| disease | Primary Nephrotic Syndrome in Children |
| alias | Nephritis, Nephrotic Syndrome |
Nephrotic syndrome (NS) is a common pediatric kidney disease caused by various disease factors that increase the permeability of the glomerular basement membrane, leading to significant protein loss in the urine. The main characteristics include massive proteinuria, hypoalbuminemia, severe edema, and hypercholesterolemia. Based on clinical manifestations, it is classified into three types: simple nephrosis, nephritic nephrosis, and congenital nephrosis. In children under 5 years old, the pathological type of nephrotic syndrome is mostly minimal change disease, while in older children, non-minimal change types (including membranoproliferative glomerulonephritis, focal segmental sclerosis, etc.) are more common.
bubble_chart Epidemiology
Nephrotic syndrome caused by glomerular disease of unknown etiology. It is reported that the annual incidence rate in children under 16 years old in the United States is 2 to 2.3 per 100,000, with a cumulative incidence rate of 16 per 100,000. According to statistics from 105 hospitals in 20 provinces and cities in China in 1982, out of 6,947 hospitalized pediatric patients in the urology department, 1,462 cases (21%) were of this syndrome, with 58.9% being first-time cases within one year of onset. Analysis of hospitalized children at Beijing Children's Hospital from 1956 to 1985 also indicates a trend of increasing numbers of patients hospitalized due to this disease.
Not yet elucidated. Minimal change disease may be related to T-cell immune dysfunction. Membranous nephropathy and membranoproliferative glomerulonephritis may be associated with immune complex formation.
bubble_chart Pathological Changes
Primary nephrotic syndrome in children can present with various pathological changes, but the majority are lesions. The reported ratios of these changes vary and can differ based on factors such as the patient's age, patient source (i.e., whether they are non-selective cases or difficult-to-treat referral cases), and indications for renal biopsy (Tables 1, 2).Table 1 Pathological types of nephrotic syndrome by age (%)
| Children | Adults | |
| Minimal change disease | 76 | 20 |
| Membranous nephropathy | 7 | 40 |
| Focal segmental sclerosis | 8 | 15 |
| Mesangial proliferative | 4 | 7 |
| Amyloidosis | 0 | 10 |
| Others | 5 | 8 |
Table 2 Pathological types of nephrotic syndrome in children by source (%)
| Non-selective cases (521 cases) | Referral cases (512 cases) | |
| Minimal change disease | 76.4 | 41.0 |
| Membranous nephropathy | 6.9 | 17.0 |
| Focal segmental sclerosis | 7.5 | 16.0 |
| Mesangial proliferative | 2.3 | 12.0 |
| Amyloidosis | 1.5 | 9.0 |
| Others | 5.4 | 5.0 |
From the above, it can be seen that children differ from adults, with minimal change disease being predominant in children. Additionally, the results vary depending on the patient source. In non-selective cases, minimal change disease is predominant (76.4%), but in referral cases, due to the majority being corticosteroid-resistant or recurrent refractory cases, the proportion of minimal change disease decreases, while non-minimal change diseases increase. According to pediatric data in China, mesangial proliferative disease is more common. For example, a report from the Pediatric Hospital of Shanghai Medical University on 72 cases of pediatric nephrotic syndrome with biopsy results showed that mesangial proliferative lesions were the most common (31.9%), followed by minimal change disease (26.3%). Reports from other regions are also roughly similar.
bubble_chart Clinical ManifestationsThe age and gender of onset peak during preschool years. The age of onset for simple cases is younger, while for tense cases it is older. Males are more affected than females, with a male-to-female ratio of approximately 1.5 to 3.7:1.
Edema is the most common clinical manifestation, often first noticed by parents. It starts from the eyelids and face, gradually spreading to the limbs and the whole body. The edema is pitting and may be accompanied by serous membrane effusions such as pleural effusion and ascites. Boys often have significant scrotal edema. Body weight can increase by 30-50%. In severe cases of edema, white or purple striae may be seen on the inner thighs, upper arms, and abdominal wall. The severity of edema is usually unrelated to prognosis. Concurrent with edema, there is often a decrease in urine output.
