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)

Patients with asymptomatic or smoldering multiple myeloma should not be treated but should be observed closely for progression. For symptomatic myeloma, chemotherapy is indicated. Melphalan, the agent of choice, should be given with prednisone for 1 week of every 6 weeks, If melphalan brings no response, or response and then relapse, cyclophosphamide (Cytoxan) should be give intravenously every 4 weeks or orally every day. BCNU, CCNU, and doxorubicin (Adriamycin) have also shown activity in myeloma. Hypercalcemia occurs in one-third of patients and should be countered with hydration, corticosteroids, Neutra-Phos, or mithramycin. Long-term hemodialysis has achieved some success. The combination of sodium flouride and calcium carbonate produces new bone formation; it seems a useful adjunct in treatment for myelomatous bone disease. Radiation should be utilized only for severe, localized pain or for solitary lesions. Survival with multiple myeloma varies, mean durations being 2 to 3 years. Multivariate analysis indicates that serum creatinine and calcium levels are the most significant indicators regarding 2-year survival. We have found monoclonal proteinuria not significantly more frequent with renal insufficiency than with normal renal function, renal insufficiency not significantly more frequent with lambda than with kappa chains, and survival not significantly greater with IgG myeloma than with IgA.
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PMID:Management and prognosis of multiple myeloma. 79 81

We combined the use of a concentrating device (Minicon) and polyacrylamide gel electrophoresis in the presence of sodium dodecyl sulfate to semi-quantitate the concentration of (a) the collective low-molecular-weight proteins and (b) of albumin excreted in the urine of patients after renal transplantation. Analytical recovery of many serum proteins from samples concentrated 100-fold in the Minicon apparatus was about 70%. It was possible to examine many urine samples by polyacrylamide gel electrophoresis after concentration with this device. The reproducibility (CV) of the technique was on the order of 20% when albumin and low-molecular-weight protein were in about equal concentration. The method was adequate to differntiate glomerular and tubular proteinuria, because in glomerular proteinuria the ratio of albumin to low-molecular-weight proteins is about 20/1, whereas in tubular proteinuria the ratio is about 1/1.
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PMID:Method for measuring the concentration of urinary proteins according to their molecular size category. 81 76

1. In four patients with nephrotic syndrome indomethacin not only reduced proteinuria but also inhibited the natriuretic effect of high doses of frusemide. 2. The inhibition of natriuresis by indomethacin could not be antagonized by albumin infusions. 3. Only the combined use of spironolactone and frusemide induced a natriuresis during indomethacin treatment. Spironolactone alone was ineffective. 4. It is suggested that inhibition of prostaglandin synthesis by indomethacin, in the presence of a stimulated renin-angiotensin system and hyperaldosteronism, may cause this strong tendency to sodium retention.
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PMID:Inhibition of frusemide-induced natriuresis by indomethacin in patients with the nephrotic syndrome. 84 48

Abnormalities of tubular cells were treated by administration of nephrotoxin and studied by specialized gel filtration methods to discern early quantitative and qualitative changes in proteinuria. Dogs given nephrotoxic doses of Diglycoaldehyde, alpha-(hydroxymethyl)-alpha1-(6-hydroxy-9H-purine-9-yl) 60 mg per kg per day intravenously, for 3 days showed a marked reduction in effective renal plasma flow from 264.91 +/- 90.05 ml per min to 125.0 +/- 19.0 ml per min as measured by 131I sodium iodohippurate, and corresponding decrease in total renal perfusion by 131I xenon wash-out from 222.2 +/- 8.6 to 124.0 +/- 28.38. However, after treating four dogs with 20 mg per kg, an increase in effective renal plasma flow was obtained. Histologic changes of glomerular and tubular damage were demonstrated. Urine from this same series of animals was examined on a daily basis by sucrose-acrylamide gradient gel centrifugation together with ultraviolet scanning. Specific patterns were also obtained using dialyzed urine which eliminated molecules greater than 3500 mol wt. The ultraviolet pattern data were digitized and analyzed on computers to augment pattern recognition. These techniques indicted that molecules (3500 mol wt or less) were excreted in response to a known nephrotoxic agent, establishing early distinctive changes in tubular cells and also relating to alteration in renal function.
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PMID:A new quantitative procedure for proteinuria. 85 63

Urinary kallikrein excretion was studied in two types of experimentally induced renal disease: anti-glomerular basement membrane nephritis (20 rats) and aminonucleoside nephrosis (five rats) with appropriate controls (23 rats) for a period of 6 to 9 weeks following disease induction. In both models there was a prompt significant decrease (p less than 0.01 - 0.001) in urinary kallikrein excretion associated with proteinuria but unrelated to urinary sodium and potassium excretion and urinary volumes. In antiglomerular basement membrane nephritis the fall in kallikrein excretion occurred within the first 24 hours concurrent with the onset of proteinuria. In aminonucleoside nephrosis the decrease antedated the onset of proteinuria by 48 hours beginning within the first 24 hours following injection of the aminonucleoside. Kallikrein inhibitors were not demonstrable in the urines of diseased animals from either model. The mechanism of the decrease in kallikrein excretion in immune and nonimmune glomerular disease associated with proteinuria is unknown.
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PMID:Urinary kallikrein in experimental renal disease. 93 67

