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| Year : 1985 | Volume
: 31
| Issue : 3 | Page : 140-5 |
Study of hyperlipidemia in adults with nephrotic syndrome.
Khanna UB, Nerurkar SV, Almeida AF, Taskar SP, Acharya VN
How to cite this article:
Khanna U B, Nerurkar S V, Almeida A F, Taskar S P, Acharya V N. Study of hyperlipidemia in adults with nephrotic syndrome. J Postgrad Med 1985;31:140 |
How to cite this URL:
Khanna U B, Nerurkar S V, Almeida A F, Taskar S P, Acharya V N. Study of hyperlipidemia in adults with nephrotic syndrome. J Postgrad Med [serial online] 1985 [cited 2023 Sep 23];31:140. Available from: https://www.jpgmonline.com/text.asp?1985/31/3/140/5396 |
An increased risk of coronary artery disease has been described in patients of nephrotic syndrome.[2],[5],[7],[13] It has also been noted that certain factors like diet, malnutrition, genetic traits etc., are known to alter the frequency and severity of lipid pattern. The Indian patient has a different dietary, constitutional and genetic background. Hence, we undertook a study to determine the spectrum of lipid abnormalities in our adult patients of nephrotic syndrome. An attempt was made also to correlate the degree of proteinuria and hypoproteinemia, with the rise in serum lipid values in cases of nephrotic syndrome. A group of nonnephrotic. proteinurias was selected to study the impact of mild to moderate proteinuria, due to various renal diseases, on the lipid levels. LCAT has been incriminated in the pathogenesis of hyperlipidemia in nephrotic syndrome[6] and hence, its estimation was carried out.
Thirty patients of proteinuria, followed up in the nephrology department of the K.E.M. Hospital, Bombay, were studied. Twenty healthy volunteers who were age and sex matched were also included in the study for comparison. Of the 30 adult patients of proteinuria, 20 had proteinuria of nephrotic range (group 1) and 10 had proteinuria of non-nephrotic range (group II). The criteria for nephrotic syndrome was proteinuria of more than 3 gm/day or 100 mg/kg/day with total serum proteins of less than 6 gm% and serum albumin of less than 3 gm%. The group of nonnephrotic proteinuria comprised patients having a 24 hour urinary protein excretion ranging from 0.5 to 3.0 gm/day. These patients had diseases like interstitial nephritis, post-streptococcal glomerulo-nephritis etc. A detailed history and clinical examination was done and other causes of secondary hyperlipidemia were ruled out. Diabetic patients, alcoholics, obese patients and patients who were on drugs known to alter the lipid profile were excluded. All patients were stable, had a good oral intake, no vomiting and were not azotemic. A detailed dietetic history was obtained with special reference to their carbohydrate and lipid intake. Biochemical tests to determine levels of serum proteins, blood sugar, creatinine and electrolytes were carried out. All patients were subjected to renal biopsy. A 24 hour urinary protein excretion was estimated by Esbach's method. Blood was collected after an over-night fast of 12 hours in a heparinised test tube and the following lipids were estimated by standardised methods as mentioned below: (1) plasma cholesterol (Abell et al).[1] (2) plasma triglycerides (vanHandel et al).[16] (3) lipoprotein electrophoresis was performed on agarose gel using barbitone buffer. (4) lecithin cholesterol acyl transferase (Rose and Juliano).[14]
The three groups studied were age and sex matched [Table - 1]
Group I patients had significantly elevated serum lipid values when compared with Group III [Table - 2]. The lipids which were found to be elevated were serum cholesterol (p < 0.001), triglycerides (p < 0.001), phospholipids (p < 0.05), LDL cholesterol (p < 0.001) and VLDL cholesterol (p < 0.001). HDL values were, however, significantly low in the group of nephrotic syndrome patients (p < 0.001).
LCAT values showed no significant difference in the three groups studied. There was no significant difference in the lipid values of Group II and Group III.
