Biochemical Signs and Clinical Symptoms of Nephrotic Syndrome

Biochemical Signs and Clinical Symptoms of Nephrotic Syndrome 

Nephrotic syndrome is a life-threatening disease. Adult patients may die of thromboembolic complications and children may die of infections, and persistent nephrotic syndrome confers a substantial risk of progression to end-stage renal failure. 

Hypoalbuminemia is a consequence of increased glomerular filtration of albumin. Loss of albumin is caused both by the loss of albumin into the urine (albuminuria) and by the reabsorption of albumin in the proximal tubule, which is mostly accompanied by its degradation. Increased tubular degradation of albumin may explain severe hypoalbuminemia in patients with only relatively moderate proteinuria, ca 3.5-4 g/day. Synthesis of albumin in the liver of nephrotic patients 

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. 

Long-lasting hyperlipidemia probably contributes also to the progression of chronic renal insufficiency (W5), possibly due to lipid (lipoprotein) deposits in 

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