from a more uniformly damaged population of nephrons.
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PMID:Concentrative transport in human renal biopsy specimens. 83 3

In order to define the possible effects of gentamicin on the course of experimental acute renal failure, the interaction between gentamicin and mercuric chloride was studied in rats. Acute renal failure was induced with 1 mg. of HgCl2 per kilogram intravenously. When given alone, HgCl2 produced a uniform, reproducible, nonoliguric, acute renal failure with a low mortality rate. Animals receiving gentamicin over the course of HgCl2-induced acute renal failure, in doses sufficient to produce a 1 hour postinjection serum concentration of 10 mug/ml., recovered glomerular filtration in a fashion similar to animals receiving only HgCl2(p greater than 0.05). Animals that recovered from HgCl2-induced acute renal failure were given 10 mg./Kg. of gentamicin every 4 hours for 15 days and developed proteinuria and decline in urine osmolality to the same degree as animals given gentamicin alone, but failed to develop azotemia. Nevertheless, morphological changes associated with gentamicin nephrotoxicity were found which were similar in severity to those seen with gentamicin alone. Animals pretreated with 10 mg./Kg. of gentamicin every 4 hours for 7 days were then given HgCl2. Acute renal failure in these animals was more severe than in animals receiving HgCl2 alone, as manifest by a greater degree of azotemia and death (p less than 0.05). The data indicate that in the rat the concomitant administration of gentamicin did not interfere with recovery from HgCl2-induced renal failure. Rats recovering from HgCl2-induced acute renal failure were resistant to a depression in glomerular filtration when given gentamicin. The prior administration of gentamicin enhanced the nephrotoxicity of HgCl2.
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PMID:The effect of concomitant mercuric chloride and gentamicin on kidney function and structure in the rat. 83 19

Serum protein electrophoresis revealed a monoclonal gammopathy in three patients who presented with glomerulonephritis. Other features of myeloma were not found. Clinical manifestations of glomerulonephritis included marked proteinuria and significant hematuria. Rate of progression of renal failure was variable. Morphologically, glomerulonephritis was characterized by diffuse proliferative lesion with predominant mesangial involvement. Immunoglobulins and complement were found deposited in the mesangium. Immunoglobulins deposited in the glomeruli were found to consist exclusively of the circulating monoclonal IgG in one patient. Immunoglobulins eluted from the glomeruli of another patient consisted of immunoglobulin (IgM) which had electrophoretic mobility similar to that of the monoclonal spike in the serum. Selective deposition of monoclonal immunoglobulins in the glomeruli indicated that an active process was involved in their glomerular localization and that the monoclonal immunoglobulins may have had a role in the pathogenesis of glomerulonephritis in these patients.
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PMID:Benign monoclonal gammaglobulinemia and glomerulonephritis. 84 51

The clinical and histopathological features of 37 patients with idiopathic membranous nephropathy are presented. Males were four times as commonly affected as females and the age at presentation ranged from nine to 70 years. The period of observation varied from three months to 23 years. Twenty-eight patients (76 percent) presented with the nephrotic syndrome and nine patients (24 per cent) presented with non-nephrotic proteinuria. At the end of the study, of the patients presenting with the nephrotic syndrome, seven (25 per cent) were in remission, seven (25 per cent) remained nephrotic, nine (32 per cent) showed only proteinuria and five (18 per cent) were dead or on dialysis. Altogether eight patients (28 per cent) developed renal failure. The nine patients who presented with non-nephrotic proteinuria appeared to do better, and none developed renal failure. The occurrence of spontaneous remission makes assessment of benefit from immunosuppressive therapy difficult. However, analysis of our data and a review of the literature suggest that in this condition oral prednisone, cyclophosphamide and azathioprine have no significant therapeutic properties. Histological assessment confirmed the occurrence of mild (Grade 1) changes in patients biopsied soon after presentation, and tubular atrophy increased with the duration of illness. Immunofluorescence confirmed deposition of mainly IgG and complement. Repeat biopsies in 14 patients showed no histological improvement and remission was not accompanied by resolution of histological abnormalities.
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PMID:Idiopathic membranous nephropathy. 86 73

Eighteen out of 57 patients (31-6 per cent) suffering from Familial Mediterranean Fever (FMF) were found to have the nephrotic syndrome, histologically proven amyloidosis and progressive renal failure. In 14 cases renal function deteriorated rapidly after the first appearance of significant proteinuria, and 12 cases (66-7 per cent) required regular haemodialysis. Seven of these patients, seen in the early stages of renal impairment, were subsequently diagnosed clinically as probably having developed renal vein thrombosis. There was radiological proof of intrarenal or major renal vein occlusion in five which in one patient progressed to inferior vena cave obstruction. Treatment with heparin, plasminogen activators and fibrinogenolytic agents was disappointing although renal function has stabilized in one patient on long term oral anticoagulant therapy. It is suggested that renal vein thrombosis is common in FMF with renal amyloidosis and usually causes rapid deterioration of function and irreversible renal failure requiring dialysis. Renal phlebography may delineate clot in the main renal veins or indicate areas of reduced blood flow due to thromboses in intrarenal venules. Treatment is only partially satisfactory but there is some evidence to suggest that renal phlebography should be undertaken promptly when renal function begins to fall followed by anticoagulant therapy to prevent further thromboembolic complications.
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PMID:Renal vein thrombosis as the major cause of renal failure in familial Mediterranean fever. 86 77

