Protein intake nephrotic syndrome

The causes of human copper deficiency include (1) low intake - malnutrition, total parenteral nutrition (TPN) (2) high loss - cystic fibrosis, nephrotic syndromes and (3) genetic factors — Menkes disease. Copper deficiency may also be associated with chronic malabsorption, a situation which is made much worse in cases of gastric and bowel resection. Several special diets, including powdered milk, liquid protein and standard hospital diets are a means of inducing copper deficiency. The amount of copper in US food has decreased steadily since 1942, and may be related to the rising incidence of coronary artery disease. A copper deficiency may also occur as the result of the use of chelators for other purposes for example, diethyl dithiocarbamate is an in vivo metabolite of ANTABUSE (disulfiram). 

Albumin is synthesized primarily by the hepatic parenchymal cells except in early fetal life, when it is synthesized largely by the yolk sac. The synthetic reserve of the liver is enormous in nephrotic syndrome, it may be 300% or more of normal. The synthetic rate is controlled primarily by colloidal osmotic pressure (COP) and secondarily by protein intake. Synthesis is decreased by inflammatory cytokines, and release (but not synthesis) is decreased by hypokalemia. Catabolism occurs primarily by pinocytosis by aU tissue, with lysosomal catabolism of the protein and use of the resulting free amino acids for synthesis of cellular proteins. The rate of pinocytosis is proportional to the local tissue metaboHc rate. Small amounts (10% to 20% of the total catabolized) are also lost into the gastrointestinal tract... 

In patients with nephrotic syndrome, dietary measures involve restriction of sodium intake to 50 to 100 mEq/day, protein intake of 0.8 to 1 g/day, and a low-lipid diet of less than 200 mg cholesterol. Total fat should account for less than 30% of daily total calories. Sodium restriction is important not only in the control of edema, but also in the control of hypertension and proteinuria. Similarly, protein restriction not only helps to reduce proteinuria, but also has a potential role in retarding the progression of renal disease. Patients should also stop smoking because a dose-dependent increase in risk for developing ESKD was observed in men with primary inflammatory (IgA glomerulonephritis) or noninflammatory (polycystic kidney disease) renal diseases. ... 

Kidney dysfunction can lead to edema formation as a result of decreased formation of urine and the subsequent imbalance of water and electrolyte (e.g., sodium ion) homeostasis. Retention of salt and water results in an expansion of the extracellular fluid volume and, thus, edema formation. Thus, when salt intake exceeds salt excretion, edema can form. Edema formation also is associated with deceased protein levels in blood, as seen in nephrotic syndrome and liver disease. Cirrhosis of the liver leads to increased lymph in the space of Disse. Eventually, the increased lymph volume results in movement of fluid into the peritoneal cavity and ascites develops. 

---