Nephrotic Syndrome Research Paper

Both of our kidneys functions to filter and excrete waste products and toxins by regulating fluids, electrolytes, and acid based balance. If the Renal blood flow is altered then the glomerular filtration rate will be altered as well. A decrease in systemic pressure stimulates the sympathetic nervous system to constrict the renal artery and decreases filtration and secretion in the kidney. In addition, a tubular obstruction can lead to the reduction of Glomerular filtration rate. An elevated intracellular calcium level due to tubular damage may alter cellular level that increases tubuloglomerular feedback and diminishes GFR. This may be prerenal, intrarenal, or postrenal. The prerenal will result from any condition outside of the kidney that disables the blood to flow to the renal vasculature causing a decrease in perfusion in the glomerulus leading to oliguria. However, both of the kidneys can still return to its full normal function on this stage. Second of the three is intrarenal, where anything can cause a direct damage to both of the kidneys such as infections, toxins, reduce blood supply, hypertension, diabetes, and even glomerulonephritis. The most common intrarenal condition is Acute Tubular Necrosis, where the epithelial layer of the nephrons are damaged causing a change in the concentration of urine, waste filtration, and an imbalance in electrolytes and acid

Capsular hydrostatic pressure (CHP): hydrostatic pressure exerted by fluid within the capsular space of the glomerular capsule, and blood colloid osmotic pressure (BCOP): osmotic pressure resulting from plasma proteins, oppose the GBHP and create the net filtration pressure (NFP) of 10mmHg under normal conditions. This pressure promotes filtration of water and solutes (Jenkins, Kemnitz and Tortora, 2010). However with the drop of GBHP, the NFP will drop and even the small supply of blood that had not bypassed and entered the capillaries will not be filtered. Change in pressure and levels of solutes will affect other levels such as concentration gradients of solutes and osmotic pressure within the peritubular capillaries, interstitial fluid and renal tubules, which are vital during tubular reabsorption and secretion. As a result, nephron function will

Facial swelling or edema is one of the signs and symptoms of APGN. It is happened because the kidney gets rid of less water in the form of less urine. As the kidney become less able to remove extra fluid, fluids build up in the body, causing periorbital or generalized edema associated with degrees of malaise, lethargy, anorexia, and not feeling good. The dark urine or hematuria is due to blood in the urine because the inflammation is allowing the leakage of red blood cells into the urine. The edema, or the hematuria is the most common clinical presentation that caused patient to seek medical care. Hypertension is another serious sign of APGN. The complications of high blood pressure such as: headache, dizziness, vomiting or even seizures that bring attention to the presence of the diagnosis. The cause of hypertension is most likely due to retention of sodium and water with resulting expansion of the extracellular space. The presence of one or all of the following signs in a child indicates the diagnosis of

Mr Goodpasture’s presentation can be explained through the pathophysiology of ESRD. The glomerular capillary membrane becomes damaged allowing proteins to escape from the blood to the glomerular filtrate (Bullock & Hales, 2013; LeMone et al., 2013). This explains the presence of protein in his urine. Due to the decrease in plasma proteins, the oncotic pressure decreases resulting in oedema (Bullock & Hales, 2013; LeMone et al., 2013). Due to the decreased protein and subsequently increased filtrate, the renin-angiotensin system (RAAS) is activated (Bullock & Hales, 2013; LeMone et al., 2013). Due to the oedema in the tissue, there is a decrease of blood volume (Bullock & Hales, 2013; LeMone et al., 2013). This leads to a decrease of glomerular filtration pressure and further stimulates RAAS (Bullock &

When arteries bring blood to the nephrons in the kidneys, material dissolved in the plasma is able to be filtered and reabsorbed, making nephrons the functional unit of excretion. The glomerulus is a ball of small blood vessels that filters out salts, urea, amino acids, water, and glucose into the Bowman’s capsule (a collecting

In a study of this phenomenon, they argued that vasopressin should normalize water absorption in terms of increasing the permeability of the distal tubule and collecting duct cells to water (Soren Nielson et al. 1997) and in doing such, would increase the concentration of AQP2 along the apical membrane of distal tube and collecting ducts (Soren Nielson et al. 1997). Such was the backbone of credence that let to their study that CHF may be a counter consequence of

Such factors may include cardiovascular diseases, kidney stones, sepsis and other factors which affect the normal function of the kidney (Neyra., 2015).

