In children with renal comprehensive common complication

1) infection is the most common complications of this disease, infection not only make the condition repeatedly affect the treatment effect, and might lead directly to death. This disease is prone to the cause of infection:
① humoral immune function is low (IgG in urine, blood loss, decreased synthesis of catabolism increase);
② often cellular immune dysfunction;
③ transferrin and zinc-binding protein is lost in the urine, influence immune regulation and lymphocyte function changes;
④ protein metabolism in malnutrition, and abnormalities of the complement system;
⑤ edema caused by local circulatory disorders;
⑥ glucocorticoids and immunosuppressants long period of time.
Infection can occur in the respiratory tract, urinary tract, skin and soft tissue; bacterial peritonitis is also not uncommon. More pneumococcal infections, mainly tuberculosis infection in recent years has also increased. Generally do not advocate routine prophylactic use of antibacterial drugs, but should be strengthened to protect, should be timely and thorough treatment of bacterial infections. Viral infection compared with the previous increase, particularly when receiving corticosteroids, immunosuppressive therapy, varicella, herpes zoster virus infection, the disease than the average children's weight, should strengthen the anti-viral treatment. Contacts should be ascertained hormones, immunosuppressants temporary reduction, and given a gamma globulin injection. Long-term application of corticosteroids, immunosuppressants patients should also be noted that the activities or spread of tuberculosis in the body, and secondary fungal infection.
2) low blood volume and electrolyte imbalance NS part of the children with low blood volume, even if the blood is dissolved is not low effective circulating volume due to hypoalbuminemia, plasma colloid osmotic pressure leaving a fragile state some incentive effect prone to cause low blood volume, or even shock. The common causes are:
① vomiting, diarrhea, diuretic, ascites, bleeding break fluid loss;
② long-term corticosteroids, causing their own adrenal suppressed under stress the body to retain sodium and water capacity;
③ sick child for a long time to ban salt or low-salt diet induced hyponatremia.
Common electrolyte disorder in patients with kidney disease have hyponatremia, hypokalemia, hypocalcemia. Some parents of children with NS inappropriate long-term ban salt or eat sodium free salt substitutes; or edema excessive use of diuretics; and infection, vomiting, diarrhea and other factors can cause hyponatremia. In the above-mentioned incentives, such as children with the sudden appearance of anorexia, fatigue, drowsiness, blood pressure, or even shock, convulsions and other performance should be considered hyponatremia may be. A large number of diuretic use high-dose diuretic or corticosteroids, should be alert to the emergence of hypokalemia. Nephrotic syndrome with massive proteinuria, 25 - hydroxy calciferol binding protein loss induced calcium metabolism disorders, intestinal calcium malabsorption, reduced the sensitivity of the bone to parathyroid hormone, can cause hypocalcemia, even a low calcium convulsion.
3) a hypercoagulable state and thrombus formation of NS patients blood Yi showing hypercoagulable state, the main Increased
① liver synthesis of clotting factors, such as II, Ⅴ, VII, VIII factor increase and hyperfibrinogenemia;
② plasma anti-clotting substances, decreased urinary loss of antithrombin Ⅲ too much;
③ high ester hyperlipidemia slow blood flow, increased blood viscosity, such as extensive use of diuretics to hypovolemia, hemoconcentration;
④ platelet count increased, the increase in adhesion and aggregation;
⑤ infection or other factors caused vascular wall damage and easy to activate the intrinsic coagulation system;
⑥ large doses of corticosteroid application may promote a hypercoagulable state. These procoagulant factors lead to the patient moving, venous thrombosis, of which the most common renal vein thrombosis, the incidence of each report is different to adult kidney disease from 5% to as high as 14%. Membrane proliferative glomerulonephritis, followed by membranous nephropathy complicated by. Children with nephrotic thrombosis can occur in different parts of the renal vein, deep venous, femoral artery, pulmonary artery, superior mesenteric artery, cerebral artery, but also the renal vein thrombosis more common, acute typical cases showed a sudden onset of gross hematuria. low back pain, spinal rib angle tenderness, kidney area, mass, in the case of bilateral renal rapid decrease in proteinuria aggravate; chronic often edema, proteinuria continued remission, and their symptoms are not obvious. X-ray examination the ipsilateral renal enlargement, ureter notch. B super addition to the kidney increases, showing that renal vein thrombosis. Renal venography can be confirmed.
In addition to renal vein thrombosis, such as sick children:
① both sides of the lower limb edema asymmetry does not change with body position changes;
② skin burst purpura, and rapidly expanding with pain;
③ scrotal edema was purple;
④ refractory ascites does not go away;
⑤ leg pain accompanied by the dorsalis pedis artery pulse disappeared, and so on, should be considered thrombosis.