In addition to edema, children may suffer from protein malnutrition due to long-term protein loss, manifesting as pale complexion, dry skin, dry and shallow yellow hair, white transverse lines on fingernails and toenails, and weak ear and nasal cartilage. Children may appear listless, fatigued, and have reduced appetite, sometimes accompanied by diarrhea, which may be related to intestinal mucosal edema and/or concurrent infections. Prolonged or recurrent episodes may lead to developmental delays. Children with nephritis may have elevated blood pressure and hematuria.
bubble_chart Auxiliary Examination
1. Urine Routine: Significant increase in urine protein, qualitative ≥ (+++), 24-hour urine protein quantification ≥ 0.1g/kg. Urine sediment microscopy may reveal hyaline casts and a few granular casts. In children with nephritis, red blood cells may also be seen, and renal epithelial cells and cellular casts are easily observed. Reduction or disappearance of urine protein is a sign of improvement in the condition.
2. Plasma Protein: Total plasma protein is lower than normal, with a more pronounced decrease in albumin, often <25~30g/L, sometimes below 10g/L, accompanied by an inversion of the albumin/globulin ratio. Among the globulins, α2, β-globulin, and fibrinogen are increased, while γ-globulin is decreased. IgG and IgA levels are reduced, while IgE and IgM are sometimes elevated. Erythrocyte sedimentation rate is increased.3. Serum Cholesterol: Often significantly elevated, other lipids such as triglycerides and phospholipids may also be increased. Due to the increase in lipids, the serum may appear milky white.
The diagnosis of nephrotic syndrome is primarily based on clinical manifestations. The presence of massive proteinuria (24-hour urinary protein excretion >0.1g/kg, or >3.5g/kg), severe edema, hypercholesterolemia (>5.7mmol/L, >220mg%), and hypoalbuminemia (<30g/L, <3Gg%) can lead to a diagnosis of nephrotic syndrome. In typical cases, serum protein electrophoresis often indicates α2↑↑, while γ is decreased. Some children may exhibit hypocomplementemia, microscopic or gross hematuria, azotemia, or hypertension. For preschool children, blood pressure >1610.6kPa (120/80mmHg), and for school-aged children >17.3/12kPa (130/90mmHg), it is classified as nephritic nephropathy. Nephrotic syndrome that is steroid-resistant (no response or partial response to full-dose steroids for 8 weeks), frequently relapsing or recurrent (≥2 times in half a year, or ≥3 times in a year), or steroid-dependent is termed refractory nephrotic syndrome. Refractory nephrotic syndrome is one of the indications for renal biopsy, which can clarify the pathological type and severity of renal lesions to guide treatment. Children with a hypercoagulable state may have shortened prothrombin time, elevated plasma fibrinogen levels, and platelet counts higher than normal. During steroid treatment, sudden onset of lumbago accompanied by hematuria, elevated blood pressure, worsening edema, or deterioration of renal function suggests renal vein thrombosis. Additionally, analysis of the primary disease aids in treatment. Massive proteinuria and hypoalbuminemia are essential conditions for diagnosis.
bubble_chart Treatment Measures
Adopt a comprehensive treatment approach combining traditional Chinese and Western medicine, primarily using adrenal corticosteroids. The treatment includes controlling edema, maintaining water and electrolyte balance, providing adequate nutrition, preventing and controlling accompanying infections, and correctly using adrenal corticosteroids. For recurrent cases or those resistant to hormones, immunosuppressive drugs are used in combination. Currently, Chinese medicinals focus on strengthening the spleen and tonifying the kidney, while mitigating the side effects of Western medicine.
1. General Treatment
(1) Rest and lifestyle: Except for cases with severe edema or concurrent infections, absolute bed rest is generally not required. Gradually increase activity levels after the condition improves. After 3-6 months of remission, patients can gradually return to studies but should avoid overexertion.
