Glomerulonephritis : A Group Of Kidney Diseases

Injury to the glomerulus and the tubules presents the onset of Intra-renal failure (Matzke, 2011). Some of the frequent causes for Intra-renal failure are glomerulonephritis; pyelonephritis; and tubular injury. Post-renal failure develops from things like ureteroliths, tumors, or anatomic impediments. Opposite of the acute form, the chronic form has a slow onset that has no early stage symptoms. It is important to know that following an acute episode a chronic renal episode often follows, and at this juncture the damage is irreversible. Glomerulonephritis and pyelonephritis combined, has been reported to be the forerunner in as much as half the cases from acute to chronic renal failure. Diabetes mellitus, renal vascular disease, such as atherosclerosis, hypertension, polycystic kidney disease, drug damage, and nephrolith are all examples of other causes of CKD (Pradeep, 2014). Biopsies of kidneys that suffered with CKD reveal smaller kidneys with scarring on the tubules.

Nephritis is the inflammation of one or both kidneys. Causes may include: kidney conditions, lupus nephritis, neuropathy etc. Types of nephritis include: acute, chronic, glomerulonephritis, and autoimmune. Symptoms include: cloudy and bloody urine or reduced urine, and loin pain.

Nephrolithiasis can be suspected based on the history and physical examination. However, lab works and diagnostic imaging are important to confirm and exclude the diagnosis of nephrolithiasis. Urinalysis is performed to examine the presence of blood, urine pH and crystals to identify the contents of the stone as well as infection. An elevated WBC count or presence of bacteria in the urine is a sign of infection. Identifying the stone composition will help to direct the medical therapy for the patient. A 24 hour urine collection is done to identify dietary and individual risk factors for recurrent nephrolithiasis. Several imaging studies can be performed to rule out nephrolithiasis. If a patient is pregnant or contraindicated for better imaging

ARF can be arranged depending upon the underlying cause. Pre-renal is the disruption of flow to the glomerulus. Decrease flow to the afferent arterioles can severely affect the nephrons ability to perform its functions. This is due to an abrupt drop in blood flow because of massive vasoconstriction in relation to decrease in volume. Intra-renal failure, however, is an actual damage to the kidneys. Damage to the nephrons may be short-term that injury to the cells and nephrons are not able to work. It could also be permanent where the damage to the nephrons is so severe that it becomes completely dysfunctional. Despite the injuries, the nephrons are capable to restore itself and recover once blood flow is brought back to normal. Post-renal is an obstruction beyond the nephron. Blockage in the ureters, bladder, and urethra can cause buildup of waste products. An example of this is BPH or benign prostate hypertrophy where the prostate gland gets so enlarged that it causes disruption of urine flow.

Glomerulonephritis is a disease that affects the glomeruli of your kidneys that filters the waste in your blood. Your glomeruli becomes damaged because of a problem with your body's immune system. Salt and extra fluid begin to build up in your kidneys, making them unable to filter properly. There are two types of Glomerulonephritis- acute or chronic. Acute Glomerulonephritis can be caused by a skin or throat infection or by other illnesses such as lupus. Chronic Glomerulonephritis can develop over time without any symptoms. Sometimes the disease runs in the family, but with most cases of glomerulonephritis disease the cause is unknown. Glomerulonephritis can affect anyone with diabetes, or other kidney diseases. It is commonly seen in young

The pathophysiology to hydronephrosis is when there is an obstruction in either upper or lower urinary tract that increases pressure into the kidney. Additionally it becomes inability to pass urine through to the bladder. The pressure delicate the tissue to make it hard to pass which leads to complication and loss of function to work properly. If the kidney swells up or there’s a blockage it cannot do what a normal kidney functioning does.

Acute nephritic syndrome is a group of symptoms that occurs with a few disorders that cause glomerulonephritis or swelling and inflammation of the glomeruli in the kidney as shown in Figure 1. Inflammation of the kidneys and glomerulus affects the function of the glomerulus – part of the kidney that filters blood, resulting in blood and protein to appear in urine – excess fluid also builds up in the body. Swelling of the body occurs when blood loses albumin, which is a vital component to the blood as it keeps fluid in blood vessels. Blood loss from damaged kidney structures progresses to allow blood in the urine. Acute nephritis is potentially life threatening as it could lead to acute kidney failure. (http://www.nlm.nih.gov/medlineplus/ency/article/000495.htm)

Glomerulonephritis is a group of diseases that injure the part of the kidney that filters blood (called glomeruli). Other terms you may hear used are nephritis and nephrotic syndrome. When the kidney is injured, it cannot get rid of wastes and extra fluid in the body. If the illness continues, the kidneys may stop working completely, resulting in kidney failure.

