Substances filter from the glomerulus into the nephron through a selective barrier called the basement membrane. Substances move through the barrier on the basis of size and electrical charge. In the nephrotic syndrome the selectivity of this membrane is impaired and the glomerulus allows albumin to escape from the blood into the filtrate. Urine therefore tests positive for protein; the amount of protein lost is often described as massive. The loss of albumin interferes with the body’s ability to balance fluids between the various body compartments. Normally, albumin levels provide oncotic pressure that counterbalances the effect of hydrostatic pressure at capillary level. In effect, normal levels of albumin are necessary to maintain fluid within the vascular space. When albumin is lost in the filtrate, hypoalbuminaemia occurs and oncotic pressure falls. The effect is that hydrostatic pressure acts with minimum opposition, fluid shifts into the interstitial space and oedema results.

Sodium levels also play a role in oedema formation. Sodium retention occurs. Traditionally, it was thought that fluid shifts cause hypovolaemia, which triggers the renin-angiotensin mechanism, which, in turn, promotes sodium retention. An alternative view is that nephrotic syndrome causes a primary defect at the tubular level, and that this causes sodium retention (Orth & Ritz 1998).

Hypoalbuminaemia is one consequence of the nephrotic syndrome; hyperlipidaemia is another. The levels of cholesterol and triglycerides in the blood rise as a result of increased synthesis by the liver and decreased clearance by the kidneys. Although the exact mechanisms for this are unknown, the potential consequences are a cause for concern. High cholesterol levels have a known association with atherosclerosis and high triglyceride levels may also have atherogenic properties and can cause further renal injury (O’Donnell 2001).

Nephrotic syndrome should be suspected when a child presents with oedema and proteinuria. In the paediatric age group, urinary protein loss of 50 mg/kg per 24 hours or greater is a firm diagnostic criterion (Roth et al 2002a); other markers are hypoalbuminaemia and hyperlipidaemia. Diagnosis is usually made without resorting to biopsy during the initial illness. This approach is taken because the majority of children have idiopathic nephrotic syndrome and their biopsies reveal the same results: they demonstrate damage to the glomerular epithelial foot processes. This is called minimal change nephrotic syndrome. A biopsy is reserved for children who do not respond to treatment. Although biopsy in these cases is still likely to reveal minimal change nephrotic syndrome (International Study of Kidney Disease in Children 1978), a few will identify other microscopic changes that might signify a different approach to treatment and different long-term outlook.

Corticosteroids are used to treat nephrotic syndrome, prednisolone being the drug of choice. The standard course is 8 weeks. A typical protocol might be 2 mg/kg daily for 4 weeks, then 1.5 mg/kg on alternate days for 4 weeks. Some children will relapse and require long-term maintenance. The earliest predictor that suggests a relapsing course is the time it takes the child to enter remission after prednisolone treatment is initiated (Constantinescu et al 2000). The child on long-term maintenance may receive prednisolone daily or every second day. There is evidence that alternate day regimes may be more beneficial and produce fewer side effects (Hiraoka et al 2003). If the child is commenced on long-term maintenance then the parents must be aware of possible side effects, such as increased appetite, weight gain and cushingoid symptoms. Parents also have to know about possible psychological side effects. Anxiety, depression and difficult behaviour are all possibilities (Soliday et al 1999).

Some children may be resistant to steroid therapy and others may suffer unacceptable side effects because of prolonged use. These children are likely to be prescribed immunosuppressive or immunomodulator drugs such as cyclosporine A, cyclophosphamide or levamisole. All these agents are associated with significant potential adverse effects and there is no consensus as to which is the most appropriate (Durkan et al 2001).

Diuretics are reserved for treating substantial oedema. Furosemide (Lasix) a loop diuretic is commonly prescribed. It is used judiciously because it may result in hypovolaemia, which in turn might increase the likelihood of thrombosis. Albumin may be used in conjunction with furosemide if severe oedema and complications such as pleural effusion or ascites are present.

