There are essentially three treatment options for children with end stage renal disease.

First:  Medical management:

This may be chosen by the family. Under these circumstances, the chance for meaningful rehabilitation is the child is very limited. Therapy should be directed at providing maximum comport for the child with minimal invasive procedures. Hospice care may be appropriate. A child with a terminal neoplasia and chronic renal failure would be an example of such a situation.

Second:  Dialysis:

This may be instituted as a form of renal replacement therapy. There are two types of dialysis.

Hemodialysis:

This is usually performed in a dialysis center. Blood must be pumped from the patient’s circulation. Uremic toxins are removed usually by diffusion across a semipermeable membrane. Fluid is removed by ultrafiltration dependent upon a pressure gradient between the blood and dialysate. Children require artificial kidneys which hold less volume and have a controlled urea filtration rate. Artificial kidneys which remove uremic toxins too efficiently may produce dialysis disequilibrium and potentially cerebral edema. Dialysis lines are adapted to child to allow slower blood flow rates and hold less volume. Children usually do not tolerate more than 10% of their blood volume outside their body at any one time. Fluid removal (ultrafiltration) is also limited when the total extracorporeal blood volume is close to or exceeds 10% of the blood volume. When performed in-center dialysis sessions usually last from 3-4 hours three days a week. Hemodialysis may be performed at home in a stable patient with a partner. Then dialysis sessions may be performed more frequently for shorter periods to simulate normal renal function.

Peritoneal dialysis:

This is essentially always performed at home. A parent is trained in the dialysis technique. An older child or an adolescent is given increasing degrees of responsibility and may become completely independent. The technique is easier to learn than hemodialysis and requires less sophisticated equipment. Both toxins and water are removed by diffusion across the peritoneal membrane. The dextrose concentration of the dialysate is varied to remove more or less water. The dialysis is done nightly at home using an automated cycler. This technique is called continuous cycling peritoneal dialysis (CCPD). Sometimes a cycler is not used and dialysate bags are simply exchanged between pass. This is called continuous ambulatory peritoneal dialysis (CAPD). The process is less efficient than hemodialysis and hence there is virtually no danger of dialysis disequilibrium. Since peritoneal dialysis is done much more often and for longer periods it gives about the same degree of uremic control especially in smaller individuals.

Both methods require access created to the vascular system or to the peritoneum.

Access to the vascular compartment may be through a central catheter usually inserted into the jugular vein. An A-V fistula may be surgically created for cannulation. The most frequently used site is the radial artery and vein. Other fistulas may be created in the groin or upper arm. Synthetic grafts may be used (e.g. Gortex®) when vessels are not large enough. In peritoneal dialysis catheters are surgically inserted into the peritoneal cavity through the abdominal wall. Central catheters, A-V fistulas, and synthetic grafts may become clotted and are at varying degrees of risk for infection. Peritoneal dialysis catheters may become occluded with fibrin or omentum. They may also develop infections along the tunnel and at the exit sight. Peritonitis is a potentially serious complication of peritoneal dialysis. The bacteria are usually introduced by contamination during the set-up of the cycler or a bag exchange. They may also be introduced from a tunnel or exit sight infection. Infections of any of the various accesses for peritoneal and hemodialysis are always potentially very serious and can result in the loss dialysis assess. Also peritonitis especially recurrent episodes can result in loss of the peritoneal membrane for dialysis. All such infections must be treated promptly and sometimes require the removal of access devices.

Third:  Renal replacement. 

In addition to dialysis, renal replacement always involves calcium phosphorus balance. Most patients with advanced renal failure and those patients receiving dialysis therapy will need a phosphorus binder. Aluminum hydroxide is never used because of the potential for aluminum to be deposited in the central nervous system and in the bones especially in younger children. Calcium acetate and calcium carbonate may be given with meals and will bind phosphorus in the gut. Sevelamer has been recently introduced under the trade name of Renagel® and purportedly lowers phosphorus without raising the calcium level. It is not clear which is the better agent.

Calcium levels must be kept at a level sufficient to moderately suppress the parathyroid hormone level.

Too much suppression can result in depressed bone turn over rates and "dead bone" syndrome.

The anemia of chronic renal failure is usually amenable to erythropoietin therapy.

Erythropoietin may be given intravenously on hemodialysis or subcutaneously if the patient is on peritoneal dialysis. Iron supplementation is always necessary unless the patient has elevated iron stores. Hyperparathyroidism, intercurrent illness, iron depletion, and immunosupressents decrease the response to erythropoietin.

Caloric supplementation is sometimes necessary in infants and children with chronic renal failure.

Often infants have a feeding aversion and must be fed by NG tubes or feeding gastrostomies. GERD and delayed gastric empting may complicate the treatment.

If the problem of insufficient caloric intake and hyperparathyroidism is addressed, growth hormone may be necessary improve growth in the infant or child with chronic renal failure

Often large doses are necessary to produce growth. One must evaluate for aseptic necrosis of the femoral head and pseudotumor cerebrae.