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)

The clinical problems and results of urinalyses of 500 dogs were reviewed and summarized to compare the sensitivities for detection of abnormalities indicative of urinary system disease among qualitative (sulfosalicylic acid [SSA]), quantitative (Coomassie brilliant blue [CBB]), and indexed (urinary protein/creatinine ratio [U(P/C)]) determinations of urinary protein loss vs microscopic examination of urine sediment. False-negative rates for the detection of microscopically abnormal urine specimens were 5.4% for SSA greater than or equal to 1+, 8.5% for CBB greater than or equal to 1.0 mg/ml, 9.7% for U(P/C) greater than or equal to 1.0, and 7.7% for CBB + U(P/C). A discriminatory U(P/C) value of 2.0 would have excluded dogs with clinically relevant proteinuria in the lower ranges. Proteinuria was not detected in 4.4% (22/500) of the specimens in which important numbers of leukocytes or bacteria were observed. False-negative rates for combined interpretation of quantitative protein concentration and U(P/C) were not significantly different (P greater than 0.10) from SSA alone. Degrees of azotemia were higher (high serum creatinine concentration, P greater than 0.10 and high serum urea nitrogen concentration, P less than 0.05) and prevalence of chronically diseased dogs was greater (P less than 0.005) in dog categories with higher U(P/C) values. More quantitative determinations of urinary protein loss as a screening test offer potential labor-saving and diagnostic advantages in the identification of urinary disease over more qualitative routine screening methods.
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PMID:Comparison of urinary protein concentration and protein/creatinine ratio vs routine microscopy in urinalysis of dogs: 500 cases (1987-1988). 279 83

Dietary polyunsaturated fatty acid modulation exerts a beneficial effect in immune-mediated glomerulonephritis. To elucidate the mechanisms underlying this phenomenon, the effects of essential fatty acid (EFA) deficiency on the heterologous phase of nephrotoxic nephritis in rats (induced by the injection of a rabbit antiglomerular basement membrane antibody) were studied. The heterologous phase of nephrotoxic nephritis was characterized by an invasion of leukocytes into the glomerulus. Polymorphonuclear neutrophils predominated early on (3 h), whereas macrophages predominated at 24 and 72 h. EFA deficiency selectively prevented the influx of macrophages into the glomerulus. The invasion of polymorphonuclear neutrophils, in contrast, was unaffected. The influx of leukocytes into the glomerulus during nephritis was accompanied by a marked enhancement (10- to 40-fold) in glomerular thromboxane and leukotriene B4 production. EFA deficiency largely attenuated this change. Renal dysfunction during the heterologous phase of nephritis was manifested as azotemia, polyuria, sodium retention, and proteinuria. With EFA deficiency, polyuria, azotemia, and sodium retention were not seen. Proteinuria was reduced by approximately 85%. To address whether the lack of macrophage migration into the glomerulus in the context of nephritis with EFA deficiency might be due to a functional defect in macrophage migration, the chemotactic responsiveness of EFA-deficient macrophages was examined. EFA-deficient macrophages displayed normal chemotactic migration toward activated C. In sum, EFA deficiency prevents the invasion of macrophages into the glomerulus in nephrotoxic nephritis and attenuates the accompanying metabolic and functional alterations, but does not affect macrophage chemotactic responsiveness. Alterations in macrophage elicitation and lipid mediator generation by inflamed glomeruli thus appear to be central to the salutary effect of dietary polyunsaturated fatty acid modification on glomerulonephritis.
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PMID:The antiinflammatory effects of essential fatty acid deficiency in experimental glomerulonephritis. The modulation of macrophage migration and eicosanoid metabolism. 280 95

