Pathophysiology of Nephritic Syndrome

The pathophysiology of nepritic syndrome is not entirely clear, but certain factors seem to be the main contributors to its development. It is often accompanied by peripheral edema and fatigue, and may initially be confused with liver disease or congestive heart failure. Luckily, these conditions are unlikely to be the cause of nephritic syndrome.

Clinical features such as proteinuria, hematuria, and a high level of hypertension may indicate the presence of nephritic syndrome. Diagnosis will also involve performing urine analysis with microscopy. Red blood cells may be small, large, or even dysmorphic and be cast. Acanthocytes are pathognomonic for glomerular inflammation, and their presence in urine analysis should prompt the use of supportive care. A multidisciplinary team should be involved in the diagnosis and treatment of this disease, and close monitoring is essential to evaluate its progression.

Inflammation of the glomerulus is one of the main causes of nephritic syndrome. It causes proteinuria, variable proteinuria, and red blood cell casts in urine. Ultimately, nephritic syndrome can lead to renal failure. When the kidneys fail to filter waste products effectively, the body can accumulate blood, protein, and electrolytes in the bloodstream.

Acute nephritic syndrome is often triggered by a streptococcal infection, such as a throat infection. In addition to infection with group A b-hemolytic streptococci, the most common cause of nephritic syndrome is hypertension. In addition to the acute onset of symptoms, nephrotic syndrome is accompanied by a significant increase in circulating volume and weight.

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