Nephrotic syndrome albumin levels

Hyperlipidemia (mainly hypercholesterolemia) is a regular part of nephrotic syndrome (K13, W6). Serum levels of cholesterol are often markedly elevated, usually above 10 mmol/L. However, in severely malnourished patients, normal or even decreased serum cholesterol level can be found. Serum levels of triacylglyc-erols fluctuate, from normal values to markedly elevated values (mainly in patients with proteinuria higher than 10 g/24 hr). There is a variable increase in plasma concentrations of very low density lipoproteins (VLDL, they correlate negatively with serum albumin level), intermediate-density lipoproteins (IDL), andLDL however, plasma concentrations of HDL are usually normal (J3). Levels of lipoprotein(a) [Lp(a)j are also increased (W4). Remission of nephrotic syndrome or decrease of proteinuria may result in the decrease of plasma concentrations of Lp(a) (G2). Concentration of free fatty acids in serum is commonly decreased because they are normally bound to albumin and albumin is lost into the urine. The activity of lecithin cholesterol acyltransferase (LCAT) is usually decreased. 

Albumin Maintains plasma oncotic pressure. Transports fat-soluble substances, e.g. bilirubin, drugs Reduced levels Low levels cause ascites and increase free plasma concentration of albumin-bound drugs, e.g. oestradiol, phenytoin Albumin is a useful clinical indicator of the liver s synthetic function. The liver produces and exports up to 12 g of albumin per day. Low levels are also seen in malnutrition, hypercatabolism and nephrotic syndrome. Half-life of 20 days, therefore indicator of chronic liver disease... 

When interpreting a patient s albumin level, possible extrahepatic causes for low levels should be considered, for example a reduction in albumin production associated with malnutrition and malignancy, or increased albumin loss seen in inflammatory bowel disease and nephrotic syndrome. 

Transferrin, fhe iron-transporting protein, occurs in urine at concentrations that are about 15 times lower fhan that of albumin. The protein has a shghtly larger effective molecular radius (around 4.0 run) than albumin (3.6 run). Its detection in fhe urine allows a more sensitive indicator of early glomerular involvement in some nephropathies such as cadmium nephropathy. A strong association has been found between the presence of albumin and transferrin in fhe urine of patients with fhe nephrotic syndrome. In these patients, increased transferrin synthesis is insufficient to compensate for urinary losses and plasma levels are reduced [94]. 

Quantitative assay of specific proteins is necessary for estimates of glomerular selectivity and for evaluation of tubular proteinuria. Nephelometry and turbidimetry are sufficiently sensitive for most of the analytes (see Chapters 3 and 9). More sensitive immunoassays are required for BMG because of the low levels that are typically excreted. In addition, this protein is susceptible to degradation at low pH, and specimens should be stored at a pH greater than 6.0 during the collection period. In assessment of the nephrotic syndrome, glomerular selectivity is estimated usually by measuring two individual proteins of different molecular size, such as albumin or transferrin plus IgG. A random urine sample and a corresponding serum are collected and analyzed for the two proteins. The ratio of the individual clearances is then calculated... 

Hypotransferrinemiacan result from protein malnutrition and accompanies hypoalbuminemia. Since transferrin has a much shorter half-life (8 days) than albumin (19 days), measurement of the transferrin level may be a more sensitive indicator of protein malnutrition than albumin measurement (see also chapter 17). Hypotransfer-rinemia also results from excessive renal loss of plasma proteins (e.g., in nephrotic syndrome). 

Low serum copper and ceruloplasmin levels are found regularly in the nephrotic syndrome with hypoproteinemia (C3, M12). These patients were found to excrete 46-75 mg ceruloplasmin per 24 hours in the urine, and this and perhaps the concomitant loss of albumin-bound copper most probably explain the development of hypoceruloplasminemia and hypocupremia in this condition. 

Signs of a nephrotic syndrome with significant albuminuria (0.3 to 0.5%) and a low serum albumin level (46.8%) were found in a two year-old affected child with marked central nervous system involvement by Zoepffel (1964) lipid chemical analyses were not performed in this case. 

Albumin formation is generally stated to take place solely in the liver. The available evidence, reviewed by Madden and Whipple (219), favors this view, but is not compelling, does not exclude other possibilities, and leaves unexplained a number of discrepancies which are noted in certain disease states, for example, the marked hypoalbuminemia observed in some instances of the nephrotic syndrome associated with relatively little albuminuria, and in so-called idiopathic hypoproteinemia. In both these conditions, the serum albumin may reach extremely low levels yet there is no impairment of hepatic function that can be demonstrated by available methods (which does not, to be sure, exclude the possibility of a specific hepatic defect such as occurs in connection with prothrombin formation and other hepatic functions). 

An important consequence of marked hypoalbuminemia is reduction of the osmotic pressure in the intravascular compartment and the formation of edema due to accumulation of fluid in the intercellular spaces, the osmotic pressure exerted by albumin constituting by far the largest counterforce to the hydrostatic pressure. There is no critical level of plasma albumin predisposing to edema formation, earlier views to the contrary. As indicated in the discussion of the nephrotic syndrome, the factors regulating water balance are too complex for any such simple relation. Further evidence of this is afforded by the observations of Keys et al. (140, 184) on production of starvation edema without significant hypoalbuminemia. 

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