Distribution of hydrostatic and oncotic pressure across the pleural and peritoneal membranes is altered. Fluid may shift into the pleural space and cause a pleural effusion. It may also shift into the peritoneal space and cause ascites. Both conditions impair lung expansion and respiratory distress may result. Treatment involves administration of diuretics and albumin.

Children with the nephrotic syndrome are prone to infection; chickenpox is a particular threat. Chickenpox is caused by the varicella-zoster virus and can have devastating effects on an immune-suppressed child. The child’s immune status should be checked and, if not immune to varicella-zoster and exposed to chickenpox, then varicella-zoster immune globulin should be administered. Acyclovir prophylaxis may also be administered as an adjunctive (Goldstein et al 2000).

Peritonitis is also a potential threat. Any abdominal pain must be carefully assessed with this complication in mind. The causative organism is usually a pneumococcus and pneumococcal immunisation is recommended for all children. Penicillin prophylaxis may be given to some subgroups (McIntyre & Craig 1998).

The final complication is thromboembolism. Children are prone to both arterial and venous thrombosis. Disturbances in clotting and fibrinolytic systems occur; antithrombin III levels may be depleted and fibrinogen levels raised. High cholesterol and triglyceride levels and low levels of albumin are other risk factors. The presence of dehydration and the use of diuretic also increase susceptibility. Nurses should be cognisant of the features of deep venous thrombosis and pulmonary embolism. With regard to the latter, the development of tachypnoea should raise concern because this might be a sign of pulmonary embolism (van Ommen et al 1998). Thromboembolism requires immediate anticoagulant treatment.

As the activity above suggests, caring for a child with oedema is a major focus when caring for a child with nephrotic syndrome. Fluid balance is also important. Fluid intake is normally controlled, the child’s previous day’s input and output being two of the factors that influence the amount prescribed. Diets high in protein (to increase albumin) or low in protein (to rest the kidneys) have been used in the treatment of this condition but they tend to be ineffective. The current approach is to determine the child’s normal dietary protein requirements and ensure that these are met. Carbohydrate intake has to be sufficient to ensure that protein intake can be utilised appropriately and not used for energy purposes. Hyperlipidaemia is not generally a cause for concern during the initial illness. If the child does not respond to treatment and hyperlipidaemia becomes a chronic state, dietary measures such as reduced saturated fat and cholesterol intake are advisable. Medications to reduce cholesterol and triglycerides may also be recommended. Finally, because sodium levels may be elevated in the nephrotic syndrome, dietary sodium has to be controlled. Foods high in sodium should not be consumed and salt should not be added to foods during cooking or at meal times.

Measures must be taken to protect the child from infection and identify it if it occurs. To this end, visitors should be infection free and the number of visitors must be controlled. The child should also be observed for signs of infection such as cough, runny nose and sore ears. Temperature, pulse and respiration should also be recorded regularly.

Deaths due to the nephrotic syndrome are rare but do occur. These deaths are normally attributed to peritonitis and thrombus. Most children with idiopathic nephrotic syndrome respond within 10–14 days of treatment; of these, two-thirds will relapse. The parents need to know about this possibility and be in the position to recognise it. They should monitor the child’s weight and test urine for protein. These children will require repeated courses of steroids, often for a prolonged period of time. Most will return to normal, although it may take many years.

The pathogenesis of poststreptococcal glomerulonephritis is not fully elucidated. There is evidence that a streptococcal component becomes lodged in the glomerular basement membrane (Cu et al 1998); this is the ‘planted antigen’ theory. Antibodies then fix to the component/antigen, forming an immune complex. The immune complex triggers a second phase, which involves activation of complement. Complement triggers a cascade of events that result in glomerular inflammation. Glomerular capillaries become blocked and impairment of glomerular filtering function occurs. Protein and blood are lost in the urine. The glomerular filtration rate (GFR) falls and urine output diminishes. In some patients, the reduction in the glomerular filtration rate may be significant and the child may develop acute renal failure. The fall in the glomerular filtration rate results in sodium and water retention and the expansion of the blood volume. Body fluid is redistributed and oedema results. Hypertension also occurs. This is partially due to sodium and water retention but other factors are thought to be involved.