A 65-year-old man underwent left-upper lobectomy for large cell carcinoma of the lung on November 8, 1984 (pT1N0M0: Stage I a). He was treated with MMC, Futraful, CDDP and CPM as adjuvant chemotherapy. In April 1985, he was re-admitted to our hospital because of progressive dyspnea. He was diagnosed as having drug-induced interstitial pneumonia, and so steroid therapy was started. In July 1985, he suffered from anemia, thrombocytopenia, proteinuria and azotemia progressively, and died due to pulmonary hemorrhage and edema. At necropsy, no cancer recurrence was found. It thus seemed that the cause of death was microangiopathic hemolytic anemia and renal failure induced by anti-neoplastic agents.
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PMID:[Microangiopathic hemolytic anemia (MAHA) and renal failure induced by anti-neoplastic agents--a case report]. 303 22

A transplanted kidney in a patient developed focal and segmental glomerulosclerosis, associated with severe systemic hypertension, proteinuria, progressive azotemia, and allograft hypertrophy. A pediatric kidney with two main arteries was used, and occlusion of the artery supplying the upper pole resulted in infarction of this portion of the allograft. Because other known factors predisposing to focal sclerosis were absent, it is postulated that renal hemodynamic changes associated with reduction in functioning renal mass, attended by striking stimuli for renal hypertrophy, resulted in progressive damage. The implications of these concepts are discussed in relation to the progression of renal diseases.
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PMID:De novo focal glomerulosclerosis after kidney transplantation. 304 72

Acute renal failure is a most challenging clinical problem when it occurs in pregnancy. It requires an understanding of the normal physiology of the kidney in pregnancy and the natural history of different underlying renal diseases when pregnancy occurs. Because patients with chronic renal disease may present with worsening proteinuria, hypertension, and renal function, these disorders must be excluded from those conditions that cause acute deterioration of renal failure in otherwise normal women during pregnancy. As in all patients who develop acute renal failure, prerenal and obstructive causes must be excluded. Particularly important causes of prerenal azotemia in pregnancy include hyperemesis gravidarum and uterine hemorrhage, especially if it is unsuspected as in abruptio placentae. Infectious causes of acute renal failure in the pregnant woman include acute pyelonephritis and septic abortion. The clinical presentation of both these conditions should be apparent, and appropriate diagnosis and treatment can then be promptly instituted. Renal cortical necrosis is another cause of renal failure that occurs more frequently in pregnancy, and it must be differentiated from the many causes of acute tubular necrosis that may be associated with pregnancy. Those conditions that cause renal failure unique to pregnancy must always be considered when renal function deteriorates in the last trimester or the postpartum period. Severe preeclampsia, acute fatty liver of pregnancy, and idiopathic postpartum acute renal failure may all present similar complications, but the approach to each of these clinical disorders must be individualized. By understanding the causes of renal functional deterioration in pregnancy, a logical differential diagnosis can be established, allowing appropriate therapeutic decisions to preserve both maternal and fetal well-being.
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PMID:Acute renal failure in pregnancy. 305 11

Since their introduction in clinical practice in 1980, ACE inhibitors have been found useful in the treatment of hypertension and CHF. In hypertension, they are effective as monotherapy in 40% to 50% of the patients, and in combination with diuretics or calcium antagonists, they are effective in up to 85% of the patients. They are well tolerated, are not associated with depression, impotence, bronchospasm or metabolic derangements such as hypokalemia, hyperuricemia or hyperglycemia, and do not have adverse effects on the quality of life. As a result, they are preferred in hypertensive patients with CHF, left ventricular dysfunction, mental depression, older age, coronary artery disease, metabolic disorders, chronic destructive pulmonary disease, and peripheral vascular disease. In CHF they cause long-lasting hemodynamic and symptomatic improvement, improve exercise tolerance, and may lower mortality in certain patient subsets. Evolving new indications for ACE inhibitors include the diagnosis of renovascular hypertension, the prediction of surgical success, the treatment of scleroderma renal crisis, the reduction of proteinuria, renal protection, cardioprotection, the improvement of arterial compliance, in Bartter's syndrome and idiopathic edema, etc. ACE inhibitors are usually well tolerated but in some instances they may cause class-specific side effects such as hypotension; usually reversible azotemia or renal failure, especially in patients with renal artery stenosis or with CHF with low blood pressure; cough; angioedema; and hyperkalemia. Differences among ACE inhibitors are emerging and include chemical class (e.g., zinc ligand), biotransformation, potency, pharmacokinetics, prodrugs, tissue effects, additional pharmacologic properties, and drug interactions.
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PMID:Angiotensin converting enzyme inhibitors. II. Clinical use. 305 46

