In nephrotic syndrome, large amounts of plasma proteins are lost in urine, causing a decrease in the plasma oncotic pressure. This leads to enhanced hepatic synthesis of albumin and other proteins, including lipoproteins, causing a secondary hyperlipidemia. Essential fatty acids such as gamma-linolenic acid (GLA) can prevent accumulation of cholesterol in the body, and spirulina has an appreciable amount of GLA. In this study 23 patients (age 2 to 13 years) with nephrotic syndrome received either medication (group I) or medication plus 1 g/day Spirulina (group II). Height, weight, and serum levels of fasting blood sugar, triglycerides, total cholesterol (TC), and low- and high-density cholesterol fractions (LDL-C and HDL-C, respectively) were measured before and after the 2-month study period. Mean height and weight were normal compared with healthy, age-matched Indian children. Lipoprotein cholesterol levels were significantly increased at baseline. TC significantly decreased by 116.33 mg/dl, LDL-C by 94.14 mg/dl, and triglycerides by 67.72 mg/dl in group II; in control group I, these values fell by 69.87, 61.13, and 22.62 mg/dl, respectively. The LDL-C:HDL-C ratio also decreased significantly, by 1.66 in group II and 1.13 in group I. TC:HDL-C decreased by 1.96 in group II and 1.19 in group I. HDL-C:LDL-C also improved significantly in both the groups. It can be concluded that spray-dried Spirulina capsules, rich in antioxidants, GLA, amino acids, and fatty acids, helped reduce the increased levels of lipids in patients with hyperlipidemic nephrotic syndrome.

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Homogentisic acid (HGA) spontaneously starts to undergo oxidation and polymerization soon after the beginning of incubation in human blood or plasma at 37 degrees C, and forms plasma soluble melanins (PSM). Haemolysis accompanies this process in blood. The addition of equimolar quantities of antioxidants delays this oxidation significantly (isoascorbic acid by 2:30-4:00 h; glutathione by 3:20-4:05 h; D-penicillamine by 5:00-5:45 h). HGA is a phenylalanine and tyrosine metabolite, related structurally to the catecholamines and other precursors of melanins. HGA is normally metabolized by the enzyme homogentisic acid oxidase. When this enzyme is genetically missing, part of HGA is excreted in the urine, another part polymerizes darkens many tissues (ochronosis), and produces widespread degenerative changes in cartilage and other connective tissues, joints, blood vessels, heart valves, kidneys and in other tissues. Collectively this disorder is known as alcaptonuria, for which no satisfactory treatment is known. The causes of both alcaptonuric arthritis and rheumatoid arthritis are thought to involve increased oxidative stress. Inflammation of joints and connective tissue damage are involved in both diseases. Oxygen radicals are suspected to cause inflammation and cellular damage. Hydroxyl radicals degrade hyaluronic acid (the viscous synovial fluid of joints). High levels of products of free radical reactions, with fluorescence excitation (ex) and emission (em) maxima in the wavelength ranges of those of PSM (ex 320-400 and em 400-470) were reported in the blood sera and synovial fluids of patients with rheumatoid arthritis.(ABSTRACT TRUNCATED AT 250 WORDS)