4), acute renal insufficiency in children with NS occurrence of acute renal failure is rare, but if the following conditions, namely, acute renal failure may occur.
① hypovolemia or hypovolemic shock, renal blood hypoperfusion can be caused by prerenal azotemia, such as its persistence can lead to tubular necrosis
② glomerular lesions, especially proliferative glomerulonephritis lesions can be caused by glomerular filtration rate decreased, the occurrence of acute renal dysfunction;
③ small lesions, but can be decreased effectively due to renal interstitial edema or renal tubular protein casts obstruction, caused by the proximal tubule and the renal capsule hydrostatic pressure increased, resulting in glomerular filtration;
④ Because the application of non-steroidal anti-inflammatory drugs, diuretics, antibiotics induced acute interstitial nephritis;
⑤ the glomerular lesions deteriorated, especially when complicated by crescentic glomerulonephritis;
⑥ acute renal vein thrombosis.
5) vitamin D and calcium metabolism disorders of children with NS massive proteinuria, can cause blood vitamin D binding protein (molecular weight 59 000) since the urinary loss of vitamin D deficiency affect intestinal calcium absorption, and therefore such a sick child more hypocalcemia associated with renal tubular change may also affect the 1-25 - (OH) 2D3 formation; long-term application of corticosteroids; further exacerbated by vitamin D and calcium metabolism disorders. Hypocalcemia, regular feedback to cause hyperparathyroidism, bone calcification exception is therefore often show clinical hypocalcemia, serum 25 - hydroxy calciferol is decreased, the blood parathyroid hormone increased, osteoporosis, osteomalacia, especially in the rapid growth in children during these changes more pronounced.
Endocrine changes in 6).
① reduce the thyroid hormone function: sick children when the NS basal metabolic rate, blood protein binding iodine value decreased. Most scholars believe that the Department of thyroid binding globulin caused by urine loss may also increase in thyroid hormone synthesis decline in its distribution of the extravascular space; there is blood when the kidney disease inhibitory factor preventing thyroxine and globulin combination.
② thymic hormone decreased significantly: with blood zinc low related, since the urine is lost outside the NS in addition to the zinc-binding protein, and also the decrease due to the lack of transferrin induced intestinal absorption of zinc. Thus affecting the synthesis of thymosin;
(3) growth hormone - abnormal peptide growth factors: NS in children with growth delay gradually cause for concern, especially long-term high-dose corticosteroid treatment of the sick child, the exact mechanism is not entirely clear, it was considered that corticosteroids may impede collagen metabolism affect bone growth, the recent report of children NS activity of serum insulin-like growth factor I and II (IGF1, 2) concentration decreased, but the relationship with growth delay is unclear. Researchers believe the NS sick child growth delay, not only with protein malnutrition, with the impact of corticosteroids on the IGF / GH axis, and impaired GH (growth hormone) and IGF gene expression is growth retardation of the latest reasons.
(4) adrenal cortical hormone and adrenal crisis: foreign reports NS blood cortisol levels decreased, and the gland to ACTH response has been reduced. Clinically more important is the feedback inhibition of corticosteroids on hypothalamic - pituitary - adrenal system, survey data show that: the application of high-dose corticosteroids to NS, its own plasma cortisol significantly inhibited by the gradual reduction children with NS to every other day 0.68mg/kg, Dayton clothing, plasma cortisol concentrations returned to normal, common, long-term therapy withdrawal in February of ACTH test 96% normal, so the application of large doses of corticosteroid therapy, such as suddenly disabled the speed of the hormone or hormone reduction during the treatment too fast, or the body to stressful situations (such as severe infection or trauma, surgery, etc.), subject to the inhibitory state of the adrenal cortex are not able to produce enough sugar, salt, corticosteroids, and failed to replenish sufficient quantities of the original sex hormone, in children with adrenal crisis, acute adrenal insufficiency: manifested as sudden onset of nausea, vomiting, abdominal pain, heart rate increased, decreased blood pressure, difficulty breathing, skin bruising hair cool, and soon to shock or even coma, if not get immediate treatment, prone to cause death.
7), renal tubular dysfunction in children with NS does not alleviate the continuing massive proteinuria, or accompanied by tubulointerstitial lesions or renal vein thrombosis who were seen varying degrees of renal tubular change, especially the proximal tubular function obstacles. Such as diabetes, urinary amino acids, phosphorus and urine, urinary potassium loss, tubular proteinuria, urinary low molecular weight proteins: lysozyme, β2-microglobulin, retinol binding protein. This is mostly temporary reversible changes, such as the persistence prompted occult renal dysfunction and poor prognosis.