Acute kidney injury (AKI) is a common clinical issue but the understanding of the syndrome has been re-evaluated, standardised and aprimorated in the past years. The change from acute renal failure to AKI happened due the fact the even mild change in function or structure of the kidney can cause abrupt clinical manifestations such as change in extracellular volume and electrolytes balance and inability to properly excrete nitrogenous waste products like urea. The old terminology is used now saved for cases were renal replacement therapy is been considered due to severity. The AKI diagnostic criteria is based in a 48 hour creatinin serum level rise by 0.3mg/dL or 1.5 times the patient baseline level or urine decrease to a volume less than

The patient was presented with throbbing back and stomach pain, which came in wave and ended into the groin. The patient had slightly distended abdomen, decreased bowel sounds were noted in addition to protein and blood traces on the urine. These symptoms represent nephrolithiasis and include nausea and flak pain. It is characterized by distal ureteral stones and its diagnosis is done with regard to clinical symptoms only, however, confirmatory tests may be performed.

3. Chronic renal failure:- Patients with decreased renal function have a high rate of complications. Moreover, useful information cannot be obtained from the biopsy of small, contracted kidneys. For these reasons, renal biopsy should be considered only in patients with almost normal-sized kidneys after careful control of hypertension and correction of coagulation

In about 95% of the patients with this disease, damage to the glomeruli occurs 1 to 3 weeks after an infection elsewhere in the body, usually caused by certain types of group A beta streptococci. It is not the infection itself that damages the kidneys. Instead, over a few weeks, as antibodies develop against the streptococcal antigen, the antibodies and antigen react with each other to form an insoluble immune complex that becomes entrapped in the glomeruli. The immune complex deposits into the glomeruli and many cells begin to increase in number. Large numbers of white blood cells become entrapped in the glomeruli, causing blockage. The acute inflammation of the glomeruli usually sub- sides in about 2 weeks, and in most patients, the kidneys return to almost normal function within the next few weeks to few months. However, in a small percentage of patients, progressive renal deterioration continues indefinitely, leading to chronic renal failure. (ACUTE GLOMERULONEPHRITIS

Since its initial description in 1968, IgA nephropathy remains the most common form of primary glomerulonephritis that can lead to chronic kidney disease. This condition is very commonly observed in Southern Europe, Australia and Asia, in Northern climates of the Western World the incidence is approximately 5-10% of biopsies for glomerulonephritis.

Nephrotoxins, acute interstitial nephritis, glomerular damage, and vascular damage also correlate with intrarenal acute renal failure (Singh, Levy, & Pusey, 2013). Postrenal acute renal failure is usually a result of a urinary tract obstruction that affects the kidneys bilaterally, which causes the intraluminal pressure upstream from the site of the obstruction to increase with a progressive decrease in the glomerular filtration rate (McCance, Huether, Brashers, & Rote, 2014). A pattern consisting of several hours of anuria with flank pain followed by polyuria is typically found in individuals with postrenal acute renal failure (McCance, Huether, Brashers, & Rote, 2014).

After the patient had present with the above signs and symptoms, further investigation was required and so was subsequently ordered by the clinician. These further tests consisted of; Blood film, taken from the vessels of the patient and analysed using light microscopy. Plasma Urea, also obtained via a blood sample from the patient which investigates the levels of Blood Urea Nitrogen to rule out renal complications. Microbiological CFU dipstick, placed into a sample of the patients urine to determine whether any urinary tract infection was present and which microorganism may be the cause (if present). Total Protein obtained from a patient’s blood sample, which can highlight any increases in Albumin and Globulin proteins outside of a normal range and so can indicate abnormal synthesis of proteins, and finally a Bone Marrow Biopsy, to investigate any possible abnormalities of the cells contained in the patient’s bone marrow. The patient also received numerous CT