Protein Loss In Nephrotic Syndrome Biology Essay


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Hyperlipidemia in conjugation with albuminuria and hypoalbuminemia is a cardinal feature of nephrotic syndrome (NS). Hyperlipidemia has been postulated to result from a coordinate increase in the synthesis of both albumin and lipoproteins as well as from their decreased catabolism. Present study was planned to evaluate serum cholesterol level in children with nephrotic syndrome and to correlate it with their serum albumin level and urinary protein excretion. Forty children comprising of 26 male and 14 female, who were clinically diagnosed as nephrotic syndrome were included in the study. Exclusion criteria were any systemic illness or signs of liver diseases, diabetes, thyroid dysfunction, or familial hyperlipidemia. The patients had normal serum creatinine level (0.89± 0.28 mg/dl). The mean serum albumin concentration (g/dl) was 1.78 ± 0.38, the serum cholesterol (mg/dl) was 166 ± 22.78 and urinary protein loss 5.3 ± 1.31 (g/day). The serum total cholesterol correlated moderately with urine protein (r= +0.618, P< 0.00002) but not with the serum albumin level (r =- 0.097, P= 0.551). The data suggest that the renal loss of protein may have some role in the deranged cholesterol metabolism seen in nephrotic syndrome.

KEY WORDS: Nephrotic syndrome, Proteinuria, Serum cholesterol, Serum albumin.


The main pathogenic abnormality in nephrotic syndrome is an increase in glomerular capillary wall permeability, resulting in pronounced proteinuria. Hyperlipidemia with increased cholesterol and triglyceride levels is a typical feature of the nephrotic syndrome (NS)(1,2) and it is not known whether it is a consequence of proteinuria or whether it arises secondarily from other effects of proteinuria such as reduced plasma oncotic pressure or hypoalbuminemia. The hyperlipidemia in nephrotic syndrome has been postulated to result from increase in the synthesis of lipoproteins, as well as from their reduced clearance from the circulation.(3) The hypoproteinemia is thought to stimulate hepatic protein synthesis which is responsible for both overproduction of lipoproteins and albumin.(4,5), Studies have tried to correlate total cholesterol with low plasma levels of albumin or degree of proteinuria, some have led to contrasting results and some did not show significant relationship.(6,7,8) In this context, present study was done in children with nephrotic syndrome to evaluate the relationship between serum total cholesterol with serum albumin and with the amount of protein excreted in urine.


Forty children comprising of 26 males and 14 females (age: 8.4 ± 4.9 years) clinically diagnosed as nephrotic syndrome were included in the study. A random urine protein-creatinine ratio of 3 and more were included in the study. (9) All patients had normal renal excretory function. Exclusion criteria were any systemic illness or signs of liver diseases, diabetes or thyroid dysfunction. The study was approved by the Institutional ethical committee and informed consent was obtained from the parents of participants of the study.

Serum albumin, serum cholesterol, and creatinine were measured using standard laboratory procedures.(10,11,12) Urinary protein was estimated by the method of Melemans O.(13) Urine creatinine by Jaffe's method .(14)

Statistical analysis:Association between study variables was assessed by Karl Pearson's correlation coefficient and student 't' test was used to test its significance. Level of significance was kept at .05.


Table 1 shows serum cholesterol and albumin levels, urine protein excretion and the correlation analysis in nephritic syndrome children. The total serum albumin concentration was 1.78 ± 0.38 g/dl, the total serum cholesterol was 166 ± 22.78 mg/dl and urine protein 5.3 ± 1.31 g per day. The serum total cholesterol correlated moderately with urine protein (r= +0.618; P= 0.00002) shown in figure 1.There was no statistically significant correlation between serum cholesterol with the serum albumin level (r = -0.097; P= 0.551).


Hyperlipidemia in nephrotic syndrome is postulated to result from a combination of reduced clearance of lipoproteins from circulation and increased hepatic synthesis of lipoproteins. (2,3) In our study there was no association between serum albumin and serum cholesterol, whereas there is a moderate positive correlation between serum cholesterol and urinary protein loss.

The mechanism causing hypercholesterolemia in nephrotic syndrome is complex and not fully understood. Earlier studies suggested that the hyperlipidemic state associated with the nephrotic syndrome might arise from reduced catabolism of apo B-containing lipoproteins (VLDL and LDL).(15,16,17) A defect in the conversion of LDL and VLDL cholesterol to HDL cholesterol has been suggested by Gitlin and Cornwell (18) and the LDL and VLDL values may increase with a corresponding decrease of HDL values.(19) Cohen et al(20) postulated that there is a loss of LCAT in the urine of nephrotic patients and this diminished LCAT activity, which catalyses the esterification of cholesterol may play a role in the altered lipoprotein metabolism in the patients.

The causal relationships between disturbances in the metabolism of albumin and apo B containing lipoproteins are not clear. Early workers in the field suggested a hypothesis that a general increase in hepatic protein synthesis is responsible for both overproduction of lipoproteins and albumin.(4) Hypoalbuminemia leads to a lack of carrier for the transport of fatty acids and this is compensated by an increase in fractions linked to lipoproteins. Hypoalbuminemia leads to an increased stimulus for synthesis of proteins and of LDL, and VLDL cholesterol by the liver.(19)

A second mechanism proposed for the increased hepatic production of apo B containing lipoproteins in nephrotic syndrome is related to reduced albumin concentration in plasma. Hypoalbuminemia is associated with a reduction in plasma oncotic pressure and the hepatic oversynthesis of apo B-containing lipoproteins may result in response to low oncotic pressure.(21) However, other studies revealed that the overproduction of apo B-containing lipoproteins does not constitute a constant feature in nephrotic patients(22) and is a drawback to the above mechanism.

Study of Demant et al(23) suggested that hyperlipidemia in nephrotic syndrome is predominantly the result of delayed lipoprotein delipidation and catabolism and there is no evidence that it is driven by a general increase of the rate of hepatic protein synthesis.

It appears that proteinuria and hypoalbuminemia both have some role in the development of hyperlipidemia. Proteinuria positively correlates with the serum total cholesterol. Atherosclerosis is a progressive condition that starts early in childhood and is accelerated in the presence of risk factors.(24) Hyperlipidemia is said to be one of the risk and is needed to be monitored.

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