Acute Nephritis Syndrome

　　The prototype of acute nephritis syndrome is poststreptococcal glomerulonephritis (PSGN), caused by certain nephritogenic strains of group A beta-hemolytic streptococcus, such as serotype 12 (with pharyngitis) and serotype 49 (with impetigo). The incidence of PSGN is decreasing in the United States and Europe. It is also prevalent in many other regions of the world, with approximately 5% to 10% of patients with pharyngitis and about 25% with skin infections developing PSGN. This disease is most common in children and young adults over 3 years of age, but 5% of patients are over 50 years old. The incubation period from infection to the onset of glomerulonephritis is 1 to 6 weeks (average 2 weeks).

　　1. Acute Congestive Heart Failure

　　Acute left heart failure in children can become the initial symptom of acute nephritis, and if not identified and treated in time, it can lead to rapid death. During acute nephritis, due to water and sodium retention, generalized edema and increased blood volume are common, leading to pulmonary congestion. Therefore, in the absence of acute heart failure, patients often have symptoms such as shortness of breath, cough, and slight wet rales at the base of the lungs, indicating pulmonary congestion. Since the patient also has respiratory tract infection, the presence of pulmonary congestion is often overlooked. Conversely, this cyclic congestion phenomenon may also be mistakenly considered as the onset of acute heart failure. Therefore, it is of great importance to correctly understand the pulmonary congestion or acute heart failure complicated with acute nephritis caused by water and sodium retention.

　　2, Hypertensive encephalopathy

　　The incidence of hypertensive encephalopathy in acute glomerulonephritis was 5% to 10% in the past. In recent years, like acute heart failure, its incidence rate has significantly decreased, and it is less common than acute heart failure. This may be related to timely and reasonable treatment. Common symptoms include severe headache and vomiting, followed by visual impairment, confusion, drowsiness, and possible paroxysmal convulsions or seizures. After controlling blood pressure, the above symptoms improve or disappear rapidly, and there are no sequelae.

　　3, Acute renal failure

　　During the acute phase of acute glomerulonephritis, mesangial cells and endothelial cells in the glomeruli proliferate in large numbers, capillaries become narrow, and intravascular thrombosis occurs, resulting in further reduction in urine output (oliguria or anuria) in patients. The large accumulation of protein catabolic products can lead to the onset of uremic syndrome during the acute phase.

　　4, Secondary bacterial infection

　　Due to reduced overall resistance, acute glomerulonephritis is prone to secondary infections, the most common being pulmonary and urinary tract infections. Once secondary infections occur, active symptomatic treatment should be given to avoid exacerbation of the original disease.

　　The diagnosis of acute glomerulonephritis is not difficult based on a history of previous infection, edema, hematuria, accompanied by hypertension and proteinuria. During the acute phase, there is often an increase in the titer of streptolysin O, a decrease in serum complement concentration, and an increase in the content of FDP in urine, which are more helpful for diagnosis.

　　Some patients may have acute congestive heart failure or hypertensive encephalopathy as the initial symptom, or only edema and hypertension at the beginning of the disease, with only slight or no changes in urine routine. For atypical cases, detailed medical history should be inquired, systemic physical examination combined with laboratory tests should be conducted for comprehensive analysis, in order to avoid misdiagnosis. For those with difficult clinical diagnosis, renal biopsy is necessary for confirmation.

　　Due to the fact that acute glomerulonephritis is a disease caused by the body's autoimmune response to Streptococcus hemolyticus infection, the most fundamental preventive measure is to prevent the infection of Streptococcus hemolyticus. If physical exercise can be strengthened, physical fitness can be enhanced, resistance can be increased, personal hygiene can be paid attention to, and infections of the upper respiratory tract, throat, and skin can be avoided or reduced, the occurrence of acute glomerulonephritis can be reduced. Once the above infections occur, appropriate antibiotics should be selected for thorough treatment in a timely manner, among which the effect of penicillin (800,000 units, intramuscular injection, twice a day) is the best, because penicillin is a bactericidal drug that can kill local bacteria, clear local foci, eliminate antigens, and avoid the occurrence of autoimmune reactions. Although this does not necessarily prevent the occurrence of acute glomerulonephritis absolutely, it can timely eliminate the spread of 'nephritis-causing strains' and reduce the occurrence of acute glomerulonephritis. It is also necessary to continuously check urine routine within 2 to 3 weeks after the injection of penicillin in order to detect the condition early and provide timely treatment. It is especially important to actively treat recurrent pharyngitis and tonsillitis.

