Glomerulonephritis

Nephrotic Syndrome, is when there is an increased in glomerular basement membrane permeability. This causes an excess loss of protein in the urine known as proteinuria. Congenital, idiopathic and secondary are forms of Nephrotic syndrome. Congenital nephrotic syndrome is rare, can be inherited and usually occur in Finnish families. Nephrotic syndrome is consider secondary if it occurs secondary to diseases like diabetes, systemic lupus erythematosus, or Henoch-Schonlein purpura. Idiopathic nephrotic syndrome, also known as minimal change nephrotic syndrome (MCNS) occurs mostly in kids with 70% occurring in kid 5 years old and younger. This paper will be focusing on MCNS (Kyle & Carman, 2013).

As the glomeruli are part of the filtration system in the nephron of the kidney, damage can hinder removal of waste products, salt and water from the blood stream. Progressive destruction of

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

A child with abrupt onset of acute kidney injury with a fever, rash, and a urinalysis with abnormal urinary sediment should be highly suspected of having acute interstitial nephritis (AIN). In 75% of cases, AIN is a drug-induced hypersensitivity reaction. It is characterized by the classic triad of fever, rash, and arthralgia, with acute renal dysfunction resulting from the infiltration and activity of inflammatory cells when the drug/antigen is exposed to the interstitium of the kidney. Medications commonly associated with AIN include nonsteroidal anti-inflammatory drugs (NSAIDs), antibiotics, diuretics, and proton pump inhibitors. Nonsteroidal anti-inflammatory drugs are the most common, the most studied, and possibly the most avoidable drugs that cause AIN-induced acute kidney injury. The mainstay of treatment of drug-induced AIN is to discontinue treatment with the offending drug as soon as possible and restore and/or maintain intravascular volume with isotonic fluids to maintain renal perfusion. Once adequate renal perfusion has been accomplished, close monitoring of fluid and electrolyte balance is of utmost importance.

The most telling is heavy proteinuria. This is when there is an excessive amount of protein in the urine. Asymptomatic proteinuria not in nephrotic range, can sometimes be the only sign of this condition. Microscopic hematuria, or blood in the urine, is occasionally present. Hypertension, renal dysfunction, swelling of the ankles and eyelids, rapid weight gain, foamy urine, fatigue, poor appetite, headache, itchy skin, shortness of breath, and nausea are some of the symptoms and signs that can point to a person having FSGS. The only way to know if your symptoms are related to FSGS is by first having a urinalysis done. The doctor will check your BUN (blood, urea, nitrogen) levels. For a normal kidney this level should be 7-20 mg/dL in adults, and 5-18 mg/dL in children. When kidney function decreases the BUN level

Haematuria, microscopic and macroscopic, is the earliest sign and is almost universal.In case of microscopic the disease may remain unnoticed for decades. Hypertension is also very common. Proteinuria can also occur but is usually a later feature. In many cases, there is slowly progressive loss of renal function leading to end stage renal disease. Clinical presentations are protean and vary with age. A particular hallmark of IgA nephropathy in young adults is the occurrence of acute self-limiting exacerbations, often with gross haematuria, in association with minor respiratory infections. This may be so acute as to resemble acute post-infectious glomerulonephritis, with fluid retention, hypertension and oliguria with dark or red urine. Characteristically, the latency from clinical infection to nephritis is short: a few days or less. Asymptomatic presentations dominate in older adults, with haematuria, hypertension and loss of GFR. Occasionally, IgA nephropathy

Similarly, patients with long-standing hypertension with hypertensive retinopathy and a family history of hypertension and CKD are likely to have hypertensive nephrosclerosis, particularly if urinalysis reveals minimal proteinuria and no hematuria22. It is worth noting that the presence of diabetes or hypertension does not rule out another cause of CKD, particularly since hypertension is a consequence of CKD. In addition, distinguishing between diabetic and hypertensive nephropathy is frequently challenging. However, a biopsy is usually not recommended because distinguishing between hypertension and diabetes as the underlying cause of CKD does not change management.

Synopsis: Acute Post-streptococcal Glomerulonephritis (APSGN) is the result of an antigen-antibody reaction where insoluble immune complexes develop and become trapped in glomerular tissue producing swelling and death of capillary cells. APSGN usually occurs after a latent period of one to three weeks following a sore throat or skin infection. It is occurs predominantly in children aged five to seven, and mainly affects boys than girls. The most likely cause of the throat infection in the six-year old child is due by a group A beta hemolytic streptococcal infection. The bacteria do not infect the kidney filters; it is the proteins from the blood that and proteins from the bacteria that injure the filers. He does not require treatment, as natural

