Proteinuria characterization

These studies led to the realization that proteinuria— the abnormal appearance of protein in the urine— could result not only from the enlargement of submicroscopic holes in the glomerular capillary wall, but also from the loss or neutralization of its negatively charged components. This finding has provided a new direction for research on the molecular basis for the nephrotic syndrome, a group of kidney diseases all characterized by massive proteinuria. 

In all forms of glomerular nephritis in tropical populations in Africa, there was increased protein in the urine. In the selective proteinuria of the nephrotic syndrome most of the protein was mainly albumin and transferrin, with lower concentrations of IgG and other globulins. On the other hand, the urine of the nonselective proteinuria of the nephrotic syndrome is characterized by much higher concentrations of IgG, IgA, a2-macroglobulins, and some IgM. Differential protein clearance to establish selectivity of proteinuria has been discussed above. 

Renal toxicity - Renal toxicity may be characterized by decreased creatinine clearance, cells or casts in the urine, decreased urine specific gravity, oliguria, proteinuria, or evidence of nitrogen retention. Renal damage is usually reversible. The relative nephrotoxicity of these agents is estimated to be Kanamycin = Amikacin = Gentamicin = Tobramycin Streptomycin. 

This syndrome is characterized by proteinuria >3.5 g/day, hypoalbuminuria <3 g/dl, hyperlip-idaemia with an elevation of serum cholesterol, edema and oval fat bodies and fatty casts in the urinary sediment. A variety of disorders may produce nephrotic syndrome but, in the majority of cases, no cause is found. It is appropriate to define the selection of studies from the history and physical examination. Tests to order are antinuclear antibody, rheumatoid factor, cryoglobulins, serum complement, HBsAg VDRL serology (syphilis), protein electrophoresis of the serum and urine and HIV. If the cause is unclear a renal biopsy is done to define the glomerular lesion as treatment may on the underlying glomerular lesion. 

Nephrotic syndrome is characterized by proteinuria and edema due to some form of glomerulonephritis. The resulting fall in plasma protein concentration decreases vascular volume, which leads to diminished renal blood flow. This in turn causes secondary aldosteronism characterized by Na and water retention and K+ depletion. Rigid control of dietary Na is essential. Therapy of the nephrotic syndrome using a thiazide (possibly with a K -sparing diuretic) to control the secondary aldosteronism, is a useful initial approach to treatment Since nephrotic edema is frequently more difficult to control than cardiac edema, it may be necessary to switch to a loop diuretic (and spironolactone) to obtain adequate diuresis. 

The nephrotic syndrome, characterized clinically by proteinuria, is a rare and idiosyncratic reaction to lithium. As with other uncommon adverse effects, the issue of causation versus coincidence must be considered. Treatment includes cessation of the drug and, when necessary, corticosteroids such as prednisone ( 322). 

Nephrotoxins Hie tenn refers to a specific target organ characterization of effect. Nephrotoxins are chemicals which produce kidney damage. Signs and symptoms are edema and proteinuria. Examples are halogenated hydrocarbons and uranium. 

Homozygotes or compound heterozygotes are characterized by the occurrence of corneal cloudings, which after the third decade become apparent upon physical examination. In addition, patients with classical LCAT deficiency develop renal disease with proteinuria and hematuria, which progresses to terminal renal insufficiency and hemolytic anemia [58,85]. 

Congenital nephrotic syndrome of the Finnish type is clinically characterized by heavy proteinuria present already in utero, which leads without nephrectomy and renal replacement therapy to the death of the affected children usually before the second year of life. Electronoptically, the glomerular basement membrane seems to be intact with the fusion of the podocyte foot processes. The chemical composition of the glomerular basement membrane is normal in patients with congenital nephrotic syndrome and all genes of the main proteins of the glomerular... 

Renal Effects. Case studies were located regarding renal effects in humans after oral exposure to chromium(VI) compounds. Acute renal failure, characterized by proteinuria, hematuria, followed by anuria, developed in a chrome plating worker who had accidentally swallowed an unreported volume of a plating fluid containing 300 g chromium trioxide/L. He was treated by hemodialysis (Fristedt et al. 

Glomerular lesions, such as those found in diabetes and glomerular nephritis, are characterized by basement membrane thickening and an increase in collagen-like substances within the mesangial regions that ultimately lead to proteinuria. Protease inhibitors prevent thickening of the basement membrane and reduce proteinuria. 

Kawasaki et al. (1992) induced crescentic glomerulonephritis with a small dose of nephrotoxic serum in WKY rats, which was characterized by the early infiltration of CD8 positive cells in glomeruli. In vivo depletion of CD8 positive cells completely prevented proteinuria and crescent formation. 

Chronic renal failure may develop in patients with poorly controlled diabetes mellitus and is characterized by heavy proteinuria, weakness, tiredness, nausea and abnormal concentrations of creatinine, electrolytes and urea (uraemia) in blood. There may also be symptoms of headache and neurological changes. 

AIN is characterized by fever, eosinophilia, hematuria, mild proteinuria and skin rash occur an average of 15 days after exposure (range 2-40). Rising serum creatinine concentration and acute renal failure with oliguria develop in about 50% of AIN cases, especially in older patients. Histologically, interstitial granulomas and variable degrees of tubular necrosis may be seen on renal biopsy. 

The nephrotoxicity of (3-lactams, such as cephaloridine, is characterized by decreased glomerular filtration rate, proteinuria, enzymuria, urinary granular casts, impaired abihty of renal cortical shces to accumulate organic ions and to synthesize glucose [27]. 

BenderWL,Whelton A, BeschornerWEetal. Interstitial nephritis, proteinuria, and renal failure caused by nonsteroidal anti-inflammatory drugs. Immunologic characterization of the inflammatory infiltrate. American Journal of Medicine 1984,-76 1006-1012. 

Compound A is nephrotoxic in rats at thresholds estimated at 180 ppm/hour [67]. Renal toxicity is characterized histologically by proximal tubular cell degeneration and necrosis in the corticomedullar region of die kidney and biochemically by proteinuria, glucosuria, and enzymuria (NAG and a-GST) with increased serum creatinine and BUN concentrations occurring with severe toxicity [67-70]. 

HIV nephropathy is characterized by heavy proteinuria, large echogenic kidneys on ultrasonography and... 

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