Nephrotic syndrome is primarily a pediatric disorder and is 1.5 times more common in children than adults. 

The incidence is 2-3/100,000 children per year and majority of affected children will have steroid-sensitive minimal change disease. 

The characteristic features are heavy proteinurea >3-4+ /24 hr, hypoalbuminemia <2.5g/dl, edema and hyperlipidemia are often associated.

  Etiology: - approximately 90% of children with nephrotic syndrome have idiopathic causes. 

 Divided into 2 groups in children 1) MCNS (High proteinuria) and  2) Nephrotic syndrome with significance lesions (low proteinuria)

 

 MCNS protein urea pathophysiology: -  Undefined mechanisms alter the permeability of the glomerular filter, resulting in massive proteinuria.  Primary abnormality of the epithelial foot process (podocytes) 

A loss of negatively charge glycoproteins within the glomerular capillary wall. 

 MCNS Oedema Pathophysiology Resultant fall in plasma oncotic pressure leads to interstitial edema and hypovolemia, stimulates the renin-angiotensin aldosterone axis and antidiuretics hormone secretion enhances Na and H2O retention. 

 Investigation shows 3-4+ g/dl proteinuria ,Serum albumin low below 2.5g/dl, serum cholesterol and triglycerides level are elevated 

 Blood urea and creatinine within normal level except when hypovolemia and fall in renal perfusion. 

AIMS: - To study the efficacy of the kukkutanda basti in hypoalbuminemia of childhood minimal changes nephrotic syndrome. 

OBJECTIVE: -Prevention of complications due to  hypoalbuminemia. To study the role of Kukkutanda Basti in arresting or prevent the complication during the progression of childhood NS.