Glomerulonephritis hematuria

The LCso for a 7-hour exposure of rats was 1480 ppm death was due to lung and kidney injury. Rabbits exposed to 800 and 1600ppm for 4—10 days showed irritation of the upper respiratory tract and lungs, severe glomerulonephritis, hematuria, and albuminuria. Oral doses of lOOmg/kg/day for 4 days produced hemorrhagic bone marrow, thymic... 

Microscopic examination of the sediment obtained from the centrifugation of a fresh urine sample wiU show the presence of a few cells (erythrocytes, leukocytes, and cells derived from the kidney and urinary tract), casts (composed predominantly of Tamm-HorsfaU glycoprotein [THG]), and possibly fat or pigmented particles. An increase in red cells or casts unplies hematuria, possibly caused by glomerular disease white cells or casts imply the presence of white cells in the tubules. Inflammation of the upper urinary tract may result in polymorphonuclear leukocytes and various types of casts, and in lower urinary tract inflammation the casts will not be present. In acute glomerulonephritis, hematuria may... 

Penicillamine onset may be seen in 1 to 3 months, and most responses occur within 6 months. Early adverse effects include skin rash, metallic taste, hypogeusia, stomatitis, anorexia, nausea, vomiting, and dyspepsia. Glomerulonephritis may occur, which manifests as proteinuria and hematuria. Penicillamine is usually reserved for patients who are resistant to other therapies because of the rare but potentially serious induction of autoimmune diseases (e.g., Goodpasture s syndrome, myasthenia gravis). 

GL/- White cells in urine proteinuria microscopic or gross hematuria nonspecific urogenital findings abnormal menses glomerulonephritis. 

Signs and symptoms of gold toxicity, the primary serious reaction, include decreased Hgb level, decreased granulocyte count (less than 150,000/mm ), proteinuria, hematuria, stomatitis, blood dyscrasias (anemia, leukopenia WBC count less than 4000/mm, thrombocytopenia, and eosinophilia), glomerulonephritis, nephrotic syndrome, and cholestatic jaundice. 

Fusion inhibitors are a new class of agents approved in the management of HIV infection. They bind to surface proteins on T-lymphocytes and prevent entry of the HIV virus. The only fusion inhibitor currently approved for use is enfuvirtide. Nephrotoxicity has not been reported with enfuvirtide, however, one patient with a previous history of proteinuria and hematuria was described to have developed membranoprolif-erative glomerulonephritis [158]. The cause and effect relationship of this event and the use of the fusion inhibitor remain unclear. 

Turpentine is a skin, eye, mucous membrane, and upper respiratory tract irritant in humans. It may also cause skin sensitization and adverse effects to CNS, gastrointestinal, and urinary tract. The lowest estimated oral dose reported to be lethal in humans is 441 mg kg Exposure to a 75 ppm concentration for 3-5 min irritates the nose and throat, and exposure to a 175 ppm concentration irritates the eyes and may be considered intolerable by human volunteers. Ingestion of turpentine causes a burning pain in the mouth and throat, nausea, vomiting, diarrhea, abdominal pain, excitement, ataxia, confusion, stupor, seizures, fever, and tachycardia and may cause death due to respiratory failure. Toxic glomerulonephritis and bladder irritation, with hematuria, albuminuria, oliguria, and dysuria, have been associated with overexposure to the vapor of turpentine in the past however, the more purified form... 

Proteinuria is a common finding in patients with kidney disease, and the use of a dipstick assay is an important screening test in any patient suspected of having renal disease. Among patients with suspected or proven CKD, including reflux nephropathy and early glomerulonephritis, and those with hypertension or previously detected asymptomatic hematuria, annual urinalysis for proteinuria is accepted as a useful way of identifying patients at risk of... 

Acute glomerulonephritis is associated with the sudden onset of proteinuria, hematuria, and the appearance of red cell casts in urine. Demonstration of the presence of red cell casts in the urinary sediment establishes the presence of active glomerular inflammation. Proteinuria is a characteristic finding in glomerulonephritis, with levels ranging from 0.5 to 3.0 g per day. Proteinuria in excess of 2.5 g per day characteristic of nephrotic syndrome are found in some cases of glomerulonephritis. 

Nephrotic syndrome characteristic of excretion of protein in urine in excess of 2.5 g per day is not present in most patients with glomerulonephritis. These patients may present with a reduced glomerular filtration rate and varying degrees of proteinuria with or without hematuria, a condition referred to as the nephritic syndrome. Patients with nephritic syndrome may recover or worsen with chronic renal failure. 

Herman [67] published a case report of a patient with hairy cell leukemia who developed membrano-prohferative glomerulonephritis during treatment with IFN-a. He developed hematuria, pyuria, and depressed complement levels. Renal biopsy revealed foot process effacement and subendothelial deposits. 

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