(2) Diet: A low-salt diet is recommended. Salt should be avoided in cases of severe edema and high blood pressure. Children with severe edema and/or oliguria should have their water intake appropriately restricted, but salt and water should be supplemented appropriately during significant diuresis or salt loss due to diarrhea or vomiting.
2. Symptomatic Treatment: Generally, diuretics are not needed as most children begin to diurese and reduce swelling within 7-14 days after hormone application. However, diuretics are often required for severe edema, concurrent skin infections, hypertension, or hormone insensitivity.
3. Adrenal Corticosteroid (hereinafter referred to as hormone) Treatment: Despite some side effects and unresolved recurrence issues, clinical practice has proven that hormones are currently effective in inducing proteinuria remission and are the first-line treatment for nephropathy. The mechanism of action is not fully understood but may involve: ① immunosuppressive effects; ② improving the permeability of the glomerular filtration membrane, reducing proteinuria; ③ diuretic effects (through effects on glomerular filtration rate and renal tubules).
The principles of medication are: ① Choose drugs with a biological half-life of 12-36 hours, such as prednisone, which not only induces remission quickly but is also suitable for long-term alternate-day therapy. ② Start treatment with a sufficient dose, administered in divided doses, to quickly induce proteinuria remission; ③ During the maintenance phase after proteinuria remission, administer the dose in the morning on alternate days. Since adrenal cortisol secretion follows a circadian rhythm with higher levels in the morning and lower at night, morning administration on alternate days minimizes the suppression of the hypothalamic-pituitary-adrenal (HPA) axis; ④ The maintenance treatment should not be too short, and medication should only be stopped after the condition stabilizes to reduce recurrence, and proteinuria recurrence should be easily controlled.
(1) Initial treatment plan: There are two types: ① Medium to long-term therapy: More commonly used domestically. Prednisone 2mg/kg/day (total dose not exceeding 60mg), divided into three oral doses. If proteinuria resolves within 4 weeks, consolidate for at least 2 weeks after resolution before starting dose reduction, switching to 2mg/kg administered in the morning on alternate days, continue for 4 weeks, then reduce by 2.5-5mg every 2-4 weeks until discontinuation, with a total treatment duration of 6 months (medium-term therapy). If proteinuria does not resolve within 4 weeks, continue until 2 weeks after resolution, generally for 8 weeks, not exceeding 12 weeks, then switch to 2mg/kg on alternate days, continue for 4 weeks, with the same reduction method, for a total treatment duration of 9-12 months (long-term therapy). ② Short-term therapy: More commonly used in Europe and America, starting with 60mg/m2 (total dose not exceeding 60-80mg), divided doses, for 4 weeks, then 40mg/m2 on alternate days, for another 4 weeks before discontinuation. Recently, there has been a tendency to extend the treatment to 12 weeks or slightly longer.
(2) Recurrent cases: Extend the alternate-day dosing period, i.e., provide medium to long-term treatment. Consider adding immunosuppressants after more than two recurrences.
(3) Hormone-dependent cases: Refer to medication history and recurrence history to find a maintenance dose for alternate-day therapy that sustains remission, maintain long-term, at least half a year, then attempt dose reduction. Generally, prednisone 1.4mg/kg on alternate days is considered to have no significant side effects. Immunosuppressants may also be added.
(4) For those resistant to hormones: Prolonging the interval of medication and/or adding immunosuppressants can lead to remission or partial remission in some cases, and may slow down the process of renal function decline. Most of these cases are non-minimal change types, so it is best to perform a renal biopsy to clarify the pathological type and decide on the treatment plan. When hormone resistance occurs, attention should also be paid to whether there are other influencing factors. For example, whether there is concurrent infection, renal tubular interstitial changes, renal vein thrombosis; or concurrent use of drugs that affect the efficacy of hormones such as phenytoin sodium or rifampicin.
