What are the complications of iga nephropathy?

A. Electrolyte imbalance.
Prevention: a low-salt rather than avoid salt, avoid strict salt will lead to hyponatremia, edema aggravated, nausea, vomiting and even convulsions. b, to avoid hypokalemia, a large number of diuretic monitoring of electrolyte levels. c, pay attention to calcium and vitamin D.
Two. Bone metabolic disorders: long term use of hormones can lead to osteoporosis, osteonecrosis.
Prevention: a watch for joint pain, hip pain. b, pay attention to calcium and VitD3, and periodic evaluation.
3. Infections.
Prevention: a, infection will be worse or cause of nephropathy repeated and recurrent. b, common respiratory tract infections, urinary tract infections, skin infections, oral infections.
4. Thrombosis.
Prevention: a watch for the sudden increase of low back pain, proteinuria, and edema. b, monitoring of blood clots to stop bleeding and laboratory treating the symptoms. c, drug prevention and treatment.
What are the complications of iga nephropathy? Change how it treated? Kidney specialists after years of clinical observation and validation and in-depth pathological analysis, discovery, development and prognosis of renal fibrosis in iga nephropathy plays an important role, and indeed can no longer be viewed "as a separate disease entity. Worldwide are at different levels of renal fibrosis and theoretical research.
IgA nephropathy mainly by iga antibodies or immune complex deposition in the mesangial area, leading to mesangial cell damage caused by a series of inflammatory reactions in pathological analysis. Mesangial cells proliferated or shrink, resulting in the microcirculation, leading to ischemia and hypoxia. Large number of renal capillary endothelial cells caused by ischemia and hypoxia, epithelial cells, renal interstitial fibroblast damage and phenotypic change in the formation of renal fibrosis; damaged leaving the basement membrane and endothelial cells or epithelial cells. The charge barrier function changed, resulting in the leakage of a large number of protein and red blood cells, the formation of proteinuria, hematuria.
Know by the above discussion, the leakage of urine protein and red blood cells of kidney disease, mainly due to the glomerular filtration membrane damage caused by resulting in increased permeability. At present, only corticosteroids inhibit the generation of antibodies and immunoglobulin iga-based, it can only be treated for primary disease; not clear already deposited iga receptor and immune complexes, can not improve renal missing blood hypoxia, can not complete the treatment and elimination of damage caused by a series of reactions due to mesangial cells, even more can not effectively repair of the glomerular filtration membrane to resume its normal filtration function. Therefore, application of hormones just because of a momentary inhibition of the generation to live in various types of receptor, and sometimes controlling the damage and the progress of the inflammation response, leaving the urine protein, occult blood, to reduce or even disappear over time.