Patients with SRNS are more likely to have complications from their disease compared to those with steroid sensitive NS.

Haemostatic abnormalities encountered in these children include :

• Increased platelet aggregability, fibrinogen, and factors V, VII, VIII, X, and XIII.
 
• Decreased levels of antithrombin III, heparin cofactor, protein C and S, and factors XI and XII.
 
• Increased fibrinolytic system components (eg. tissue plasminogen activator, plasminogen activator inhibitor-1)

The majority of thrombotic events are silent and symptomatic disease is found in only about 30% of patients. However in a study by Hoyer et al [5], systematic ventilation perfusion scans demonstrated defects consistent with pulmonary embolism in 28% of patients with steroid dependant or resistant NS. Thrombosis can occur in both arteries and veins.

Pathogenesis

The pathogenesis of glomerulosclerosis is still unknown. Several factors, including hemodynamic factors, cytokines and growth factors, hyperlipidemia, and platelet activation, lead to an increase of mesangial matrix production by resident cells in patients with FSGS. These patients have glomerular hypertrophy even if typical findings of FSGS are absent. There are several growth factors involved in the sclerotic process including platelet derived growth factor, TGF-ß, angiotensin II, thromboxane A2, coagulation factors and lipids [6,7,8].