Acute nephritis after elderly acute infection

　　In the 19th century, people had observed that acute nephritis was associated with certain Streptococcus infections, but it was later confirmed that not all Streptococcus infections could lead to acute nephritis; only the nephritogenic strains had this pathogenic effect. It is now known that the nephritogenic strains mainly exist in group A beta-hemolytic Streptococcus, mainly type 12, including types 1, 2, 3, 4, 18, 25, 49, 55, 57, and 60, and occasionally infections by group C or G beta-hemolytic Streptococcus can also be pathogenic. The preceding infections caused by these nephritogenic strains are mainly upper respiratory tract infections (such as pharyngitis or tonsillitis), but skin infections (such as impetigo, often caused by group A type 49 bacteria) are also common. Which components of the Streptococcus are responsible for the pathogenic antigens that cause immune reactions in the body is not yet fully clear. It was long thought to be the M protein in the cell wall of Streptococcus, but later it was confirmed that this antigenic component mainly exists in the cell membrane or cell body, such as the intracellular chain in the cell membrane and the nephritogenic strain-associated protein in the cell body. In addition, there are reports that a positively charged antigen in the extracellular components of Streptococcus cells may also be pathogenic.

　　Most patients with this disease have a history of prodromal infection (pharyngeal or skin), and mild cases may not show clinical manifestations of infection. As the condition worsens, the following complications may occur:

　　1. Circulatory congestion state and acute congestive heart failure

　　This complication starts abruptly and is severe, occurring on average within 3 to 5 days after onset and is often misdiagnosed as pneumonia complicated with heart failure. In recent years, the mechanism and clinical manifestations of this complication have been recognized, and timely early diagnosis has greatly improved the prognosis.

　　2. Hypertensive encephalopathy

　　In recent years, due to timely and reasonable treatment, the incidence of this complication after acute chain infection nephritis has significantly decreased, with an incidence rate of about 0.5%. Although hypertension often coexists with this disease, its role in the disease has not been confirmed. From a pathological perspective, multiple small thrombi (due to vascular spasm) and cerebral edema may occur in the brain, and there may also be cerebral hemorrhage. Vascular spasm and water and sodium retention are related to cerebral edema. Dizziness, headache, vomiting, confusion, and amaurosis are common, and severe cases may have paroxysmal convulsions and coma. A diagnosis can be made if one of the following three conditions - hypertension with visual impairment, convulsions, or coma - is present.

　　The clinical manifestations of this disease range from subclinical mild to acute renal failure, with a significant fluctuation in severity.

　　1. Hematuria

　　Hematuria is often the first symptom of onset, with almost all patients having hematuria, among whom gross hematuria has an incidence rate of about 40%. The urine color is uniform brown turbidity or like wash water, but without blood clots. The dissolution and destruction of red blood cells in acidic urine often makes the urine appear soy sauce-like brown. It usually disappears within a few days to 1 to 2 weeks. Severe hematuria patients may experience discomfort and frequency during urination. Microscopic hematuria usually disappears within half a year, and some may persist for 1 to 3 years.

　　2. Proteinuria

　　Almost all patients show positive urinary protein (by routine qualitative methods), and proteinuria is generally not severe, ranging from 0.5 to 3.5g/d, often non-selective proteinuria, with only about less than 20% of patients having urinary protein above 3.5g/d. At this time, urinary FDP is often increased, and some patients may have urinary protein turn negative and become extremely微量 when seeking medical attention, thus without a record of urinary protein positivity.

　　3. Edema

　　Edema is also often an early symptom of the onset, with an incidence rate of 70% to 90%, which is due to a significant decrease in glomerular filtration rate, and more than 60% of cases show this as the main manifestation of the disease. The mild form is early eyelid edema, presenting as so-called 'nephritic face' (nephritic faces), which can extend to the whole body in severe cases. The indentation after finger pressure is not obvious, and the weight may increase by more than 5kg compared to before the disease. Chest and abdominal effusions may occur, and most patients can urinate and reduce edema spontaneously within 2 to 4 weeks. If edema or nephrotic syndrome persists, it often indicates a poor prognosis.

　　4. Hypertension

　　Hypertension is seen in about 80% of cases, more common in the elderly, mostly moderate blood pressure elevation, occasionally severe hypertension, and more than 80% of cases show an increase in diastolic pressure, but fewer than 50% of patients have blood pressure exceeding 16kPa (120mmHg), and it is often not accompanied by fundus changes indicative of hypertension.

