Other patients eat well and only use the tube for medicine or supplemental feeds. The tube is also useful for patients needing to drink large amounts of fluids around the time of transplant.While infants with infectious causes of congenital nephrotic syndrome may improve with antibiotics or antiviral medications, those with genetic causes progress to end-stage renal disease and require dialysis, and ultimately a kidney transplant. Prognosis
Congenital nephrotic syndrome can be successfully controlled with early diagnosis and aggressive treatment including albumin infusions, nephrectomy, and medications. Affected children have rapid decline in kidney function resulting in end-stage renal disease within the first years of life, and require treatment with dialysis and kidney transplantation. Most children live fairly normal life post-transplant but will spend significant time hospitalised pre-transplant and have numerous surgeries to facilitate treatment. Kidney transplantation outcomes for children with congenital nephrotic syndrome are similar to those of other patient groups. Nephrotic syndrome typically does not reoccur following kidney transplantation, however recurrences have been seen in children with NPHS1 mutations who develop anti-nephrin antibodies.Due to the protein (albumin) losses many patients have reduced muscle tone and may experience delays in certain physical milestones such as sitting, crawling and walking. Similarly many patients experience growth delays due to protein loss. Delays vary from mild to significant but most patients experience growth spurts once they receive their transplanted kidney. Physical therapy may be useful for the child to strengthen muscle tone.
Congenital nephrotic syndrome is a rare kidney disease which manifests in infants during the first 3 months of life, and is characterized by high levels of protein in the urine (proteinuria), low levels of protein in the blood, and swelling. This disease is primarily caused by genetic mutations which result in damage to components of the glomerular filtration barrier and allow for leakage of plasma proteins into the urinary space. Signs and symptoms
Urine protein loss leads to total body swelling (generalized edema) and abdominal distension in the first several weeks to months of life. Fluid retention may lead to cough (from pulmonary edema), ascites, and widened cranial sutures and fontanelles. High urine protein loss can lead to foamy appearance of urine. Infants may be born prematurely with low birth weight, and have meconium stained amniotic fluid or a large placenta. Complications
Frequent, severe infections: urinary loss of immunoglobulins
Malnutrition and poor growth
Blood clots (hypercoagulability): imbalance of plasma coagulation factors from urine protein loss
Hypothyroidism: urinary loss of thyroid-binding protein
Poor bone health associated with vitamin D deficiency: urinary loss of vitamin D binding protein
Acute kidney injury
Chronic kidney disease and ultimately end-stage kidney disease

Causes
Primary (genetic) causes
Mutations in the following five genes account for greater than 80% of the genetic causes of congenital nephrotic syndrome:
NPHS1 (Finnish Type): The gene NPHS1 encodes for the protein nephrin. This genetic variant is characterized by severe protein loss in the first several days to weeks of life.