Case report academic papers A case report of nephrotic syndrome
Nephrotic syndrome; infect
Doi:10.3969/j.issn.1004-7484 (x) .2012.08.292 Article number:1004-7484 (20/kloc
Nephrotic syndrome is proteinuria and a group of clinical manifestations caused by various renal pathological damages. Its main feature is massive proteinuria, defined as? 3.5g/d with hypoalbuminemia? 30g/L, hyperlipidemia and edema. Because the syndrome can be caused by many diseases with different etiology and pathology, it has its own characteristics in clinical manifestations and treatment measures. This paper reports the cases of 1 in our hospital.
Clinical data of 1
Patient, male, age 14, went to the local hospital in February for edema of face and lower limbs. There was no abnormality in urine routine, and the edema gradually subsided after oral administration (details are unknown). Five days before coming to the clinic, the patient had no obvious inducement to have edema of face and lower limbs again, accompanied by abdominal distension, and no discomfort such as fever and vomiting. Local urine routine showed occult blood 2+ and protein 3+, but patients didn't pay attention to it and treat it. 1 The day before seeing a doctor, the patient's symptoms worsened, and his right abdomen and waist were painful and feverish, so he came to see a doctor in our hospital. Physical examination: T38.9℃, BP 120/75mmHg, facial edema, voiced motion (+), obvious percussion pain in both kidneys, scrotum and lower limbs edema, and no obvious positive signs in other physical examinations. Auxiliary inspection: WBC 18.0? 10? 9/L，N%89.5%，HGB 12 1g/L，PLT343？ 10? 9/L, Cr 1 18.3umol/L, ALB 1 1.6g/L, 24h urine protein quantification >: 10g, coagulation function: PT16./. CT showed increased lung markings, a large amount of ascites in abdominal cavity, and nothing else was special. After admission, anti-infection and fresh frozen plasma infusion were given symptomatic support treatment. Because the patient was complicated with severe infection, hypoproteinemia and coagulation dysfunction, renal biopsy was not performed. After 10d, the patient's general condition improved and the infection was controlled. After methylprednisolone treatment, the patient's edema gradually decreased, urine volume increased and plasma albumin level increased. After that, the patient's condition improved and he was discharged.
2 discussion
The etiology of nephrotic syndrome can be divided into primary and secondary, and the latter is mainly diagnosed after excluding the former. There are many reasons for secondary nephrotic syndrome, including diabetic nephropathy, hepatitis B-related nephritis, lupus nephritis, amyloidosis, drugs and infection [1]. The pathological types of primary nephrotic syndrome mainly include minimal change nephropathy, mesangial proliferative nephritis, focal glomerulosclerosis, membranous proliferative nephropathy and membranous nephropathy. Among them, minimal lesion type is more common in children and adolescents, and it is sensitive to hormone therapy; Membranous nephropathy is mainly seen in middle-aged and elderly people; Mesangial proliferative lesions are mainly IgA nephropathy and non-IgA type, and they are also the most common pathological types of nephrotic syndrome.
The clinical manifestations and pathophysiological changes of nephrotic syndrome mainly include proteinuria, changes in plasma protein concentration, hyperlipidemia and edema. Hypoalbuminemia is mainly the loss of protein in urine, but the plasma albumin level is not completely parallel to the loss of urine protein. The changes of other plasma protein components such as IgM, fibrinogen, a 1, a2 globulin and large lipoprotein are normal or slightly increased. In addition, the levels of fibrinogen, factor VIII, antithrombin III, protein C and protein S, which are prone to thrombosis, increased, but their activities decreased. When the level of plasminogen decreases, the level of plasminogen activator inhibitor-1(PAI- 1) increases, or the interaction between plasmin and fibrin is destroyed due to the low level of albumin [2]. Edema is mainly the retention of extravascular sodium and water. When the volume of tissue fluid increases more than 5kg, clinically detectable concave edema can occur. The degree of edema is generally consistent with the degree of hypoproteinemia.
The main complications of nephrotic syndrome are infection, thromboembolic complications, malnutrition and renal injury. Infection is mainly due to the obvious decrease of blood IgG level [3], the decrease of complement components, especially the influence of factor B and factor D on the activation pathway of complement bypass [4], the decrease of leukocyte function [5] and the low transferrin and zinc deficiency [6]. The complication of thromboembolism is one of the serious and fatal complications. Nephrotic syndrome is in hypercoagulable state [7], and the tendency of thrombosis is more serious because of the increase of blood concentration and viscosity caused by low protein and hyperlipidemia. In addition, excessive use of diuretics will also increase the blood drug concentration.
The treatment of nephrotic syndrome can be divided into three aspects: the treatment of proteinuria, the symptomatic treatment of systemic pathophysiological changes and the protection of residual renal function. The treatment of proteinuria mainly includes glucocorticoid, cytotoxic drugs, immunosuppressants, ACEI and so on. The symptomatic treatment includes detumescence and anticoagulation. Other Chinese medicines, such as Astragalus membranaceus, have protective effects on chronic kidney diseases.
The patient is consistent with the manifestations of nephrotic syndrome and has other clinical manifestations. The patient was complicated with serious infection, severely impaired coagulation function and obvious bleeding tendency. Obviously, anticoagulant therapy is not suitable for this situation. We should first correct the coagulation function, control the infection, and give various symptomatic support treatments. The patient's general condition improved, and after the infection was controlled, he was given regular hormone therapy.
refer to
[1] Liu Gang, Ma, Zou, et al. Comparative analysis of renal diseases in renal biopsy patients in recent ten years. Journal of Clinical Internal Medicine, February 20041:834-838.
[2] Kaisenga. Plasma components of nephrotic syndrome. A j-renol, 1993, 13:347-359.
[3] Giangiacomo J, Cleary TG, Cole BR, et al. Serum immunoglobulin in nephrotic syndrome. Possible causes of minimal change nephrotic syndrome. British Medical Journal,1975,293: 8-12.
Anderson DC, York Taylor, Ross G, et al. Evaluation of serum factor B, serum opsonin, granulocyte chemotaxis and infection in children with nephrotic syndrome. J Infectious Dis, 1979,140:1-1.
Aube D, Chapman S, Brown Z, et al. Inhibition of normal lymphocyte transformation by serum from patients with minimal change nephropathy and other forms of nephrotic syndrome. Clinical renal cells, 198 1, 15:286-290.
[6] Cameron JS. Clinical consequences of nephrotic syndrome. In: Cameron JS, Davl? Oxford Textbook of Clinical Kidney Diseases, first edition 1. Oxford: Oxford University Press, 1992:276.
[7]Mehls O, Andrassy K, Koderisch J, et al. Hemostasis and thromboembolism in children with nephrotic syndrome: differences with adults. J Pediatrics, 1987,1/kloc-0: 862-867.
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