(5) Methylprednisolone intravenous pulse therapy: High-dose intravenous administration has a more potent immunosuppressive and anti-inflammatory effect, which can rapidly induce the conversion of urinary protein to negative. Although this method can be used for initial treatment, it is more commonly used in China for refractory nephropathy, i.e., for those who are resistant to hormones or require high-dose maintenance and have obvious hormone side effects. The dose is 15-30mg/kg (total dose not exceeding 100mg), diluted with 5-10% glucose 100-200ml and intravenously infused over 1-2 hours. It is administered once daily or every other day, with 3 times constituting a course of treatment, and repeated after one week if necessary. After 48 hours of the pulse, hormone is administered orally every other day. The side effects include occasional facial flushing, tremor, nausea, and altered taste during the infusion, and may also cause transient hypercoagulability, hypertension, arrhythmia, and gastrointestinal ulcer bleeding.
(6) Observation of the efficacy of hormone therapy:
1) Short-term efficacy: The sensitivity of children to hormones is related to their type. According to clinical classification data in China, 78.9% of cases with simple sexually transmitted disease show complete response; while for nephritis type, it is 34.3%. In terms of pathological tissue types, according to the International Study of Kidney Disease in Children (ISKDC) report, 368 out of 471 children with primary nephrotic syndrome showed hormone response (78.1%). Among the cases showing hormone response, 93.1% were minimal change disease, 29.7% were focal segmental sclerosis, 55.6% were mesangial proliferative, and only 6.9% were membranoproliferative nephritis. The pediatric department of the First Hospital of Beijing Medical University treated 123 cases, with 96 cases (78%) showing hormone response in an 8-day cycle, consistent with the results of ISKDC.
2) Long-term efficacy: Sensitivity to hormone therapy but easy relapse is a common phenomenon. Foreign reports indicate that only 23% of cases do not relapse after initial remission. The duration of initial treatment seems to some extent related to relapse. Foreign reports show that after 4 weeks, 8 weeks, and 12 weeks of treatment, the relapse rates within 12 months are 81%, 61%, and 36%, respectively. The pediatric department of the First Hospital of Beijing Medical University followed up 80 cases showing hormone response after medium and long-term treatment for 2 years, with 32 cases (40%) not relapsing at 6 months, 38 cases (47.5%) being non-frequent relapsers, and 19 cases (23.7%) being frequent relapsers. 80% of relapses occurred within 2 years, and some children could still relapse after many years of remission. If multiple relapses or recurrences occur within the first half year of initial treatment, it can predict frequent relapses. Frequent relapsers have long-term active disease, and a few may even develop varying degrees of renal insufficiency; due to long-term continuous use of hormones, hormone side effects often occur. 20% of frequent relapsers may have a course of disease lasting 10-15 years or more, but the activity tends to gradually weaken with the course of disease. Generally, those sensitive to hormones, despite multiple relapses, their sensitivity remains unchanged, and a few may change from hormone-sensitive to hormone-resistant.
The course of intermittent treatment for relapsed cases can be extended to 1-several years, and immunosuppressants can be added for those who relapse 1-2 times or more.
As mentioned earlier, most resistant cases are non-minimal change disease. In recent years, long-term every-other-day administered at draught therapy has been used to treat membranoproliferative nephritis, membranous nephropathy, focal segmental sclerosis, and resistant minimal change disease in children, giving prednisone 1.5-2.0mg/kg every other morning at draught, with a course of 1/2-3 years, gradually reduced to 0.5-1.0mg/kg every other morning at draught, lasting 3-5 years, and the condition can also improve to varying degrees, achieving remission or partial remission and maintaining good renal function.
(7) Side effects and complications of hormone therapy: There are two types.
1) The effects of long-term supraphysiological doses of hormones on the body: such as lipid metabolism disorders, manifested as obesity, abnormal fat distribution, and Cushing's appearance; due to enhanced protein catabolism, negative nitrogen balance, muscle atrophy and weakness, and poor wound healing occur; glucose metabolism disorders can cause hyperglycemia and glycosuria; due to water and electrolyte disturbances, water and sodium retention and hypertension occur; calcium and phosphorus metabolism disorders lead to hypercalciuria and osteoporosis. Gastrointestinal tract may develop peptic ulcers, even perforation. Neuropsychiatric aspects include euphoria, excitement, insomnia, and in severe cases, psychosis and epileptic seizures. Due to the suppression of antibody formation, infections or the activation and dissemination of latent infection foci (such as subcutaneous node disease) are prone to occur. Long-term medication can also lead to internal visual obstruction and aseptic necrosis of the femoral head. In children during the growth period, growth, especially height, may be affected.