　　5. Oliguria

　　Most patients have less than 500ml/d of urine at the onset, which can cause azotemia due to oliguria. Two weeks later, the urine volume gradually increases, and renal function recovers. Only a few patients (less than 5%) develop anuria from oliguria, indicating severe renal parenchymal lesions.

　　6. Renal function damage

　　Patients often have transient azotemia, with mild elevation of blood creatinine and urea nitrogen. Severe cases (blood creatinine > 352μmol/L (4.0mg/dl), urea nitrogen > 21.4mmol/L (60mg/dl)) should be vigilant of acute renal failure. After several days of diuresis, nitrogenemia can return to normal. A few elderly patients may not recover renal function even after diuresis, indicating poor prognosis.

　　7. General manifestations

　　Patients often have fatigue, anorexia, nausea, vomiting (not completely proportional to azotemia), drowsiness, dizziness, blurred vision (related to the degree of hypertension, cerebral ischemia, and cerebral edema), and dull pain in the腰部 (due to the expansion of renal parenchyma stretching the renal capsule, and pulling on the terminal branches of sensory nerves).

　　To prevent the occurrence of old-age acute post-infection nephritis, everyone can refer to the following three-level preventive measures:

　　First-level prevention

　　1. Enhance the body's ability to resist streptococcal infection, appropriately exercise, strengthen nutrition, and try to avoid contacting flu patients in public places during the winter and spring seasons.

　　2. Strengthen health education and publicity, avoid upper respiratory and skin infections, and actively treat various chronic foci, such as tonsillitis, sinusitis, caries, and otitis media.

　　3. Strengthen the research on the relationship between the disease and HLA and the relatives of the patients, in order to further clarify the relationship between the two.

　　Second-level prevention

　　1. Early treatment, close observation, and timely urinary routine testing should be carried out for patients with existing glomerulonephritis to prevent the disease from persisting and causing chronic kidney changes.

　　2. Urinalysis, renal function determination should also be performed for patients with hypertension and anemia to avoid missed diagnosis of chronic nephritis.

　　3. Those who have the conditions can undergo renal biopsy early, so as to correctly select drugs.

　　Three-level prevention

　　1. Low-protein diet.

　　2. Control blood pressure.

　　3. Prevent interstitial tubular damage.

　　6. Avoid using drugs harmful to the kidneys.

　　Old-age acute post-infection nephritis is a group of diseases caused by many etiologies. Generally, this disease can be diagnosed by the following examinations.

　　1. Urinalysis

　　In addition to red blood cells and proteinuria, various types of casts (red blood cells, granular, and white blood cells) as well as white blood cells can be seen. Occasionally, white blood cell casts may be present, but this does not indicate the existence of urinary tract infection. Mild cases may show no change in urine, and the recovery of urinary routine changes is slower than that of clinical symptoms, especially the microscopic red blood cells often persist for several months to over one year. Persistent large amounts of proteinuria suggest the presence of nephrotic syndrome.

　　2. Blood routine

　　During edema, due to blood dilution, hemoglobin and red blood cells may decrease, which can recover after diuretic edema subsides. White blood cell count is normal, but white blood cells and neutrophils may increase when there is an infection focus.

　　3. Renal function

　　Patients often have varying degrees of renal dysfunction, with decreased glomerular filtration rate and endogenous creatinine clearance. During oliguria, serum urea nitrogen and creatinine may temporarily increase. In cases of concurrent acute renal failure, significant azotemia may occur with metabolic acidosis and other electrolyte disturbances. In cases of concurrent heart failure, the reduction in renal blood flow is more significant.

　　4. Immunology and complement system examination

　　Examination shows that antistreptolysin O (ASO), antistreptokinase (ASK), antihyaluronidase (AH), antideoxyribonuclease (ADNase), and other antibodies are increased, indicating that most of this glomerulonephritis is post-infection glomerulonephritis. The proportion of patients with increased ASO is 70% to 80%. If the three indicators mentioned above are checked simultaneously, the positive rate can reach 100%. The positive rate of ASO can be reduced to 15% in patients treated with penicillin early. Serum IgG and IgM increase and return to normal within 1 to 2 months after onset; IgA is basically normal. In the first week of onset, 32% to 42% of patients have increased rheumatoid factor. Serum cryoglobulin and circulating immune complexes can be found in the first few weeks of onset.