antidiuretic hormone (ADH) in the distal convoluted tubules. Therefore, resulted into ANP pathway turning off ADH, renin and aldosterone. At T=30 to T=90, there was increase in urine flow rate for drinking group which increased in plasma volume and blood, decreased in aldosterone concentration and plasma vasopressin (Evans, et al., 2009). Additionally, increment in urine flow rate, Atrial natriuretic peptide (ANP) attributed to the increase in the Glomerular filtration rate (GFR) and glomerular permeability; Atrial natriuretic peptide (ANP) had a direct contribution to the increase of radius and the large glomerular pores (Theilig, Wu. 2015). The Glomerular filtration rate (GFR) rate increased as the surface area of the capillaries increased.

Sodium and potassium transport can be related to kidney function and dialysis. The level of potassium is managed by the kidneys. A balance has to be maintained between sodium and potassium. The main organ that controls the balance is the kidney. By removing excess potassium in the urine, the balance of potassium is controlled. For those that have a kidney disease, some may be told by the doctor to avoid foods that are high in potassium. Kidney losses

The second compensatory mechanism is increased preload via renal conservation of sodium and water that is caused by the activation of the renin-angiotensin-aldosterone system. Increased blood volume means improved venturical filling and thus causing increased stroke volume, which increases the pressure exerted on the artery walls. Prolong increase stroke volume can overwork the heart and lead to hypertrophy. In addition, the increased extracellular volume expansion can lead to dilutional hypoproteinaemia, exacerbate third

Kidney disease and diabetes tend to go hand in hand as the kidneys of diabetics slowly thicken and become progressively scarred over time. The nephrons, which are the basic functional and structural units of the kidneys, become leaky and allow albumin, a protein made by the liver, to pass freely into the urine. The damage to the kidney may be ongoing for many years before a patient becomes symptomatic and loses the ability to filter the blood, control the fluid balance of the body and remove waste products.

The prognosis of nephrotic syndrome depends the sensitivity to the corticosteroid treatment, the underlying cause and the patient factors. Patients who are sensitive to corticosteroid treatment have a good prognosis and their risk to develop renal failure is small, while in the other hand patients who are resistant to corticosteroid treatment have a poor prognosis and they have a high risk up to 50% to develop renal failure. The second factor is the cause of nephrotic syndrome for example idiopathic membranous nephropathy is one of the primary form of the NS and the most common type, it has an appropriate prognosis in general and the prognosis can follow one of three pathways, one is a good course with high rate of cure from the disease, another one the patient may develop edema with normal renal function and the last one may progress to renal failure within 10

When the nephron is compromised, it is unable to perform the many functions required of it. Twenty percent of the blood contents get filtered through the glomerular capillaries. The blood contains water and electrolytes, protein and sugar. The body filters about 180 liters of blood per day and the

All the forms of diabetes have chronic hyperglycemia as common symptom which leads to the development of many of diabetes-specific disorders. These include microvascular disorders (due to the damage to small blood vessels) affecting vessels of retina, renal glomerulus, peripheral nerve and/or accelerated atherosclerotic macrovascular disorders (due to damage to larger blood vessels) affecting arteries that supply the heart, brain and lower extremities (Fowler, 2011). The microvascular pathologies make diabetes a leading cause of blindness, end-stage renal disease and a variety of unbearable neuropathies (Control et al., 1993; Turner et al., 1998).

Kidney diseases are one of the major concerns in the USA and with this, thousands of Americans currently on the national waiting list for a deceased donor. Patients can wait for years to find a compatible donor, and for the more sensitized patients the waiting is long. For sensitized patient the transplantation is a nightmare, because even if they find a living donor candidate willing to give away a kidney, the recipient may not be able to receive the transplant due to the incompatibility of their donors. The shortage of kidney and many other organs for transplantation is the key factor that prolongs the waiting time, which is up to 5 years, and some patients may never receive the an organ. The shortage of deceased donors increased the demand of live- donors, which can be from a family member if lucky. However, not everybody has that opportunity to get it from a sibling and the demand from non- relative donors have increased even if they are a positive cross match or HLA incompatible (1). In Kidney transplant the best possible donor is one whose HLA is very closely matched to the recipient that would make it more likely for the transplant to work and not being rejected. The closer the family member the better options it would have the recipient to have a more compatibility with the donor and this is because HLA markers are passed on from parents to their kids with a 50% chance to match and 25% chance of matching for brothers and sisters. Reducing the mismatch HLA antigens