Kidney Health Notes (IV) | How to diagnose and treat glomerulonephritis in children? Just look at these 6 points!

Glomerulonephritis (GN) is one of the common glomerular diseases in children, which often affects the health of children's kidneys. Reasonable diagnosis and clear treatment have a vital impact on the protection of children's kidney health. Therefore, this article summarizes 6 key points on the clinical diagnosis and treatment of GN in children for the learning and communication of clinical physicians.

Point 1: Clarify the four characteristics of GN

(1) GN refers to a spectrum of diseases in which glomeruli are damaged, and the characteristic changes are usually inflammatory changes in the glomerular capillary loops and glomerular basement membrane.

(2) The injury may affect all or part of the glomerulus or glomerular capillary loops.

(3) Inflammation is mostly immune-mediated.

(4) Clinical manifestations include hematuria (including microscopic hematuria and macroscopic hematuria) and proteinuria (including microalbuminuria, non-nephrotic level proteinuria and nephrotic level proteinuria), with or without oliguria/edema, hypertension, abnormal renal function and extrarenal manifestations.

Point 2: Clarify GN classification and staging

(1) Etiology classification: According to the etiology, GN is divided into primary GN, secondary GN and hereditary GN. Primary GN includes IgA nephropathy, GN after streptococcal infection, GN after non-streptococcal infection, etc.; secondary GN includes lupus nephritis, purpuric nephritis, ANCA-associated vasculitis renal damage, hemolytic uremic syndrome, and secondary glomerular damage caused by inherited metabolic diseases such as methylmalonic aciduria combined with hyperhomocysteinemia, etc.; hereditary GN includes Alport syndrome.

(2) Disease course staging: In the past, GN was divided into four stages: acute, progressive, protracted, and chronic GN, based on the clinical course and complications. At present, with the popularization of the concept of chronic kidney disease, GN is also clinically divided into two types: acute and chronic according to the course of the disease. That is, those with a course of less than 3 months are acute, and those with a course of ≥3 months are chronic. The course of disease classification no longer involves related complications such as renal function and hypertension.

(3) Pathological classification: GN is a type of glomerular hypercellular disease characterized by proliferation of renal intrinsic cells and/or leukocyte infiltration. Based on the different etiologies/pathogenesis, combined with immunofluorescence/histochemistry, light microscopy and electron microscopy results, GN is divided into the following five categories: immune complex-mediated GN, ANCA-associated GN, anti-glomerular basement membrane GN, monoclonal Ig-mediated GN and C3 nephropathy.

① Immune complex-mediated GN is the most heterogeneous group of diseases, characterized by immunoglobulin deposition in renal pathological immunofluorescence, and the type and location of deposition are related to the cause, often accompanied by complement deposition, and light microscopic glomerular damage varies. Therefore, immunofluorescence and electron microscopy are needed to make a clear diagnosis.

②ANCA-related GN, immunofluorescence immunoglobulin or complement are mostly negative, immunoglobulin and C3 segment deposition are occasionally seen, and light microscopy is mostly necrotic or crescent GN, with various volumes and periods of change. Therefore, cellular, cellular fibrous and fibrous crescents can all be seen.

③ Anti-glomerular basement membrane GN, characterized by the presence of anti-glomerular basement membrane antibodies in the serum, immunofluorescence IgG linear deposition along the glomerular basement membrane, necrosis can be seen at the interruption, often accompanied by C3 segment deposition, light microscopy shows progressive crescents or necrotizing GN, and renal puncture in the early stage of the disease often shows large cellular crescents in the same period. About 25% of patients may also be accompanied by ANCA positivity.

Key point 3: Clarify the stage of renal function

GN is often accompanied by abnormal renal function. Currently, pediatric and adult clinical practice tends to use acute kidney injury and chronic kidney disease instead of abnormal renal function. The Kidney Disease Improving Global Outcomes Organization divides acute kidney injury into three stages based on serum creatinine levels: stage 1 is a serum creatinine increase of ≥26.5 μmol/L or 1.5-1.9 times; stage 2 is a serum creatinine increase of 2.0-2.9 times; stage 3 is a serum creatinine increase of more than 3.0 times, or a serum creatinine increase of ≥353.6 μmol/L, or the need to start renal replacement therapy, or the patient is <18 years old and the estimated glomerular filtration rate is <35 ml/(min·1.73m2).

Chronic kidney disease is divided into five stages according to the glomerular filtration rate (GFR), as shown in Figure 1.

Figure 1 Stratification basis

Key point 4: Identify typical clinical manifestations

In the acute phase, symptoms often include general discomfort, fatigue, lack of appetite, fever, headache, dizziness, cough, shortness of breath, nausea, vomiting, abdominal pain and nosebleed.

(1) Edema: 70% of patients have edema, which usually only affects the eyelids and face. In severe cases, it can spread throughout the body within 2 to 3 days and is non-pitting.

(2) Hematuria: 50% to 70% of cases have macroscopic hematuria, which usually turns into microscopic hematuria after 1 to 2 weeks.

(3) Proteinuria: The degree varies. 20% of cases can reach nephrotic levels. Pathologically, patients with proteinuria often present with severe mesangial hyperplasia.

(4) Hypertension: 30% to 80% of cases have elevated blood pressure.

(5) Decreased urine volume: Severe cases of macroscopic hematuria may be accompanied by decreased urine volume.

In addition, a small number of children may experience symptoms such as severe circulatory congestion, hypertensive encephalopathy and acute renal insufficiency in the early stages of the disease, which requires clinical diagnosis and accurate judgment based on the actual situation of the children.

Point 5: Complete diagnosis in 6 steps

The diagnosis of GN should follow the following procedures: (1) Symptom diagnosis, whether the clinical diagnosis is consistent with GN (hematuria and proteinuria are necessary conditions). (2) Course diagnosis, to determine whether the course is acute or chronic. It should be noted that if the cause is considered a hereditary disease, it should be diagnosed as chronic even if the time of discovery is less than 3 months. (3) Etiology diagnosis, to determine whether it is primary, secondary or hereditary GN. (4) Primary disease name diagnosis. (5) Pathological diagnosis. (6) Renal function diagnosis.

Point 6: Take multiple measures and treat together

(1) Pay attention to rest: In the acute phase, patients need to stay in bed for 2 to 3 weeks until the visible hematuria disappears, the edema subsides, and the blood pressure returns to normal. Then they can get out of bed and do some light activities. If the ESR is normal, they can go to school, but they should avoid strenuous physical activities. They can resume physical activities only after the urine test is completely normal.

(2) Diet: A low-sodium diet is important. Patients with severe edema or hypertension need a salt-free diet. Patients with azotemia should limit protein intake.

(3) Anti-infection treatment: such as the use of antibiotics.

(4) Symptomatic treatment: mainly diuresis, lowering blood pressure and treatment of related organs.

References:

[1] Zhang Hongwen. Classification/staging and diagnostic procedures of glomerulonephritis in children[J]. Journal of Clinical Pediatrics, 2023, 41(01): 73-76.