This long-term study analyzes the prognostic value of the quantitative urinary protein excretion during and following steroid administration, the renal functional status three years after the onset of disease, and the degree of histologic damage in adult patients with steroid-treated idiopathic nephrotic syndrome (INS). No patient who had a complete (proteinuria less than 0.1 gm/day) or partial (proteinuria less than 2.0 gm/day) remission during steroid administration progressed to renal failure. Furthermore, no patient in whom urinary protein excretion subsequently fell to below 2.0 gm/day ever progressed to renal failure. Only 3 of 49 patients in whom renal function was normal three years after the onset of INS developed renal failure. Finally, renal failure occurred in only 2 of 28 patients with mild abnormalities by light microscopy, compared with 12 of 21 patients with more advanced glomerular abnormalities. Thus, a partial, as well as a complete remission during steroid administration, subsequent reduction in proteinuria to below 2 gm/day, persistence of normal renal function beyond three years, or the presence of mild histologic abnormalities auger a favorable long-term prognosis in patients with INS.
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PMID:Prognosis in steroid-treated idiopathic nephrotic syndrome in adults. Analysis of major predictive factors after ten-year follow-up. 87 28

Two patients reacting with transitory, massive proteinuria after diagnostic renal arteriography with a commonly used non-ionic contrast medium, metrizoate, are described. One of them developed temporary renal failure; the concentration of urinary albumin reached 330 g/g creatinine. It is suggested that intratubular precipitation of proteins, obstructing urinary flow, might be one factor in the development of her renal failure.
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PMID:Proteinuria following renal arteriography. Report of two cases. 89 76

Twenty-eight patients with SLE and distinct, well-defined renal morphologic lesions of membranous nephropathy were followed up for 4 years. These patients comprised approximately 8% of the patients evaluated for SLE during a 12-year period. The patients with membranous lupus nephropathy had typical systemic features of SLE, and most of them had positive LE cell tests and ANA, low serum complement concentrations, and mildly elevated serum antinative DNA levels. Proteniuria and microscopic hematuria were usually discovered years after systemic symptoms of SLE had developed, Only two patients had slowly progressive renal failure, and most patients continued to have proteinuria. Prednisone treatment did not influence either proteinuria or renal function. In only one patient, the renal character of the disease changed drastically, demonstrating membranoproliferative glomerulonephritis. Six patients died (21%); most of these died of cardiovascular illnesses. The relatively benign and stable renal course of membranous lupus nephropathy in patients with otherwise typical SLE suggests that the renal pathogenesis is different from that of proliferative lupus nephritis.
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PMID:Membranous lupus nephropathy: a clinicopathologic study. 91 91

The blood levels of 25-hydroxyvitamin D (25-HCC) in 26 patients with nephrotic syndrome (proteinuria of 6.5 g/24 h +/- 0.8 SEM) ranged between 1 and 18.6 ng/ml (8.6 +/- 1.0 SEM). This value was significantly lower (P less than 0.01) than that in normal subjects (21.8 +/- 2.3 ng/ml) and patients with chronic renal failure (24.8 +/- 2.3 ng/ml). There was inverse correlation (P less than 0.01) between levels of 25-HCC and magnitude of proteinuria and a direct relation (P less than 0.01) with serum albumin. Reduction in proteinuria was rapidly followed by a rise in blood 25-HCC toward normal. Ionized calcium levels were low in 16 of 26 nephrotic patients irrespective of degree of renal failure. In four of seven nephrotic patients with normal renal function, ionized calcium levels were low and showed an inverse relation with levels of parathyroid hormone. These data show that patients with nephrotic syndrome have low blood levels of 25-HCC probably due to its loss in urine. This derangement is probably responsible for the disorders of calcium metabolism in nephrosis.
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PMID:Blood levels of 25-hydroxyvitamin D in nephrotic syndrome. Studies in 26 patients. 93 Dec 2

Two patients with intractable massive proteinuria and uremia were followed and treated with standard mecial therapy and dialysis. After a period of study and demonstration of clinical deterioration both patients were given solutions containing sodium mercaptomerin. Within days there was a decline in urine protein excretion and a variable increase in serum protein concentration. The patients demonstrated an increase in blood pressure, which made hemodialysis treatment possible. No deleterious effects from the mercury salts were noted. These observations suggest that in selected cases nephrotoxic agents may be of value in decreasing massive proteinuria, and improving protein homeostasis in uremic patients. Table I: Possible advantages of medical nephrectomy. 1. Reversal of hypotension and shock 2. Ability to perform hemodialysis 3. No anesthesia or surgical risk 4. No angiography related complications 5. Preservation of endocrine function of kidney. Possible advantages of medical nephrectomy (Table I), are: 1) Correction of proteinuria and hypotension; 2) Ability to perform hemodialysis; 3) No anesthesia or surgical risk; 4) No angiography related complications; and 5) Preservation of remaining endocrine function of the kidney, including erythropoietic and vitamin D action. The ideal agent should be non-toxic to other organs and produce selective renal ablation. Obviously mercury is not the ideal agent, although in these cases it did not produce observable side effects. It appears that this agent should be used with caution and only in patients with irreversible renal failure.
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PMID:Medical nephrectomy. The use of metallic salts for the control of massive proteinuria in the nephrotic syndrome. 95 62


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