El prototipo de la glomerulonefritis aguda es la glomerulonefritis aguda post- infecciosa. Recientemente, se ha asociado un aumento en la cantidad de. La glomerulonefritis aguda postinfecciosa es una enfermedad que afecta principalmente a los niños de 2 a 10 años. La forma clásica aparece de manera . Glomerulonefritis aguda postinfecciosa. Mycoplasma pneumoniae. Neumonía Activación del sistema inmunológico debido a la infección.
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Nephritic syndrome associated to skin infection, hepatitis A, and pneumonia: Pediatrician, Universidad de Cartagena, Cartagena, Colombia.
Glomerulonefritis e infecciones | Nefrología al día
Posrinfecciosa is the most common glommerulonefritis of acute and chronic renal disease. The prototype of acute glomerulonephritis is acute post-infectious glomerulonephritis.
Recently, increased cases of glomerulopathy have been associated with bacterial, viral, and other infections. Acute nephritic syndrome is part of glomerulonephritis with an acute beginning, characterized by hematuria, hypertension, edema, and oliguria due to the reduction of glomerular filtration reflected in an increase of nitrogen compounds.
This paper shows a male infant at 2 years and 7 months of age with nephritic syndrome associated to a skin infection, pneumonia, and hepatitis A virus infection. Acute glomerulonephritis may be associated to streptococcus or another coincidental infection. Children with skin infection, hepatitis A, or pneumonia who reveal abnormal urinalysis, hypertension, azotemia, or oliguria should be evaluated for concomitant glomerulonephritis.
El prototipo de la glomerulonefritis aguda es la glomerulonefritis aguda post-infecciosa. Acute nephritic syndrome ANS or acute glomerulonephritis AGN consists of the sudden appearance of hematuria, hypertension, oliguria, edemas, and deterioration of the renal function in varying degrees. Not all these symptoms will be present in all cases of acute glomerulonephritis 1.
This is the most common of childhood renal syndromes, predominating gpomerulonefritis pre-school and grade school age, with a maximum frequency between 6 and 7 years of age 2. Clinical manifestations are rare in children under 3 years of age, but cases have been described during breastfeeding stages, adolescence, and adulthood 23. It is more frequent in boys than in girls at a ratio of 2: In developing nations, the incidence remains high because of the following factors: Product of the fourth pregnancy of mother G: Maternal breastfeeding up gglomerulonefritis one year of age and weaning at 6 months postinnfecciosa mashed potatoes and soups.
Complete vaccination with postinfeccciosa records. Physical exam upon admission: Jaundice glomerulonefriris sclerae, non-toxic, good general status, normocephalic, mobile neck without masses. Symmetrical thorax without retractions and with diminished vesicular murmur in the right pulmonary field, absence of crackles, with mobilization of secretions in both pulmonary fields, and with rhythmic cardiac sounds without murmurs.
Nephritic syndrome secondary to: The following clinical exams were done: Urinary red blood cell morphology: Acs hepatitis A IgM: Thorax posterior-anterior and lateral X-ray: Antibiotic therapy was ordered crystalline penicillin to work on the pneumonia. The patient was hospitalized for 10 days, presenting improvement of the diuresis, non-feverish, normalized laboratory workups: The classical example of acute nephritic syndrome is constituted by acute post-streptococci glomerulo-nephritis.
Although there are multiple causes of acute nephritic syndrome Table 1among the most common, after post-streptococci there are: The main infectious agent is the group A b-hemolytic streptococcus S. The serotypes keeping a relationship with pharyngeal infection are: The most commonly isolated serotype in both foci is ,3. In studies carried out of epidemic outbursts, the incidence was Among other bacterial causes we may mention: Toxoplasma gondii, Trichinella, Rickettsia, Plasmodium malariae and falciparum, filaria.
The literature has mentioned the virus for varicella, rubella, cytomelovirus, parvovirus B19, Epstein-Barr virus, enterovirus, measles, parotitis, and the virus for hepatitis, as in the clinical case presented previously. Viral hepatitis is a well-recognized cause as a chronic and acute renal disease 3.
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The hepatitis B virus has been related with glomerulonephritis, but it has been more associated with membranous and mesangiocapilar nephropathy 4. The hepatitis C virus causes several forms of glomerulonephritis, including that mediated by cryoglobulinemia. There are reports in literature of the association between glomerulonephritis and virus, but cases reported with hepatitis A virus are few and rare.
Acute glomerulonephritis in these patients may be only associated to hepatitis A virus or to another coincidental infection, including streptococcus, as in the patient in our clinical case, who presented prior coetaneous infection with hypochromic spots on the extremities pyodermatitis stigmapneumonia, hepatitis A documented with IgM antibodies for hepatitis A virus.
It is possible that the physiopathology of these rare cases of glomerulonephritis associated to hepatitis A virus infection derive immunologically from reactions similar to acute glomerulonephritis. These reactions can occur with other viral infections. The mechanisms involved in the production glomerulnefritis the glomerular lesion associated with viral infection are diverse.
The viruses may directly infect the glomerular cells and induce glomerulonefriitis cytopathogenic effect. Patient data published in literature reveal that acute glomerulonephritis may be caused by hepatitis A virus infection, as well as by other viruses. More case reports are needed in the future glomerulonefrktis determine the exact mechanism of renal disease during this infection.
With respect to clinical findings, this clinical case presented: Furthermore, oliguria was present with elevated creatinine, which required administration of furosemide; there was no evidence of proteinuria in the urine test.
The edema and the oliguria presented by the patient ceased with the use postinfeccciosa diuretics.
This patient did not reveal blood hypertension, with systolic blood pressure within the 50 th Percentile and diastolic blood pressure within the 90 th percentile. Among hematologic manifestations, we observed moderate anemia due to possible dilutional hypervolemia. The diminished complement C3 fraction was documented. Aside from antecedents of coetaneous infection and hepatitis A viral infection, the patient reported in this revision also presented pneumonia evidenced via thoracic X-ray.
Literature has reported cases of acute glomerulonephritis associated with pneumonia 5 – 7.
Cases have been reported with positive cultures for S. Because of the high prevalence of pulmonary, coetaneous, and pharyngeal infections in our environment due to streptococcus and hepatitis a viral infection, these have become problematic issues in public health that can lead to a variety of renal diseases. Understanding the mechanisms of why these infectious agents can postinffecciosa renal damage will permit more effective treatment strategies to revert the renal disease produced by said infections.
Due to the aforementioned, studies are needed with a sufficient number of patients to analyze the main renal lesions secondary to these infectious agents and to propose management strategies to avoid the final phase of renal disease. In conclusion, acute glomerulonephritis may be only associated to streptococcus or to another coincidental infection.
Also, children with coetaneous infection, viral hepatitis, or pneumonia, who have revealed abnormalities in the urinalysis, hypertension, azotemia, or oliguria, must be evaluated to discard associated glomerulonephritis.
Golmerulonefritis NK, Gaglio P. Viral hepatitis as a cause of renal disease.
Nat Clin Pract Nephrol. Pneumonia associated acute glomerulonephritis. Glomerulonephritis associated with acute pneumococcal pneumonia: Acute nephritis and respiratory tract infection caused by postinfecciisa pneumoniae: Pediatr Infect Dis J.