The study of the relationship of dietary fat to the lipid abnormality in nephrotic syndrome revealed no significant difference of serum lipids in the two subgroups with different fat intake [Table - 3].
Type IIb variety of hyperlipidemia (Friedrikson's classification) was seen in 50% of patients. The other common pattern was type IV which was seen in 25% of cases. Type V was seen in only 5% of cases while type Ha and type III were each encountered in 10% of cases.
In patients of nephrotic syndrome the severity of proteinuria correlated positively with serum cholesterol (r = + 0.620) and with serum triglyceride (r = + 0.604) [Table - 4].
Severe hypoalbuminemia was found to be associated with increased lipid changes [Table - 5] Serum albumin correlated inversely with serum triglycerides (r = - 0.604) and serum cholesterol (r = - 0.620).
Hyperlipidemia forms an important component of nephrotic syndrome. In keeping with the results of two western studies,[4],[12] all our patients of nephrotic syndrome had hyperlipidemia. However, the western studies differed from ours in one important aspect: the average lipid values in our study in both the patients of nephrotic syndrome as well as control subjects were lower than those observed by the western workers.[3],[4],[11],[12] This difference in the lipid pattern could be due to different dietetic patterns of Indian people as regards to the carbohydrate and fat content of the diet. It is well known that a high-carbohydrate, low-calorie, low-fat diet lowers cholesterol and triglyceride values.[17] Moreover, fibre content in the diet, genetic factors, physical activity and habits like smoking and drinking in a particular population can alter the lipid spectrum.
The lipid profile in our nephrotic patients revealed a significant, elevation of serum total cholesterol, esterified cholesterol, triglycerides and phospholipids. The LDL and VLDL cholesterol values were elevated but HDL cholesterol values were significantly low. This low value of HDL cholesterol predisposes an individual to atherogenesis. An increased risk of coronary artery disease has been demonstrated in some studies.[2],[13]
Chopra et al[4] reported a series of 17 nephrotic patients with hyperlipidemia. Twelve of these had a type IIb variety of Friedrikson's hyperlipoproteinemia classification. In contrast, in another study from the Mayo clinic,[12] the pattern of lipoprotein profile fell into equal groups among types IIa, IIb and V. Of the, 20 nephrotic patients in our study, 50% had type IIb pattern. Type I was not seen at all. Type IV, which is the commonest abnormality in patients with chronic renal failure, was less commonly seen (25% of cases only).
Our nephrotic patients showed a strong positive correlation between the degree of proteinuria and the lipid values. In fact, patients with severe nephrotic syndrome exhibited lactescence of the serum. Nonnephrotic patients such as those with chronic renal failure etc., did not reveal any hyperlipidemia, probably implying that a significant degree of proteinuria leading to hyproteinemia is needed for the development of hyperlipidemia.
Serum albumin levels also were found to be negatively correlating with cholesterol and triglycerides. A similar finding was also obtained by some western workers[4],[9],[12],[15] and in one Indian study by Katiyar et al.[10] 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. Also synthesis of lipids and albumin takes place in the liver. Hypoalbuminemia leads to an increased stimulus for synthesis of proteins and of LDL, and VLDL cholesterol by the liver. Gitlin and Cornwell[8] take into consideration, a defect in the conversion of LDL and VLDL cholesterol to HDL cholesterol. Thus, LDL and VLDL values may go up with a corresponding decrease of HDL values, as also seen in our study. The role of lipoprotein lipase in nephrotic syndrome is less than in chronic renal failure as is seen by the decreased incidence of fasting chylomicronemia in ours and other studies. Cohen et al[6] postulated that there is a loss of LCAT in urine of nephrotic patients and this diminished LCAT activity (which catalyses the esterification of cholesterol) is blamed as the likely modulator of lipid values. In the present study, however. LCAT levels were not altered and hence they could not be incriminated in the altered lipid patterns noted in our nephrotic patients.
