Patient with Nephrotic Syndrome

Patient with Nephrotic Syndrome

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From the results of the numerous tests carried out according to the patient history of frothy urine with a significant oedema over a maximum period of 5 days, the patient was diagnosed with Nephrotic Syndrome. This is condition that occurs due to leakage in the kidney filtration part leading to a large amount of protein leaking from the blood into the urine. This is mainly due to fluid retention known as oedema which is as a result of low protein level in the blood. It occurs due to abnormal functioning or a part of the kidney is affected (glomeruli). This syndrome can be caused by numerous diseases coming together to cause or form one particular disease; these causes range from minimal change disease, membranous nephropathy, focal segmental glomerulosclerosis (FSGS) and other conditions, disorders of the glomeruli. The membranous nephropathy also known as the membranous nephritis or membranous glomerulonephritis, only causes diseases in adults and very uncommon in children. Leakage occurs from this due to the thickening of the membranous in the glomeruli which is the filter of the glomeruli. Focal segmental glomerulosclerosis is a causative due to the formation of small scars (sclerosis) on some of the kidney glomeruli. Another form of cause of nephrotic is minimal change which is due to lack of virtual change detected in the glomeruli when examined under the microscope. This causes the syndrome in 9 out of a total of 10 children under the age of 5 years.
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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Under normal circumstances the passage of most plasma proteins (particularly albumin) into the urine is prevented by the glomerular capillary wall (GCW). The GCW is a trilaminar structure comprised of fenestrated glomerular endothelial cells, the glomerular basement membrane (GBM), and podocytes. It is richly decorated throughout with an anionic glycocalyx which electrostatically repels negatively charged proteins. In addition, the structure of the GBM and the podocyte intercellular junctions (slit-diaphragms) restricts the passage of proteins according to molecular size. Oedema; Oedema is thought to result from two distinct mechanisms: Under-fill Model and overfill model. The under-fill model is most common in children in which reduction of the oncotic pressure helps in the promotion of the translocation of fluid from the body vascular part into the extracellular fluid section. When plasma volume decreases it’s stimulate the initiation of renin-angiotensin-aldosterone system, and also the discharge of vasopressin, resulting in the reabsorption of sodium and water in the distal nephron. Elevation of capillary hydrostatic pressure promotes further fluid movement into the extravascular compartment. While overfill model is due to defects in the secretion of sodium in distal nephron. The causes of the defects are yet unclear but guesses indicated that it may be related to the tubulointerstial inflammation that frequently complements proteinuria. The retention of sodium leads to an increased in the volume of blood that accompanies suppressed vasopressin and angiotensin or aldosterone levels. The increased intra-capillary hydrostatic pressure and the low oncotic pressure favours movement of fluid into the extravascular compartment. Finally retention of sodium that accompanies GFR reduction in patients with history of CKD or AKI can also contribute.
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.

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