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 &

Diabetic nephropathy (DN) refers to a characteristic set of structural and functional kidney abnormalities in patients with diabetes.1 It is the most important long-term complication of diabetes mellitus (DM). It is a progressive condition with high cardiovascular morbidity and mortality. It progresses in both Type 1 and Type 2 diabetes in a relatively predictable manner through the stages of normoalbuminuria, microalbuminuria and macroalbuminuria which often heralds increasing creatinine as the final manifestation of overt diabetic nephropathy.2 One study at BPKIHS has reported 16.6% prevalence of diabetic nephropathy.3 In another study done at BPKIHS among 177 Type2 DM patients, 14.69% had frank proteinuria, 44.64% had micro-albuminuria and 40.68% were without proteinuria.4 Diabetes nephropathy is now the most common cause of End Stage Renal Disease (ESRD) in United States accounting for 45%.5 From several studies it is seen that ESRD develops in 50% of Type 1 DM individuals with overt nephropathy within 10 years and in >75% by 20 years. In the absence of treatment a greater proportion with patient with Type 2 Diabetes compared with Type 1 Diabetes have microalbuminuria and overt nephropathy at or shortly after diagnosis of diabetes. This is because the disease may have been present for several years before

Glomerulonephritis is a group of kidney diseases in which the glomeruli of the kidney becomes inflamed. The glomeruli of the kidney filters protein and blood out of the incoming blood vessels and redistributes them back into circulation. In the case of Glomerulonephritis, the inflamed glomeruli are unable to redistribute the blood and protein back into circulation and thus is released in the urine. Glomerulonephritis is a broad term used for a few specific types of glomerular damage. The specific name is given once tissue samples are examined under a microscope and key features have been identified (www.hopkinsmedicine.org/nephrology/glomerulonephritis.html). While it cannot be used as definitive diagnosis, a few key symptoms can help to determine the tests needed for diagnosis. Commonly abdominal pain, diarrhea, excessive urination (polyuria), fever and edema of the ankles, feet, abdomen, and face (including eyes) are experienced. Once these symptoms have been evaluated by a doctor, a complete urinalysis would be requested in helping to diagnose the disease. With Glomerulonephritis protein (proteinuria) and blood (hematuria) would be found in the urine sample. (www.nlm.nih.gov/medlineplus/ency/article/000484.htm). If the urinalysis is returned positive with these findings a kidney biopsy will be performed. Positive confirmation of which type of Glomerulonephritis can then be made if the results of the biopsy show abnormal tissue and the result of the

Chronic kidney disease (CKD) is a long-term condition characterized by presence of kidney damage or a decrease of glomerular filtration rate (GFR) less than 60ml/min/1.73m2 for 3 months or longer periods (Levey, Bosch, Lewis, 1999). Kidney disease always being neglected as it was asymptomatic in the early stage. Chronic kidney disease was divided into 5 stages and according to its severity. The staging system is based on the estimated GFR and remaining kidney function. In each stages of chronic kidney disease, there is certain medical action and investigation need to be carry out to monitor the progression of disease. Medical practitioners can use this as basis guidelines to monitor the deterioration of kidney disease. Patient will increase severity of uremic and suffer from clinical manifestations of azotemia when GFR drop to less than 25% of normal (Schrier, 2010). When GFR drop to less than 15ml Stage 5 CKD patient need to be undergo renal replacement therapy, either dialysis or renal transplant in order to avoid complication such as uremic and fluid overload.

Nephrotic syndrome occurs when filtering units of the kidneys become damaged. As a result, protein which is usually kept in the plasma begins to leak into the urine in excessive amounts, which decreases the amount of protein in your body (Nephrotic Syndrome , n.d.). Nephrotic syndrome is caused by various disorders that can damage the kidneys. This damage results in too much protein being excreted in the urine. In addition to this, Nephrotic syndrome consists of various symptoms such as protein in the urine, elevated cholesterol levels, low blood protein levels in the blood, high triglyceride levels, and swelling. This condition can be diagnosed, upon arrival to the doctor’s office a physical exam will be performed. Laboratory tests will be

Chronic Kidney Disease (CKD) is among the leading causes of mortality throughout the world, and its prevalence and the health care costs resulting from it are considerable and increasing. CKD commonly is silent and asymptomatic until its late stages. Accordingly, CKD is diagnosed prior to symptomatic stage of kidney failure, resulting in delays in proper interventions and the emergence of adverse consequences in the CKD patients

“I would buy skates for myself instead!” I said these words when my friends approached me to make some contribution for the gift they were going to buy for one of my pal recovering from nephrotic syndrome. Later that week we went to see him (visualize) and he was so surprised to see all of us and was happy when he received a gift. He said (feeling) to me, “Thank you that is an amazing car I ever had”. I said (feeling), “Sorry I made no contribution to that gift.” He still thanked me for stopping by. I had a feeling of guilt and that inspired me to give him something to make him happy from my side. As days passed I observed one of my friend making a battery operated car and that inspired me to make one. I started making car so that I can give