What are the serious complications of chronic kidney disease?

(1) infection
The main reason for the decrease of the resistance to infection with nephrotic syndrome patients is ① losing too much IgG in the urine.② The deficiency of B factor (complement pathway component) leads to the deficiency of immune regulation. ③Malnutrition, the body's non-specific immune response ability weakened, resulting in impaired immune function. ④A large number of transferrin and zinc were lost from the urine, transferrin was necessary to maintain the function of normal lymphocytes. ⑤The local factors, ascites, pleural effusion, skin edema caused by highly skin breakdown and severe edema which local humoral factor dilution, defense function, are susceptible to patients with nephrotic syndrome factors in antibiotics before bacterial infection was one of the main causes of death in nephrotic syndrome patients, severe infection mainly occurred in children and the elderly, adults are rare, common clinical infection: primary peritonitis, cellulitis, respiratory tract infection and urinary tract infection, once the infection is diagnosed, should be treated immediately.
(2) hypercoagulable state and venous thrombosis
Nephrotic syndrome with hypercoagulable state, mainly due to the changes in blood coagulation factors, including factor IX, Xi decreased V, X factor VIII, fibrinogen, beta thromboglobulin and platelet levels increase, enhanced platelet adhesion and aggregation, antithrombin and anti plasmin activity decreased, therefore, to promote the aggregation and coagulation factor increased, decreased and fibrinolytic mechanism of anti coagulation and anti coagulation factor damage, nephrotic syndrome is a hypercoagulable state, antibiotics, glucocorticoid and diuretic for aggravating factors of venous thrombosis, coagulation proteins play a role by hormone, and diuretic makes the blood concentration. Increase in blood viscosity.
Nephrotic syndrome, when plasma albumin is less than 2.0g/d1, the risk of renal vein thrombosis increased, most of that first and then extended thrombus formation, in small veins, eventually involving renal vein, renal vein thrombosis in patients with membranous nephropathy can be as high as 50%, in which he pathological type, its occurrence the rate is 5% ~ 16%, the acute type patients with renal vein thrombosis can be manifested as a sudden onset of back pain, hematuria, urine white blood cells, increased urinary protein and renal dysfunction, chronic patients without any symptoms, but after thrombosis of renal blood stasis often result in increased proteinuria, or poor response to treatment, because thrombosis, renal embolism symptoms, pulmonary embolism can occur, can also be associated with renal tubular damage, such as diabetes, amino acid in urine and renal tubular acidosis, diagnosis to renal vein angiography, Doppler Ultrasound, CT, IMR and other non traumatic examination also contributes to the increase of plasma thrombomodulin beta diagnosis, suggesting the potential for thrombosis, blood alpha 2- antifibrinolysin increase also is considered a sign of renal vein thrombosis, the rate is about 6% in peripheral deep vein thrombosis, deep vein common Yu Xiaotui, only 12% there are 25% clinical symptoms, can be found by Doppler ultrasound, the incidence of pulmonary embolism was 7%, 12% still have no clinical symptoms, other venous involvement is rare, arterial thrombosis is rare, but in children, although the incidence of thrombosis is relatively low, but the arterial and venous involvement as common.
(3) acute renal failure
Acute renal failure nephrotic syndrome was the most serious complication, often requiring dialysis treatment, common causes are: ①hemodynamic changes: nephrotic syndrome often hypoalbuminemia and vascular lesions, especially in elderly patients with renal arteriosclerosis, the blood volume and blood pressure drop are sensitive, so when the acute blood loss, vomiting diarrhea, caused by the loss of body fluid, surgical injury, ascites, a diuretic and antihypertensive drug use, can make blood pressure drops further, leading to renal perfusion decreased abruptly, which reduced glomerular filtration rate and tubular epithelial cell swelling after acute ischemia, degeneration and necrosis, leading to acute renal failure. ②The renal interstitial edema, hypoproteinemia can cause edema, also may cause renal interstitial edema, renal interstitial edema of renal tubular compression, the proximal tubule of Bowman capsule hydrostatic pressure increased, GFR decreased.③ Drug induced acute interstitial nephritis. Bilateral renal vein thrombosis. Vasoconstriction: some nephrotic syndrome in patients with low blood pressure when the concentration of renin, renin contraction of the renal artery, GFR decline, this situation in the elderly who have more vascular lesions. The concentration of protein tube blockage in renal distal tubule: nephrotic syndrome may be involved in the mechanism of acute renal failure. Often accompanied by glomerular epithelial foot process effacement, nephrotic syndrome, fracture hole disappeared, the effective filtration area was significantly reduced. The rapidly progressive glomerulonephritis. To urinary tract obstruction.
(4) renal tubular dysfunction
The renal tubular function in nephrotic syndrome decreased, to see more children, that is the mechanism of renal tubular filtration protein heavy absorption, the tubular epithelial cell damage, Changbiaoxianwei glycosuria, aminoaciduria, hyperphosphaturia, renal tubular potassium loss and hyperchloremic acidosis, where the renal tubular function a variety of defects often indicates poor prognosis.
(5) abnormal bone and calcium metabolism
Nephrotic syndrome in the circulation of VitD binding protein (Mw65000) and VitD syndrome complex in the urine in the blood loss, 1, 25 (OH) 2VitD3 level decreased, resulting in intestinal calcium malabsorption and bone of PTH tolerance, thus nephrotic syndrome often occurs in hypocalcemia, osteitis fibrosa and sometimes paraungual hyperactivity caused by bone softening, in nephrotic syndrome complicated by renal failure progression of bone malnutrition, generally non nephropathy caused by uremia is more serious.
(6)endocrine and metabolic abnormalities
Nephrotic syndrome and urinary loss of thyroid binding protein (TBG) and cortical hormone binding protein (CBG), clinical thyroid function may be normal, but the levels of TBG and T3 decreased, free T3 and T4, the TSH is normal, because the blood CBG and 17 hydroxycorticosteroid are reduced, and combined with the free cortisol ratio can be changed. The organization of pharmacological doses of cortisol response is different from normal, because ceruloplasmin (Mw151000), transferrin (Mw80000) and urinary albumin loss from nephrotic syndrome, often in serum copper, zinc and iron concentrations decreased, zinc deficiency can cause impotence, taste disorders, wound healing and cell mediated immune damage. Continue to reduce transferrin can cause clinical treatment of anemia of iron, with the resistance of microcytic hypochromic and severe hypoproteinemia can lead to metabolic persistent alkali poisoning due to plasma protein Reduce 10g/L, the plasma bicarbonate will be reduced by 3mmol/L.