| 1. | Abell, L. L., Levy, B. B., Brodie, B. B. and Kendall, F. E.: Simplified method for estimation of cholesterol. J. Biol. Chem., 195: 357-366, 1952.  |
| 2. | Berlyne, G. M. and Mallick, N. P.: Ischaemic heart disease as a complication of nephrotic syndrome. Lancet, 2: 399-400, 1969. |
| 3. | Castelli, W. P., Cooper, G. R., Doyle., J. T., Palmieri, M. G., Gordon, T., Holmes, C., Hulley, S. B., Kagan, A., Kuchmak, M., McGee, D. and Vicie, W. J.: Distribution of triglyceride and total LDL and HDL cholesterol in several populations. A cooperative lipoprotein phenotyping study. J. Chron. Dis., 30: 147-169, 1977. |
| 4. | Chopra, J. S., Mallick, N. P. and Stone, M. C.: Hyperlipoproteinemia in nephrotic syndrome. Lancet, l: 317-321, 1971. |
| 5. | Chugh, K. S.: Nephrotic syndrome. In, "API Text Book of Medicine." Section 6, Chapter, 5, 3rd Edition, API Publications, Bombay, 1979, pp. 408-412. |
| 6. | Cohen, S. L., Cramp, D. G., Lewis, A. D. and Tickner, T. R.: The mechanism of hyperlipidemia in nephrotic syndrome. Role of low albumin and the LCAT reaction. Clin. Chim. Acta, 104: 393-400 1980. |
| 7. | Curry, R. C. Jr. and Roberts, W. C.: Status of the coronary arteries in the nephrotic syndrome. Analysis of 20 necropsy patients aged 15-35 years to determine if coronary atherosclerosis is accelerated. Amer. J. Med., 63: 183-192, 1977. |
| 8. | Gitlin, D. and Cornwell, D.: Plasma lipoprotein metabolism in normal individuals and in children with nephrotic syndrome. Paper presented at the 48th Annual Meeting of the American Society of Clinical Investigations, Atlanta City, 1956. J. Clin. Invest., 35: 706. 1956. |
| 9. | Heymann, W., Nash, G., Gilkey, C. and Lewis, M.: Studies on the causal role of hypoalbuminemia in experimental nephrotic hyperlipemia. J. Clin. Invest, 37: 808-812, 1958. |
| 10. | Katiyar, G. P., Singh, C. K., Agarwal, K. N. and Singh, R. N.: Study of serum lipid pattern in nephrotic syndrome in children. Indian Paediatrics, 13: 83-88, 1976. |
| 11. | Nerurkar, S. V., Iyer, I. and Taskar, S. P.: Apolipoprotein B in normolipemic and hyperlipoproteinemic subjects from the city of Bombay. J. Postgrad. Med., 28: 13-17, 1982. |
| 12. | Newmark, S. R., Anderson, C. P., Donedeo, J. V. Jr. and Ellefson, R. D.: Lipoprotein profiles in adult nephrotics. Mayo. Clin. Proc., 50: 359, 1975. |
| 13. | Porro, G. B. and Bianchessi, M.: Ischaemic heart disease complicating nephrotic syndrome. Lancet, 2: 804, 1969. |
| 14. | Rose, H. G. and Juliano, J.: Regulation of plasma lecithin-cholesterol acyl transferase in man. I-Increased activity in hypertriglyceridemia. J. Lab. and Clin. Med., 88: 29-43, 1976. |
| 15. | Rosemann, R. H., Friedman, M. and Byers, S. 0.: The causal role of plasma albumin deficiency in experimental nephrotic hyperlipemia and hypercholesterolemia. J. Clan. Invest., 35: 522-532, 1956. |
| 16. | van Handel, E. and Zilversmit, D. B.: Micromethod for direct determination of triglycerides. J. Lab. and Clin. Med., 50: 152-157, 1957. |
| 17. | Vishwanathan, M., Snehalata, C., Ramachandran, A. and Shobha, R.: The effect of calorie-restricted, high-carbohydrate, high-protein, low-fat diet on serum lipids in diabetes. J. Assoc. Phys. India, 26: 162-168. 1978. |
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