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The pathophysiology of Nephrotic syndrome figure 4
According to the results of the tests, the patient syndrome is caused by either of the two; minimal change and focal segmental glomerulosclerosis. The pathophysiologies of the disease are primary glomerular defect and circulating permeability factor and inhibitors. The primary glomerular defect of nephrotic syndrome leads to leakage of high molecular mass proteins that’s equivalent to the size of albumin of approximately 66 kD, with haemostatic proteins of a similar size also being excreted pathologically in the urine (Eddy AA and Symons JM, 2003). Due to these excretion; prominent loss of important coagulation regulatory proteins such as antithrombin and protein S.
As mentioned above; Hypoalbuminaemia is a predominantly events that occur due to losses of protein urinary. In response to this, hepatic albumin synthesis increased but they are still insufficient to prevent the fall in the serum albumin concentration. Proteinuria, Nephrotic range proteinuria is almost invariably due to glomerular disease.
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Some nephrotic syndrome occurs in known pattern while others occur in differentiable patterns that can be characterized by proteinuria levels above 3.5 g per day and lipiduria. Patients with advance or other diseases such as edema and hyperlipidaemia (mature nephrotic syndrome) normally have numerous marked glomerular leaks than patient with proteinuria occurrence alone.
Other tests to confirm these diagnoses are; microscopy midstream urine, culture and sensitivities to the excluded urinary tract infection. Full blood count and coagulation screening can also be carried out. Renal function tests and biopsy under ultrasound. ESR and CRP, immunoglobulins, serum and urine electrophoresis, autoimmune screen if suspected (for autoantibodies and complement levels), and hepatitis B and hepatitis C, can all be carried out to check for other systemic diseases and nephrotic syndrome.
According to Machuca et al (2009); the urinary losses of macromolecules present in nephrotic syndrome replicates the dysfunction rate of the permselective glomerular filtration barrier. Genetic studies produced a results that led to the identification of the proteins involve in slit-diaphragm signalling, regulation of actin cytoskeleton dynamics, responsible for the maintenance of the podocyte integrity and for cell matrix interactions. Evidence indicated the link between minimal change nephropathy and Hodgkin’s disease indicating evidence that interleukin 13 (IL - 13) is an autocrine growth factor responsible for the Reed Stemberg cells. This result shows that IL-13 correlate with the induction of structural changes in podocytes which are capable of alteration in the selectivity of the filtration in patients leading to nephrotic syndrome.