The present studies were designed to characterize the extent and pathogenesis of the glomerular lesions which occur in the viable portion of the kidney following partial renal infarction in rats. Control rats with two normal kidneys had a mean blood pressure of 112 mm Hg, minimal proteinuria and no glomerular pathology on light (LM), electron (EM) or immunofluorescence microscopy (IFM). Rats with two-thirds infarction of one kidney (stage II) became hypertensive, although less than 4% of the glomeruli from either kidney were abnormal. Rats with two-thirds infarction of one kidney and contralateral nephrectomy (stage III) developed proteinuria and hypertension whether fed a normal, low or high Na+ diet. By light microscopy 37% of glomeruli were abnormal 28 days after partial infarction and contralateral nephrectomy and thereafter the percent of abnormal glomeruli increased. Detectable amounts of immunoglobulin and complement (C3) were present in kidneys of stage II or III rats but were always accompanied by more extensive albumin and fibrin deposits. Basement membrane deposits characteristic of immune complexes were not seen on EM. Administration of antihypertensive medication to stage III rats significantly lowered blood pressure and reduced the number of abnormal glomeruli on LM; however, IFM abnormalities remained prominent. Platelet thrombi seen by EM and abundant glomerular fibrin deposits seen on IFM suggested that coagulation mechanisms may be prominent in the pathogenesis of the renal lesion. Heparin-treated stage III rats had significantly lower blood urea nitrogen concentrations, blood pressures and proportion of abnormal glomeruli although glomerular deposition of serum proteins was still present on IFM. These observations suggest that this glomerulopathy is initiated by an unknown agent(s) which increased capillary permeability. This lesion progresses via thrombotic mechanisms which are prevented by heparin administration.
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PMID:Pathogenesis of the glomerulopathy associated with renal infarction in rats. 94 Feb 76

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

No differences were found at the 30th week of pregnancy in total body water, serum sodium, potassium, chloride and osmolality, plasma volume, total protein concentration, intravascular protein mass, serum albumin concentration, intravascular albumin mass, and urinary estriol and pregnanediol in 94 primigravidae who remained normotensive, 35 who developed mild preeclampsia, and 23 who developed severe preeclampsia (i.e. hypertension and significant proteinuria in the third trimester). In twin pregnancies no differences were found between 13 primigravidae who remained normotensive and nine who subsequently developed proteinuria and hypertension.
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PMID:Changes preceding the development of preeclamptic toxemia. 95 65

An unusual electrophoretic pattern of the urine from a patient with malignant lymphoma was observed. One of the major proteins, identified Zn-alpha2-glycoprotein (Zn-alpha2), was isolated from the urine and partly characterized. The Stokes radius was found to be 3.24 nm and the molecular weight, determined by sodium dodecyl sulfate polyacrylamide electrophoresis, 42,000. The plasma level in healthy individuals was 39 +/- 7 (SD) mg/liter. In 12 of 25 healthy individuals, Zn-alpha2 was measurable in the urine and was found to be 1.0 +/- 1.1 mg/liter. In 23 patients with chronic glomerulonephritis (CGN), in 9 with proximal tubular dysfunction (PTD), in 23 with various renal diseases (VRD), and in 10 with malignant lymphoma, the plasma level and the urinary excretion were compared with those of albumin (mol wt 67,000) and of the retinol-binding protein (RBP, mol wt 21,000). A close correlation was found between the urine-to-plasma (U/P) ratios of Zn-alpha2 and albumin in the patients with CGN, whereas in the PTD patients the U/P ratios of Zn-alpha2 and RBP were correlated. No significant renal arteriovenous difference in Zn-alpha2 could be demonstrated. The Zn-alpha2 excretion was increased also in two patients with malignant lymphoma and proteinuria of a tubular pattern. The plasma Zn-alpha2 varied inversely with the glomerular filtration rate in the patients with renal disease, but was normal in those with malignant lymphoma. The results are consistent with the assumption of a sieving coefficient of Zn-alpha2, substantially exceeding that of albumin, but notably lower than that of smaller low-molecular-weight proteins. An increased excretion of Zn-alpha2 may be due to increased glomerular permeability as well as to defective proximal tubular reabsorption.
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PMID:Renal handling of Zn-alpha2-glycoprotein as compared with that of albumin and the retinol-binding protein. 98 27

Compared with a group of normal pregnant women, matched for age, parity, posture, and length of gestation, women with hypertension and proteinuria in the last trimester had significantly lower plasma concentrations of renin, renin substrate and angiotensin II. Plasma aldosterone and DOC concentrations were also lower in the hypertensive group. The plasma levels of cortisol, corticosterone, and ADH showed no significant difference. Plasma renin concentration was raised throughout normal pregnancy, and part of this increase appeared to be due to the presence of an inactive form of renin. Plasma concentrations of renin substrate, angiotensin II, and aldosterone were also raised in normal pregnant women, but concurrent measurement of these substances showed no significant relationship between them, renin, and plasma electrolytes in mid- or late gestation. A study of five women in the weeks immediately after conception showed increases in plasma angiotensin II and aldosterone concentrations, which were significantly related at this very early stage of pregnancy. Total 24-hour urinary sodium increased gradually from about two weeks after gestation to the end of the study five weeks later. This increase was due mainly to a rise in overnight sodium excretion, with a fall in the day/night ratio. No relationship was found between plasma angiotension II or aldosterone concentrations and day, night, or total 24 hour sodium excretion.
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PMID:Studies of the renin-angiotension-aldosterone system, cortisol, DOC, and ADH in normal and hypertensive pregnancy. 100 39


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