2) Another category is acute adrenal cortical insufficiency and withdrawal syndrome caused by hormones: a large amount of exogenous corticosteroids feedback inhibits the hypothalamic-pituitary-adrenal system, reducing adrenal cortical secretion, decreasing function, and even causing gland atrophy. If the medication is suddenly stopped or encounters stress states such as infection or surgery, the adrenal cortex secretion becomes relatively or absolutely insufficient, leading to symptoms of acute adrenal cortical insufficiency, manifested as nausea, vomiting, abdominal pain, pre-shock, and even shock.
4. Immunosuppressive therapy Indications include: refractory nephropathy and/or severe side effects of hormones, where immunosuppressants can be added or substituted.
(1) Cyclophosphamide: Can reduce relapse and prolong the stage of remission; for those partially sensitive to hormones, adding it can induce complete remission; for those resistant to hormones, it can sometimes improve the child's response to hormones. The dose is 2～2.5mg/(kg·d), with a course of 8～12 weeks, total dose 200～250mg/kg, and it is contraindicated to repeatedly apply within one year. Side effects: short-term gastrointestinal reactions, liver function damage, alopecia areata, bone marrow suppression, hemorrhagic cystitis, and increased susceptibility to bacteria and viruses. Long-term effects on gonads have recently gained attention, as its use in adolescent or pre-adolescent boys can affect testicular spermatogenic function, causing infertility. Gonadal injury is related to the dose, so indications and dose should be carefully considered when applying.
(2) Chlorambucil: Can reduce relapse in hormone-sensitive individuals. The usual dose is 0.2mg/kg daily, with a course of 6～8 weeks, total dose not exceeding 10mg/kg. Side effects are similar to cyclophosphamide, with certain gonadal injury, and there are reports of leukemia and solid tumors.
(3) Nitrogen mustard hydrochloride: Administered by rapid intravenous drip or slow intravenous push every other day: 10～20 times as a course. Start with a small dose, first use 1～2mg, then gradually increase, up to 0.1mg/kg. Side effects are gastrointestinal symptoms, which can be prevented by giving sedatives before medication, and local venous inflammation, so a larger vein should be chosen for administration.
(4) Cyclosporin A: This drug specifically inhibits the activation and proliferation of helper T cells and cytotoxic T cells, without affecting B cells and granulocytes. The dose is 6～8mg/kg daily, often requiring blood concentration monitoring to adjust the dose. The course is 8 weeks. Its efficacy for nephrotic syndrome can be summarized as effective for those responsive to hormones, and for such patients when hormone side effects are severe, this drug can be substituted, but relapse is possible after stopping, and it remains effective upon reuse; for those resistant to hormones, if applied early, some cases can be alleviated. Its most notable side effect is nephrotoxicity. Acute nephrotoxicity manifests as pre-renal azotemia, generally reversible changes, related to dose. Chronic nephrotoxicity involves changes in renal tissue structure, manifested as interstitial and tubular lesions. Clinically, there are hypertension, hyperuricemia, sodium retention, hyperkalemia, and decreased creatinine clearance. Besides nephrotoxicity, it can also cause hirsutism, gingival hyperplasia, and hypomagnesemia.
(5) Root Leaf or Flower of Common Threewingnut glycosides: Extracted from the root of the Celastraceae plant Root Leaf or Flower of Common Threewingnut, it has immunosuppressive effects. The dose is 1mg/kg daily, maximum 30mg daily divided into three doses. The course is 3 months. Side effects include leukopenia, gastrointestinal reactions, skin pigmentation, and may also affect gonadal function (manifested as menstrual disorders, amenorrhea in women, and reduced sperm motility or quantity in men).
