Haematuria

Glomerulonephritis (GN), or the inflammation of glomeruli, is a leading cause of renal failure worldwide. Inflammation is characterized by vascular fragility, infiltration of leukocytes, and edema. Glomerular disease may manifest by three major syndromes: nephritic syndrome, nephrotic syndrome, and rapidly progressive glomerulonephritis (RPGN). Nephritic syndrome consists of sudden onset of hematuria, non-nephrotic range proteinuria (1.5 g/24 h), active sediment with red blood cell (RBC) casts or dysmorphic RBCs, acute renal failure, and hypertension. Nephrotic syndrome is characterized by heavy proteinuria (>3.5 g/24 h), edema, hypoalbuminemia, and hyperlipidemia. RPGN is characterized by active sediment (RBC casts and dysmorphic RBCs) and rapid development of acute renal failure usually over a period of weeks to months. Glomerulonephritis accounts for the majority of progressive renal disease in many parts of the world.

Acute renal failure occurs quickly over a period of days or weeks with a reduction in GFR and elevation of BUN, plasma creatinine and crystatin C levels. Oliguria (urine output of < 30ml/hr or < 400 ml/day) is usually associated with ARF, although urine output may be normal or increased as well. Fluid is still filtered at the glomerulus but there is an alteration in tubular secretion or reabsorption. Most types of ARF are reversible if diagnosed and treated early (Perrin, 2009).

Glomerulonephritis is a glomerular kidney disease in which the kidneys' filters become inflamed and scarred. There are different types of glomerulonephritis which include kidney disease of diabetes, IgA nephropathy, and lupus nephritis.Membranous nephropathy. GN is an immunologically mediated disease in which deposits of IgG and complement complexes collect in the basement membrane. The glomerular basement membrane becomes thickened and does not function normally, allowing large amounts of protein to be lost in the urine. In time, the kidneys slowly lose their ability to remove wastes and excess fluid from the blood to make urine.

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

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

In order to distinguish between primary and secondary FSGS, disease presentation and associated medical conditions are very helpful. Suggestive of secondary FSGS are conditions, such as infections, hypertension and obesity, as well as proteinuria that is within nephrotic range, but not accompanied by full blown nephrotic syndrome. Moreover, patients with secondary FSGS will tend to have gradually increasing amounts of protein in the urine. Hence, it is important to find out if the onset of the disease was sudden or subtle with gradual

Chronic glomerulonephritis occurs when there is slow, progressive destruction of the glomeruli of the kidney, with progressive loss of kidney function. In some cases, the cause is found to be a specific attack to the body's immune system, but in most cases, the cause is unknown. Iit is generally thought that a still-unidentified abnormality of the immune system is to blame.

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

Thrombotic microangiopathy (TMA) entails microvascular thrombosis, consumptive thrombocytopenia, and microangiopathic hemolytic anemia (MAHA) that leads to ischemic organ damage. Severe hypertension may induce TMA within the renal vasculature. We describe the first case of chronic thrombotic microangiopathy as a cause of nephrotic range proteinuria, not associated with clinical or laboratory features suggestive of TMA.

Low serum albumin levels are usually associated with acute glomerulonephritis, the normal albumin levels for Patient B implies that acute glomerulonephritis could be eliminated from list of conditions provided. Thus suggested for both Patient B and Patient N there were no leakage of the serum albumin in the urine. Nevertheless, (McClatchey, 2002) identified that low albumin levels may also signify impaired liver function. Conditions such as hepatic cirrhosis and chronic hepatic cirrhosis can also be dismissed because of the normal level of albumin in blood. This implies that no anomalies were present thus signifying accurate results.

JH’s infection from pneumococcal pneumonia results to inflammation of the capillaries in the glomeruli affecting the ability of the kidney to filter urine and eliminate wastes.

We collected data on the disease status (like renal histology, duration of nephrotic syndrome, number of relapses) and treatment status (like immunosuppressive treatments used before RTX, number of courses of RTX) of the patients. RTX response was measured at 1, 3, 6, 12, 18 and 24 months post RTX therapy in terms of proteinuria, spot urine protein/creatinine ratio (Up/Uc) or creatinine clearance. Complete blood counts, lipid profile and serum albumin levels were monitored regularly.

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