Complications In addition to the glomerulopathy described above, kidney complications of<unk> <unk>  disease include cortical infarcts leading to loss of function, persistent bloody urine, and perinephric hematomas. Papillary infarcts, demonstrable radiographically in 50% of patients with<unk>  trait, lead to an increased risk of bacterial infection in the scarred kidney tissues and functional tubule abnormalities. The presence of visible blood in the urine without pain occurs with a higher frequency in<unk>  trait than in<unk> <unk>  disease and likely results from infarctive episodes in the renal medulla. Functional tubule abnormalities such as nephrogenic diabetes insipidus result from marked reduction in vasa recta blood flow, combined with ischemic tubule injury. This concentrating defect places these patients at increased risk of dehydration and, hence,<unk> ng crises. The concentrating defect also occurs in individuals with<unk>  trait. Other tubule defects involve potassium and hydrogen ion excretion, occasionally leading to high blood potassium, metabolic acidosis, and a defect in uric acid excretion which, combined with increased purine synthesis in the bone marrow, results in high blood uric acid levels.
Sickle cell nephropathy
IgA nephropathy
Malarial nephropathy
Analgesic nephropathy
Mesoamerican nephropathy
Phosphate nephropathy
Uddanam nephropathy
Membranous glomerulonephritis