5. Other treatments
(1) Use of anticoagulants: Nephrotic syndrome often presents a hypercoagulable state, so some advocate the addition of anticoagulants or antiplatelet aggregators, such as heparin, dipyridamole, invigorating blood and resolving stasis Chinese medicinals Salvia, etc.
(2) Levamisole: It is an immunomodulator. Generally used as an adjunctive therapy for hormones, especially in cases of frequent relapses or hormone-dependent cases often accompanied by infections. The dose is 2.5mg/kg, administered every other day. After use, it can reduce concurrent respiratory infections and decrease the dosage of hormones for hormone-dependent patients.
(3) Captopril: As an angiotensin II converting enzyme inhibitor, it has been considered in recent years to improve the hemodynamic state of the glomerulus, thereby reducing urinary protein excretion. It can be used as an adjunct to hormone therapy, especially in patients with hypertension.
6. Chinese Medicine Treatment: In addition to treating edema through dialectical treatment, it can also address the side effects caused by hormones and immunosuppressants. For edema and oliguria, Plantain Herb, Christina Loosestrife, Grass of Common Knotgrass, and corn silk can be used. For symptoms of blood stasis, add Salvia, Sichuan Lovage Rhizome, Chinese Angelica, Motherwort Herb, and Shiny Bugleweed leaves. For those with spleen qi deficiency and kidney deficiency, tonify the spleen and strengthen the kidney with Astragalus Root, Tangshen, Poria, White Atractylodes Rhizome, Chinese Yam, Psoralea, Epimedium Herb, Dodder Seed, and Barbary Wolfberry Fruit. During hormone induction, if there is a red tongue texture, wiry pulse, and flushed excitement, use yin-enriching and anti-inflammatory herbs, with a basic formula of Anemarrhena, Scrophularia, Unprocessed Rehmannia Root, Moutan Bark, Alisma, Raw Liquorice Root, Phellodendron Bark, and Gentian. During hormone reduction, if qi deficiency and kidney deficiency appear, add qi-tonifying and kidney-tonifying herbs, with a basic formula of Astragalus Root, Prepared Liquorice Root, Dodder Seed, and Schisandra Fruit. For yang deficiency, add Psoralea and Epimedium Herb; for yin deficiency, add Glossy Privet Fruit and Yerbadetajo Herb, and additionally take Six-Ingredient Rehmannia Pill. If white blood cell count decreases during the use of immunosuppressants, provide qi-tonifying and blood-tonifying herbs, such as Solomonseal Rhizome, Chinese Angelica, Suberect Spatholobus Stem, Motherwort Herb, and Hairyvein Agrimonia Herb.
Over the past half-century, the advent of effective antibacterial drugs, corticosteroids, and immunosuppressants has significantly improved the prognosis of nephrotic syndrome in children. The five-year mortality rate has decreased from 60-70% in the era without antibacterial drugs to about 10% with the use of prednisone, and has further declined with the application of immunosuppressants, especially in cases of minimal change disease. It should be noted that the prognosis of this syndrome is closely related to its pathological type. According to Habib et al. (1971), in a 1-18 year follow-up, cases progressing to chronic kidney failure or death included 7% with minimal change disease, 38% with focal segmental sclerosis, and 8% and 41.5% with membranous nephropathy and membranoproliferative glomerulonephritis, respectively.
1. Infection is the most common complication and the leading cause of death; according to the International Study of Kidney Disease in Children (ISKDC) statistics in 1984, infections directly or indirectly accounted for 70% of deaths in children with nephropathy. Infection is also often a trigger and precursor for disease recurrence and/or exacerbation, and can affect the efficacy of hormone therapy.
The reasons why this syndrome is prone to infection include: ① low humoral immune function (loss of immunoglobulins in urine, reduced synthesis, increased catabolism); ② often accompanied by insufficient cellular immune function and complement system function; ③ protein malnutrition, edema leading to local circulatory disorders; ④ frequent use of corticosteroids and immunosuppressants.