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The clinical severity of poststreptococcal glomerulonephritis is variable, with some children having mild disease and being asymptomatic (Tasic & Polenakovic 2003). When children have symptoms the onset is usually abrupt. The child suffers from haematuria, mild to moderate proteinuria and oedema. The degree of oedema varies. Mild periorbital oedema may occur or it may be more extensive. In some cases it may be severe with accompanying ascites or pleural effusion. Urine assumes a dark colour because of the presence of blood and protein. Urine output is diminished, some children are oliguric and, as mentioned above, may present with acute renal failure. Hypertension is common; this might be mild but can be severe. If severe, associated symptoms such as headache and visual disturbance occur. The child is usually fatigued. Anaemia, uraemia and hypervolaemia contribute to feelings of tiredness.

Diagnosis is made on history, examination and a number of investigations. Urinalysis reveals blood, protein and high specific gravity. Throat swabs (or skin swabs) may be positive for streptococcal infection. Blood samples are taken and examined for antibody to streptococci and their extracellular products (Lang & Towers 2001). Antistreptolysin O (ASO) is one example. The normal ASO is < 166 Todd units, in poststreptococcal glomerulonephritis this is raised. Blood is also examined for evidence of complement activity. A reduction in complement elements C3 and C4 are suggestive of poststreptococcal glomerulonephritis.

Antibiotics are administered to eliminate any persistent streptococcal infection; penicillin is the drug of choice. Hospitalisation is not always required but when hypervolaemia, oedema or hypertension are concerns the child is admitted.

Hypervolaemia and the resultant oedema make fluid balance an important focus. All input and output should be accurately documented. The child’s weight should also be recorded. Hypervolaemia and oedema can be addressed by restricting fluids and sodium intake. The child’s diet should not contain salty foods and salt should not be added. Dietary manipulation alone may be insufficient to deal with more severe problems and diuretics may be required. Loop diuretics such as furosemide act quickly and effectively.

Hypertension may be mild, moderate or severe. The frequency of recording will differ depending on the circumstance. The dietary measures and administration of diuretics taken to relieve oedema and hypervolaemia may be all that is required to reduce the blood pressure. If hypertension is not alleviated by these means then antihypertensive agents are employed. Severe rises in blood pressure require intravenous antihypertensive agents.

The prognosis of poststreptococcal glomerulonephritis is excellent (Kasahara et al 2001). Most children who develop the condition will recover, with blood pressure and renal function returning to normal. However, a small number of children do not recover and go on and develop renal failure (Baldwin et al 1974).

The ureters enter the bladder at an oblique angle on the posterior right and left lateral surface. The oblique course is continued through the bladder wall. Each ureter terminates in a ureteral orifice found at both sides of the upper level of the trigone. When the intravesical pressure is increased during micturition the detrusor muscle contracts and the intravesical section of the ureters are passively compressed. This valvular mechanism normally prevents reflux. The effectiveness of this mechanism is dependent on an adequate length of intravesical ureter (Belman 1997).

VUR predisposes to urinary tract infection because urine that is refluxed into the ureter(s) trickles back into the bladder, producing an increased urine residual, which provides the conditions for an infection to take place. Reflux then provides a route by which the infection can reach the kidney. Urinary tract infection with VUR is associated with renal scarring and is an important cause of hypertension and chronic renal failure in later life.

Prophylaxis is usually discontinued when reflux disappears. This can be expected between 6 and 10 years (Huang & Tsai 1995). Management also emphasises the importance of measures designed to minimise the likelihood of urinary tract infection. The parent/child is taught the importance of adequate fluid intake, appropriate wiping action, regular toileting, double voiding to expel refluxed urine, and avoidance of constipation.

Surgery is considered for patients with grade IV and V reflux. It is considered as an option because spontaneous resolution is less likely. Surgery is also considered when prophylaxis fails to prevent urinary tract infection or further renal damage. Open surgery involves re-implantation of the offending ureter or ureters. The aim of re-implantation is to create an adequate intravesical tunnel, to allow compression of the ureter against the detrusor muscle. The success rate of reimplanation is 95% (Birmingham Reflux Study Group 1984).