Mini Review - Archives of General Internal Medicine (2023) Volume 7, Issue 4
Glomerulonephritis in Children: An Overview of Inflammatory Kidney Diseases.
Department of Nephrology, University of Michigan, Michigan, US
- *Corresponding Author:
- Andrew Martini
Department of Nephrology
University of Michigan
Received:31 Jul-2023, Manuscript No. AAAGIM-23-109484; Editor assigned:05-Aug-2023, PreQC No. AAAGIM-23-109484 (PQ); Reviewed:18-Aug-2023, QC No. AAAGIM-23-109484; Revised:23-Aug-2023, Manuscript No. AAAGIM-23-109484 (R); Published:30-Aug-2023, DOI:10.35841/ aaaa-7.4.189
Citation: Martini A. Glomerulonephritis in Children: An Overview of Inflammatory Kidney Diseases. Arch Gen Intern Med. 2023;7(4):189
Glomerulonephritis, a group of inflammatory kidney diseases, poses significant challenges to the health and well-being of children worldwide. This complex condition affects the glomeruli, the tiny filtering units within the kidneys responsible for removing waste and excess fluids from the blood. When these essential structures become inflamed, it can lead to impaired kidney function and various health complications. Understanding Glomerulonephritis in children is crucial for healthcare professionals, parents, and caregivers alike. Early recognition and appropriate management are essential to mitigate the impact on a child's renal function and overall health. We will delve into the treatment options and supportive care measures that can help alleviate symptoms and slow the progression of the disease, aiming to improve the quality of life for young patients facing this challenging condition.
In most cases, glomerular inflammation starts with an antigen-antibody response, either with a direct antibody binding to an antigen expressed or trapped in the glomerulus or with the localization of a circulating complex in the kidney. This causes harm by activating one or more inflammatory mediator systems, including the complement cascade, coagulation factors, cytokines, growth factors, and others. Proliferation of resident glomerular cells and infiltration of lymphocytes or neutrophils are signs of inflammation. Glomerular inflammation and expansion limit microcirculation, lowering GFR and frequently resulting in a rise in Blood Urea Nitrogen (BUN) and creatinine. This decrease in GFR, in turn, causes salt and water retention, resulting in fluid overload. The degree of fluid overload in Acute Glomerulonephritis (AGN) varies greatly. It might emerge as life-threatening hypertension and pulmonary edoema in severe cases. Indeed, in some children with AGN, hypertensive encephalopathy may be the presenting ailment.
In certain cases, AGN is the primary process, and almost all clinical signs are a result of the renal lesion. The best example is poststreptococcal AGN. In other circumstances, the AGN is just one symptom of a systemic sickness that has affected numerous organs, each of which can be harmed independently. The AGN linked with Henoch Schoenlein purpura in youngsters serves as a model for this. Fortunately, most occurrences of AGN in children are self-limiting or treatable, however there may be devastating sequelae during the acute phase. Less frequently, what begins as an obvious AGN may foreshadow the onset of a chronic process that eventually leads to irreversible end-stage renal disease (ESRD). Obviously, a good urinalysis is the first step in evaluating a child with suspected AGN. The appearance of red blood cell casts, while not always present, is indicative of glomerulonephritis. Because AGN is an inflammatory condition, white blood cells in nephritic urine are not uncommon. Unfortunately, this can sometimes result in an incorrect diagnosis of urinary tract infection.
Proteinuria is almost always present in AGN, albeit any cause of extensive hematuria can result in some urine protein. If the urine is not visibly bloody, the presence of hematuria and proteinuria almost always indicates glomerulonephritis. The first blood work necessary in suspected AGN is actually limited; for example, more advanced immunologic tests are basically "second tier" studies once the initial results are known. Assessing renal function and electrolytes, as well as performing a hemogram, are obvious first steps. Mild anaemia is common with AGN and is most likely dilutional; more substantial anaemia would indicate that the condition is persistent. In most cases of AGN, there are no significant changes in the white blood cell or platelet counts. The usual finding in HSP is a normal platelet count in the presence of petechiae and purpura.
Aside from these fundamental criteria, only a few more are useful in the initial examination. Serum albumin is frequently included; a modest degree of hypoalbuminemia is common in many inflammatory disorders such as HSP, but levels of 2.0 gm/dL are relatively unusual in uncomplicated AGN and indicate a process with a nephrotic syndrome component. The most crucial (and sometimes overlooked) initial examination is an evaluation of the complement system. This usually entails getting serum C3 and C4 levels; the total hemolytic complement ("CH50") is solely of historical importance. Poststreptococcal AGN is distinguished by a very low C3, with very minor declines in C4. The latter is relatively brief and is most likely caused by Type III cryoglobulin activation. The significance of timely C3 measurement cannot be overstated. Poststreptococcal AGN hypocomplementemia is transient, usually returning to normal in six to eight weeks. Urinary irregularities, on the other hand, may last much longer. Thus, if a child has had irregular urine for a few weeks and has not had a C3 measurement, it may be tough to make a clear diagnosis of poststreptococcal AGN without a kidney biopsy .
Glomerulonephritis in children is still a complex and difficult group of inflammatory kidney illnesses that requires ongoing attention and research. We have received significant insights into the impact of this illness on paediatric patients as well as the critical components of its diagnosis and management as a result of this comprehensive review.
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