In four adults with idiopathic nephrotic syndrome and azotemia, percutaneous renal biopsy showed diabetic glomerulosclerosis, yet none had oral glucose tolerance tests diagnostic of diabetes mellitus or funduscopic evidence of diabetic retinopathy. Possible concomitant glomerular disease that may have produced proteinuria was excluded. Well documented cases of diabetic glomerulosclerosis without concurrent glucose intolerance are uncommon, and almost 30% of such patients have a past history of diabetes. Despite the absence of overt diabetes at onset of diabetic glomerulosclerosis, these patients warrant careful monitoring of plasma glucose levels and strict control of systemic hypertension.
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PMID:Diabetic glomerulosclerosis without concurrent diabetes mellitus. 305 23

The nephropathy complicating insulin-dependent diabetes mellitus (IDDM) has been well studied, but that complicating non-insulin-dependent diabetes mellitus (NIDDM) is less well defined. In patients with IDDM, the glomerular filtration rate is often increased early in the course of the disease, approaches normal with insulin therapy, but tends to remain slightly elevated throughout the ensuing 10-15 yr of insulin dependency. After the onset of overt azotemia, end-stage renal disease (ESRD) develops in approximately 5 yrs. Proteinuria may be intermittently positive in the earliest stages of diabetes, evolving into intermittent and then persistent microalbuminuria, which in turn blossoms into macroalbuminuria. Because 40-50% of IDDM patients develop proteinuria and two-thirds of this subpopulation develop ESRD, some 20-30% of any given cohort of IDDM patients eventually need dialysis or transplantation. Evidence indicates that diabetic nephropathy is associated with a greater incidence of eye, nerve, heart, and peripheral vascular disease. Nondiabetic renal disease complicating IDDM and NIDDM is associated with a lesser frequency and severity of these extrarenal manifestations. The prevalence of retinopathy increases with advancing nephropathy. Roughly two-thirds of the deaths from IDDM are related to renal failure, and most of the remainder are caused by associated cardiovascular disease. Transplantation from living relatives carries the best prognosis for survival, and little difference is seen between hemodialysis, peritoneal dialysis, and cadaver transplantation. The health-care costs of treating diabetic nephropathy are also reviewed.
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PMID:Clinical features and health-care costs of diabetic nephropathy. 307 74

Mild, transient proteinuria and azotemia were produced in three cynomolgus monkeys (Macaca fascicularis) and a chimpanzee (Pan troglodytes) following intravenous inoculation with Prospect Hill virus, a hantavirus isolated from meadow voles in the United States. This is the first demonstration of an acute nephropathy in nonhuman primates with the viruses causing hemorrhagic fever with renal syndrome.
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PMID:Experimental hantavirus infection in nonhuman primates. 313 14

Heavy proteinuria in patients with essential hypertension raises the question of underlying primary renal disease. While malignant hypertension may be associated with proteinuria in the nephrotic range, it is generally held that protein excretion in benign nephrosclerosis is almost invariably less than 0.5-1.0 g/24 h. We report 18 patients with biopsy-proven hypertensive nephropathy and heavy proteinuria, of which only 6 had malignant hypertension. In the remaining 12 patients with benign nephrosclerosis, protein excretion reached up to 6.5 g/24 h, and nephrotic range proteinuria was present in 3 patients. All patients with heavy proteinuria suffered from long-standing moderate or severe, poorly controlled hypertension and were azotemic. We suggest that hypertensive nephrosclerosis be included in the differential diagnosis of massive proteinuria accompanying azotemia in poorly controlled hypertensives.
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PMID:Marked proteinuria in hypertensive nephrosclerosis. 316 Feb 40


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