Term Paper: Nephrotic Syndrome

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[. . .] Focal segmental glomerulosclerosis (FSGS) is the scarring of the glomeruli in random scattered patterns or in specific areas. Biopsies, which are typically suggested to determine diseased kidneys, are difficult as a diagnostic tool in the case of FSGS. Repeated biopsies become necessary in the hope of retrieving scarred renal tissue, since it is non-uniformly dispersed. This is one condition that is idiopathic in nature. There is no known associated disease (or causes as described above) for FSGS. Nephrotic syndrome is diagnosed through proteinuria.

While diabetic nephropathy is the commonest cause of Nephrotic Syndrome, membranous glomerulopathy (nephropathy) is the second highest cause of nephrotic syndrome. As in FSGS, more than seventy five percent of patients that present MG have no associate causes.

The rest show MG from diabetes, lupus, immune deficiency disease and cancer. MG is said to have been caused by the deposition of immunglobulin G. And C3 in the glomeruli. MG is progressive. Approximately 20 to 40% of the cases end in ESRD. Most show remission. Or, even in case of progression of disease do not see renal failure. A significant proportion of the patients recover even without treatment. How to treat a patient, and how aggressively to do so is often a matter of debate. Steroids, ACEs and ARBs are varyingly used to treat membranous glomerulopathy.

Minimum change disease (MCD) is glomerular disease that afflicts children more than it does adults. In MCD, a biopsy of a diseased portion of tissue does not a significant change from normal tissue. In some cases, small amounts of lipids (fats) may be present. But no scarring is observed. The origins of MCD are indeterminate. It is idiopathic in nature. Steroids are not often prescribed for MCD. A changed diet often helps. Also, ARBs ACEs and other anti-inflammatory drugs also help. (EdREN, 2004)

Amyloidosis, which is the stiffening of kidneys due to excess protein deposits often affects the elderly.

Effects of Nephrotic Syndrome

Let's consider the ill effects of nephrotic syndrome. These effects were alluded to in the first paragraph of this work. They are proteinuria, hematuria, hypoproteinemia and edema. Proteinuria, as described above is a high preponderance of protein in the urine. A person with normal kidney function loses approximately 150 mg of protein in one day. Contrast that with a person with proteinuria whose average protein excretion (through the urine) is more than three grams per day. This number can rise up to more than 25 times normal protein secretions. These proteins improperly filtered into the urine are essential to the normal functioning of the body. Proteins are built from units called amino acids. They are essential for functions, which are varied and involuntary. Breathing, muscle control, the clotting of blood, the balance and functioning of the immune system all depend on proteins. Proteinuria is often specifically called albuminuria. That is because of the albumin, which is a relative smaller protein. It can pass through the glomerular layers easily if the latter is damaged. Larger proteins may be blocked and are not detectable unless the damage in the glomeruli is significant. A qualitative test to test for proteinuria and nephrotic syndrome and other kidney diseases often detects the presence of albumin. In fact, microalbuminuria (detection of small amounts of albumin) is a precursor to proteinuria. (Weiner, 2004)

One might suppose therefore depending on the levels of proteinuria, large amounts of albumin is lost. The function of albumin is to retain water in the blood. This water retention maintains the blood volume. It acts as a sponge does. Edema, the secretion of salts away from the blood and tissue and retention in areas where it causes discomfort, is therefore a consequence of the loss of albumin. The blood volume decreases due to the loss of albumin. The body perceives this loss and retains more salt. In order to maintain concentrations, fluid moves into these areas to combat this excess salt. This causes fluid retention. Also, due to inefficient filtration, excess sodium is sometimes retained in the blood and consequently, so is fluid. Edema is evident if the person afflicted, not realizing this consumes more salt than the body can excrete. Edema is the result of this intake-excretion imbalance. While swelling in the ankles can result from edemas after a person is on their feet for extensive periods, edemas can also occur around the eyes. This is observed when the patient wakes up in the morning.

