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Treatments for glomerulosclerosis depend on what caused the scarring of the glomeruli. This is determined by a renal biopsy. Immunosuppressive drugs stop proteinuria in some patients, but once the treatments have ended, proteinuria will continue. The drugs may sometimes damage the patient's kidneys even more.
Glomerulonephrosis is a non-inflammatory disease of the kidney presenting primarily in the glomerulus (a glomerulopathy) as nephrotic syndrome.The nephron is the functional unit of the kidney and it contains the glomerulus, which acts as a filter for blood to retain proteins and blood lipids.
Genetic disorders: congenital nephrotic syndrome is a rare genetic disorder in which the protein nephrin, a component of the glomerular filtration barrier, is altered. Drugs ( e.g. gold salts, penicillin , captopril ): [ 25 ] gold salts can cause a more or less important loss of proteins in urine as a consequence of metal accumulation.
Glomerulonephritis is characterized by inflammation and thinning of the glomerular basement membrane and the occurrence of small pores in the podocytes of the glomerulus. These pores become large enough to permit both proteins and red blood cells to pass into the urine (yielding proteinuria and hematuria , respectively).
Glomerular hyperfiltration and an aberrant regulation of RAAS lead to increased intraglomerular pressure, causing stress on the endothelial cells, the mesangial cells and the podocytes. This exacerbates the dysfunction caused by the metabolic effects of hyperglycemia. [citation needed]
As the glomerulonephritis progresses, the tubules of the kidney become infected, leading to atrophy and hyalinisation. The kidney appears to shrink. Treatment with corticosteroids is attempted if the disease progresses. [citation needed] In extremely rare cases, the disease has been known to run in families, usually passed down through the females.
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These presenting symptoms are relatively non-specific and are often seen in other glomerular disorders. Preceding upper respiratory tract infection or post-streptococcal glomerulonephritis may contribute to hematuria, as both have been identified in patients presenting with hematuria in the context of mesangial proliferative glomerulonephritis. [2]