　　The prevention of acute nephritis mainly involves the prevention and treatment of other diseases that can cause nephritis (also known as the predisposing diseases of nephritis), especially the prevention and treatment of diseases caused by streptococcal infection, such as upper respiratory tract infection, acute tonsillitis, pharyngitis, scarlet fever, erysipelas, and boils. It takes a period of time for the human body to develop nephritis after infection with the above diseases, which is called the incubation period. For example, the incubation period for upper respiratory tract infection and acute tonsillitis is about one to two weeks; for scarlet fever, about two to three weeks; for boils, about two to four weeks. The incubation period is the process in which the body reacts. If timely treatment is given when infected with the above predisposing diseases, the occurrence of immune response can be prevented. According to clinical observations, recurrent attacks of tonsillitis, pharyngitis, and other chronic infection foci can cause acute nephritis and transform it into chronic nephritis. Therefore, if it is confirmed that acute nephritis is caused by tonsillitis, timely tonsillectomy can help cure and prevent recurrence. Other bacteria, viruses, protozoa, and other pathogens can also cause nephritis. Therefore, the active and timely prevention and treatment of predisposing diseases to nephritis are of great significance for preventing the occurrence of acute nephritis and preventing the transformation of acute nephritis into chronic nephritis.

　　Urine protein excretion can be greater than 0.5-2g/m2 per day; the arbitrary urine protein/creatinine ratio may be less than 2 (normal 0.1-0.3), and the urine sediment contains atypical red blood cells, leukocytes, and renal tubular cells. Casts including red blood cell casts and hemoglobin casts are characteristic, and leukocyte casts and granular casts (protein droplets) are more common.

　　The antibody titer against pathogenic infectious factors usually rises within 1-2 weeks, and the increase in antibodies against streptococcal antigen products can be detected: Antistreptolysin O (ASO) is the best indicator of upper respiratory tract infection, as well as antihyaluronidase and antideoxyribonuclease B against pyoderma. C3 and C4 are usually reduced during the active phase of the disease, and the complement level can return to normal within 6-8 weeks in 80% of PSGN cases. However, it is actually not the case for all membranous glomerulonephritis (MPGN), cold agglutinin disease often lasts for several months, and circulating immune complexes can only be detected within a few weeks.

　　Tubular function is often disrupted due to inflammatory changes in the interstitium, leading to decreased urine concentration ability and acid secretion ability, as well as impaired solute exchange in renal units. Because of certain inherent glomerular hypertrophy capabilities, tubular dysfunction usually occurs before GFR significantly decreases. As glomerular function disorder gradually progresses, the total filtration area decreases significantly, GFR decreases, azotemia appears, and GFR can be estimated from serum creatinine concentration or urine creatinine clearance rate. Although GFR usually returns to normal within 1-3 months, proteinuria may persist for 6-12 months, microscopic hematuria may last for several years, and transient changes in urine sediment may occur again during mild upper respiratory tract infections.

　　One to six weeks before the onset of this syndrome, there is a history of sore throat, impetigo, or culture-confirmed Streptococcal infection, and an increase in the serum titer of anti-Streptococcus antibodies can help with diagnosis. Red blood cell casts are visible in any glomerulonephritis, but when associated with clinical manifestations, it strongly suggests acute nephritis syndrome. Ultrasound examination can help differentiate between acute disease (usually kidney volume is normal or slightly increased) and chronic disease exacerbation (kidneys shrink).

　　Acute Nephritis Syndrome Diet

　　1. Acidic foods include squid, fish paste, chicken, crucian carp, meat, seaweed, peanuts, rice, flour, etc.

　　2. Alkaline foods include wakame, kelp, mushrooms, spinach, soybeans, chestnuts, bananas, rapeseed, carrots, potatoes, radishes, juices, milk, tofu, etc. In addition, tea and coffee also belong to alkaline foods.

　　3. Increase the intake of soup dishes or beverages in the diet to ensure adequate water intake.

　　Antimicrobial treatment for infection before PSGN occurrence seems unable to prevent PSGN. If bacterial infection is present at diagnosis, antimicrobial treatment should be performed, and treatment with other any secondary causes should be ineffective with immunosuppressive drugs. Corticosteroid hormones may worsen the condition. If azotemia and metabolic acidosis are present, dietary protein intake should be limited. When circulatory overload, edema, or severe hypertension is present, sodium intake should be reduced. Diuretics (such as thiazides, loop diuretics) may be helpful for controlling the expanded extracellular fluid volume. Severe hypertension requires vigorous treatment, and dialysis may be necessary for severe renal failure.