There are several reasons for hematuria. Some of these are as simple as bleeding due to exercise or external trauma to the kidneys. Hematuria occurs from nephrotic syndrome. This is because the damage to the glomeruli allows the blood to filter into the tubule. This blood shows up in the urine. A urine test generally reveals blood in the urine when it is invisible to the naked eye. On the other hand, in severe cases, the urine is the color of blood or a dark brown color.

Renal failure occurs due to the inefficient filtration of waste. This leads to the buildup to toxins in the blood and the tissue. The effects are varied, as are the levels of seriousness.

The symptoms of renal failure from acute nephrotic syndrome can be fatal unless dialysis or a transplant is not recoursed. Two primary waste products are creatinine and urea. Excess build up of these can lead to fatigue, weakness, loss of appetite and vomiting.

Acids that are not discarded can build up leading to metabolic acidosis. Phosphate waste when accumulated causes blood phosphate to increase decreasing the level of other calcium salts, as that can be used to strengthen bones. Thus, bone brittleness can result. The body can decrease its production of erythropoietin. This can result in anemia. The resulting edema can result in complications that include breathlessness. (Weiner, 2004)

While the short-term effects are used in the diagnosis of nephrotic syndrome and its underlying causes, the condition if remained unchecked can result in acute or chronic renal problems. Eventually, end stage renal failure may occur. The previous section indicated how PSGN could result in nephrotic syndrome. Acute renal failure will occur within a short time after the throat or skin infection in PSGN. Dialysis is often called for in these cases. Though the effects of acute renal failure are not lasting, it can devolve into Chronic Renal Failure.

Acute renal failure, while it lasts, is extremely dangerous and can be life threatening. Chronic renal failure, on the other hand takes longer to manifest. Chronic renal failure leads to end stage renal failure. It is incurable and the only way to slow down the failure is to treat the problems that may have caused it. Chronic renal failure is due to the destruction of nephron function. Nephrons once destroyed cannot be regenerated. End Stage Renal Failure means that kidney function has completely shut down. Kidney function can only be treated by a transplant or dialysis. In dialysis, there are two types. The most common is hemodialysis where the blood is circulated outside the body. It is outside the body that the blood is divested of wastes. Dialysis has to be performed about thrice a week for three to four hours at a time. (Kidney-Failure-Symptoms, 2003)

Recent Studies

The previous two sections have shown that the exact mechanism for and from Nephrotic Syndrome is not known, especially in patients that present symptoms from idiopathy. This section is devoted to recent studies without a specific theme. These studies contribute information that will enable researchers to understand the complex renal processes in nephrotic syndrome better

Exactly how the filtration occurs is also a matter for debate. We know that smaller proteins such as albumin can flow through the damaged pores. Recent studies have also shown that the glomerular membrane not only acts as a size filter but also as a shape filter. In addition, the charge presented by the molecule being filtered is also an important consideration. According to the authors, the filtration should not be considered as a static process, but dynamic depending on the type of molecule it needs to filter. Studies conducted on normal rats showed that different components of the glomerular membrane are responsible for specific functions. The glomerular capillary wall is responsible for the filtration. The podocytes are responsible to size filtration. Podocytes are epithelial cells that mix of the glomerular cells. These cells are branched. The branches are called pedicles and the branches infiltrate the glomeruli creating a network.

This interconnection creates the slits through which molecules escape into the urine or are retained in the blood. The endothelial cell coat is responsible for charge filtration. (Ohlson, 2000)

The responsibility of podocytes in the size filtration is becoming more and more evident. Four proteins have been recently discovered through genetic engineering. These are podocin, alpha-actin, CD2AP (CD2 Associated Protein, which is a binding protein) and nephrin as major components of podocytes. Problems arising from… [END OF PREVIEW]

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Nephrotic Syndrome.  (2004, February 29).  Retrieved May 25, 2019, from https://www.essaytown.com/subjects/paper/nephrotic-syndrome/8682200

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