Among bacterial infections, pneumococcal infections were predominant in the past, but infections caused by bacilli have also increased in recent years (e.g., large intestine bacilli). Common infections include respiratory infections, urinary tract infections, skin erysipeloid, and primary peritonitis. Prophylactic use of antibiotics is generally not recommended because the effect is unreliable and can easily lead to the proliferation of drug-resistant strains and dysbiosis; however, once an infection occurs, it should be treated promptly and aggressively.
Children are also more sensitive to viral infections, especially during the course of receiving corticosteroids and immunosuppressants. Complications such as chickenpox, measles, and seasonal herpes zoster are often more severe than in general children; for those with a history of exposure, the dose of hormones and immunosuppressants can be temporarily reduced, and γ-globulin injections can be given. There have been individual reports of temporary remission of nephropathy after measles infection.
2. Hypercoagulability and thromboembolic complications. In nephropathy, the body's coagulation and fibrinolysis systems may undergo the following changes: ① increased fibrinogen; ② increased plasma coagulation factors V and VIII; ③ decreased antithrombin III; ④ decreased plasma plasminogen activity; ⑤ increased platelet count, increased adhesion and aggregation. The result can lead to a hypercoagulable state and thromboembolic complications, with renal vein thrombosis being the most clinically significant. Acute cases present with sudden onset of gross hematuria and abdominal pain, with tenderness in the costovertebral angle and renal mass on examination, and acute renal dysfunction in bilateral cases. Chronic renal vein thrombosis has less obvious clinical symptoms, often only with worsening edema and unresolved proteinuria. X-ray examination shows enlarged kidneys and ureteral notches. B-ultrasound can sometimes detect it, and renal venography is necessary for confirmation if needed. In addition to the renal vein, other venous or arterial sites can also develop such complications, such as the femoral vein, femoral artery, pulmonary artery, mesenteric artery, coronary artery, and intracranial artery, causing corresponding symptoms. Clinically, when venous blood sampling shows easy coagulation, the possibility of hypercoagulability should be considered. The simplest method is to measure fibrinogen and platelet count for initial screening, and other indicators can be measured if conditions permit.
3. Calcium and vitamin D metabolism disorders. In nephropathy, vitamin D-binding protein (VDBP, molecular weight 59000) is lost in the urine, leading to insufficient vitamin D in the body, affecting intestinal calcium absorption, and feedback leading to hyperparathyroidism. Clinical manifestations include hypocalcemia, insufficient circulating vitamin D, and poor bone calcification. These changes are particularly prominent in growing children.
4. Hypovolemia. Due to low plasma albumin and reduced plasma colloid osmotic pressure, this syndrome often has insufficient blood volume, and some children have long-term inappropriate salt restriction. When there is a relatively rapid loss of body fluids (such as vomiting, diarrhea, large dose diuretic use, large amount of ascites drainage, etc.), symptoms of varying degrees of hypovolemia can occur, such as orthostatic hypotension, prerenal azotemia, and even shock.
5. Acute Renal Function Decline This sign is not uncommon in the acute onset of transient grade I azotemia. Acute renal function decline may occasionally occur during the course of the disease. The reasons are: ① Hypovolemia, inappropriate large-scale necrosis. ② Severe renal interstitial edema, renal tubules blocked by protein casts leading to increased hydrostatic pressure in the renal capsule and proximal tubules, resulting in reduced glomerular filtration. ③ Drug-induced renal tubular interstitial lesions. ④ Complicated by bilateral renal vein thrombosis.
6. Renal tubular dysfunction can manifest as glycosuria, aminoaciduria, potassium and phosphorus loss in urine, and impaired concentrating ability.
7. Stirred pulse atherosclerosis may occasionally occur in children with persistent hyperlipidemia. When the coronary stirred pulse is involved, symptoms such as chest tightness, colicky pain, electrocardiogram changes, and even sudden death may occur.
8. Children may occasionally experience neurological symptoms such as headache, spasm, and visual disturbances, which may be caused by various factors including hypertensive encephalopathy, cerebral edema, dilutional hyponatremia, hypocalcemia, and hypomagnesemia.
