<unk>  is a type of nephropathy associated with<unk> <unk>  disease which causes kidney complications as a result of<unk> ng of red blood<unk> s in the small blood vessels. The hypertonic and relatively hypoxic environment of the renal medulla, coupled with the slow blood flow in the vasa recta, favors<unk> ng of red blood<unk> s, with resultant local infarction (papillary necrosis). Functional tubule defects in patients with<unk> <unk>  disease are likely the result of partial ischemic injury to the renal tubules. Also the<unk> <unk>  disease in young patients is characterized by renal hyperperfusion, glomerular hypertrophy, and glomerular hyperfiltration. Many of these individuals eventually develop a glomerulopathy leading to glomerular proteinuria (present in as many as 30%) and, in some, the nephrotic syndrome. Co-inheritance of microdeletions in the -globin gene (thalassemia) appear to protect against the development of nephropathy and are associated with lower mean arterial pressure and less protein in the urine. Mild increases in the blood levels of nitrogen and uric acid can also develop. Advanced kidney failure and high blood urea levels occur in 10% of cases. Pathologic examination reveals the typical lesion of "hyperfiltration nephropathy" namely, focal segmental glomerular sclerosis. This finding has led to the suggestion that anemia-induced hyperfiltration in childhood is the principal cause of the adult glomerulopathy. Nephron loss secondary to ischemic injury also contributes to the development of azotemia in these patients __TOC__
Sickle cell nephropathy
IgA nephropathy
Malarial nephropathy
Analgesic nephropathy
Mesoamerican nephropathy
Phosphate nephropathy
Uddanam nephropathy
Membranous glomerulonephritis