　　Patients with acute post-infection nephritis in the elderly need to pay close attention to their diet to prevent the deterioration of the condition.

　　1. Fluids

　　At the early stage of onset, especially in patients with obvious edema, hypertension, and complications, the intake of fluids should be limited, and water should be given according to thirst to avoid exacerbating edema or complications and the burden on the kidneys.

　　2. Sodium salt

　　Patients with edema, hypertension, and circulatory congestion should strictly limit the intake of sodium salt, use a salt-free diet for a short period of time, and then transition to a low-sodium diet (calculated at 1.5g per day). For patients with severe hyponatremia and reduced urine output, control the intake of water, not exceeding the urine output per day, plus the amount of insensible water loss.

　　3. Protein

　　When there is no obvious oliguria and azotemia, protein intake should be limited to 1g/kg per day. Unanalyzed control of protein intake is not beneficial to the repair of renal units, but excessive protein intake can promote glomerulosclerosis.

　　There is no specific treatment plan for this disease so far. The main treatment principle is to prevent and treat water and sodium retention, control the blood volume, and thus alleviate symptoms and prevent complications.

　　Rest

　　During the acute phase, bed rest is required until macroscopic hematuria disappears. Bed rest can improve renal blood flow and reduce the occurrence of complications, taking about 2 weeks. Activities can be gradually increased after clinical symptoms disappear and blood creatinine returns to normal. Avoid strenuous physical activities within 3 months.

　　Treatment of infection foci

　　There is no definite opinion so far on the role of penicillin or macrolides and other antibiotics targeting Streptococcus in the treatment of acute nephritis, as to their ability to control infection foci and eliminate residual antigens. Most authors have observed that the use of antibiotics for the treatment of nephritis after the onset of the disease has no effect on the condition and prognosis of the disease.

　　Third, symptomatic treatment

　　1. Diuresis

　　After controlling the intake of water and salt, if edema is still obvious, diuretics should be used. Thiazide diuretics are commonly used, and loop diuretics such as furosemide (Lasix) and bumetanide (Bumetanide) can be used when necessary. These two drugs may still have diuretic effects in cases where the glomerular filtration function is severely impaired and creatinine clearance is less than 5-10ml/min, possibly by adjusting the distribution of renal blood flow, increasing the blood volume entering the glomerulus, and decreasing the blood volume entering the renal medulla, thereby correcting the 'glomerular-tubular imbalance phenomenon'. The dosage of furosemide (Lasix) may sometimes need to be 400-1000mg/d, and attention should be paid to the fact that high doses of furosemide (Lasix) may cause serious damage to the hearing and kidneys. In addition, various drugs that can relieve vascular spasm, such as dopamine, can be used to achieve the purpose of diuresis. Mercury diuretics (damage renal parenchyma), osmotic diuretics (increase blood volume, increase the burden on the heart and complications), and potassium-sparing diuretics should not be used.

　　2. Antihypertensive Drugs

　　Active and steady control of blood pressure is very necessary for increasing renal blood flow, improving renal function, preventing heart failure and complications. Thiazide diuretics are commonly used, and blood pressure control can be achieved after diuresis. Calcium channel blockers such as nifedipine (nifedipine) 20-40mg/d and hydralazine (hydralazine), prazosin can be used to enhance the effect of vasodilation when necessary. Renin-angiotensin blockers are generally not needed. For severe hypertension, the traditional method of hypomagnesia sulfate injection is often used, which is prone to hypermagnesemia under poor renal function, causing respiratory depression. Currently, there are many effective rapid blood pressure lowering drugs, such as diazoxide (hypotension), sodium nitroprusside, which have replaced magnesium sulfate.

　　3. Treatment of Hyperkalemia

　　Attention should be paid to limit dietary potassium intake, and the use of potassium-wasting diuretics can prevent the progression of hyperkalemia. If urine output is very low, leading to severe hyperkalemia, ion exchange resins, intravenous glucose insulin drip, and high-tonicity bicarbonate sodium drip can be used. However, all these measures can exacerbate water and sodium retention, expand blood volume, so they should be used with caution. In necessary cases, peritoneal dialysis or hemodialysis can be used.