Find information on thousands of medical conditions and prescription drugs.


Glomerulonephritis is a primary or secondary autoimmune renal disease featuring inflammation of the glomeruli. It may be asymptomatic, or present with hematuria and/or proteinuria (blood resp. protein in the urine). There are many recognised types, divided in acute, subacute or chronic glomerulonephritis. Causes are infectious (bacterial, viral or parasitic pathogens), autoimmune or paraneoplastic. more...

Gardner's syndrome
Gastric Dumping Syndrome
Gastroesophageal reflux
Gaucher Disease
Gaucher's disease
Gelineau disease
Genu varum
Geographic tongue
Gerstmann syndrome
Gestational trophoblastic...
Giant axonal neuropathy
Giant cell arteritis
Gilbert's syndrome
Gilles de la Tourette's...
Gitelman syndrome
Glanzmann thrombasthenia
Glioblastoma multiforme
Glucose 6 phosphate...
Glycogen storage disease
Glycogen storage disease...
Glycogen storage disease...
Glycogenosis type IV
Goldenhar syndrome
Goodpasture's syndrome
Graft versus host disease
Graves' disease
Great vessels transposition
Growth hormone deficiency
Guillain-Barré syndrome

Acute glomerulonephritis

Acute diffuse proliferative GN

Histopathology: the majority of glomeruli present hypercellularity due to proliferation of endothelial and mesangial cells, inflammatory infiltrate with neutrophils and with monocytes. The Bowman space is reduced (compressed). Tubules are not affected.

Rapidly progressive GN (Crescentic GN)

Histopathology: The majority of glomeruli present "crescents". Formation of crescents is initiated by passage of fibrin into the Bowman space as a result of increased permeability of glomerular basement membrane. Fibrin stimulates the proliferation of parietal cells of Bowman capsule, and an influx of monocytes. Rapid growing and fibrosis of crescents compresses the capillary loops and decreases the Bowman space which leads to renal failure within weeks or months.

Mesangial proliferative GN

This type is due to deposition of polymerised IgA1 in the mesangium, with a localised proliferation of tissue. It is consistent with IgA nephritis (Berger's disease) and usually presents with macroscopic hematuria.

Minimal change GN

This form of GN usually (though not exclusively) presents in children with nephrotic syndrome and massive proteinuria. It is controlled with steroids. As the name indicates, there are no changes on light microscopy.

Chronic glomerulonephritis

Chronic glomerulonephritis represents the end-stage of all glomerulonephritis with unfavorable evolution.

Histopathology: few glomeruli may still present changes which permit to discern the etiology of CGN. The majority of the glomeruli are affected. Depending on the stage of the disease, they may present different degrees of hyalinization (hyalinosclerosis - total replacement of glomeruli and Bowman's space with hyaline). The hyaline is an amorphous material, pink, homogenous, resulted from combination of plasma proteins, increased mesangial matrix and collagen. Totally hyalines glomeruli are atrophic (smaller), lacking capillaries, hence non-functional. Obstruction of blood flow will produce secondary tubular atrophy, interstitial fibrosis and thickening of the arterial wall by hyaline deposits. Functional nephrons have dilated tubules, often with hyaline casts in the lumens. In the interstitium is present an abundant inflammatory infiltrate (mostly with lymphocytes).

This general (glomerular, vascular and interstitial) affection constitutes the so-called "end stage kidney". In most cases, it is associated with systemic hypertension.


[List your site here Free!]

Outbreak of severe rotavirus gastroenteritis among children—Jamaica, 2003
From Morbidity and Mortality Weekly Report, 11/14/03 by D Ashley

In late May 2003, the Jamaican Ministry oft health (MoH) identified a sharp increase in the number of acute gastroenteritis (AGE) cases reported throughout the country (Figure), accompanied by increases in AGE-associated hospital admissions and deaths among children. The greatest increase in AGE cases was observed among children aged <5 years in the southeastern parish of Kingston and St. Andrew. During June-July, 12 AGE-associated deaths were reported among children aged <8 years. MoH began an investigation to determine the etiology of the outbreak, ascertain risk factors for illness and death, and identify appropriate control measures. This report presents the preliminary results of that investigation, which determined that the AGE cases were associated with rotavirus and deaths might have been reduced by appropriate AGE case management, indicating a need for additional education of caregivers regarding AGE treatment.


The increase in AGE cases was detected by Jamaica's National Sentinel Surveillance System (NSSS), which receives weekly reports that include the number of patient visits for AGE among children at 55 sentinel sites. In addition, review of admissions at two Kingston and St. Andrew hospitals identified an increase in the number of children hospitalized for AGE. Mandatory investigation and reporting to MoH found a concurrent increase in the number of diarrheal deaths among children.

Interviews with primary caregivers suggested that eight of the 12 deaths were attributable to diarrhea. These eight deaths occurred among children aged 4 months 3 years (mean: 17 months). All eight children had watery diarrhea and vomiting that began 1-5 days before death. All had visited a public or private health-care provider at least once for treatment. Five children had received oral rehydration therapy (ORT) for their diarrheal illness; three received no ORT during their clinic visits. Three children were treated with antibiotics, two with antidiarrheals, and three with antiemetic injections.

Testing for Salmonella, Shigella, Vibrio cholerae, and Escherichia coli O157:H7 on 43 stool specimens collected during June-July as part of NSSS surveillance identified four Shigella spp. and nine Salmonella spp. isolates. This was an expected finding for that time of the year. However, rotavirus was identified by latex agglutination in 21 (49%) of the initial 43 stool specimens and by enzyme-linked immunosorbent assay in 33 (50%) of an additional 66 stool specimens collected from children aged <5 years as part of the MoH investigation. Further testing at CDC identified rotavirus in five of seven stool specimens from persons aged >5 years. Testing of 32 stool specimens was negative for norovirus, sapovirus, and astrovirus; however, adenovirus was identified in three specimens, all of which also had evidence of rotavirus. Initial characterization of 23 rotavirus samples obtained as part of the MoH investigation indicated the presence of three common serotypes; no vaccine strain was identified.

An epidemiologic investigation of this rotavirus-associated outbreak continues to identify risk factors for severe illness and death. As of November 12, no food or water source had been identified. Preventive efforts have focused on advising parents and physicians of the benefits of ORT for children with AGE.

Editorial Note: In Jamaica, rotavirus is usually confined to winter months (1), occurs among children aged <3 years, and is no longer associated with substantial mortality. Identification of rotavirus as the etiologic agent of this large outbreak of severe AGE seemed improbable because the outbreak occurred during the summer, included children aged >3 years, and resulted in multiple deaths. However, laboratory tests confirmed rotavirus as the etiologic agent, and identified multiple common rotavirus strains. Environmental exposures are being considered as explanations for this unusual outbreak. Ongoing studies are examining heavy rainfalls that occurred in late May and might have flooded latrines in crowded urban areas, causing fecal contamination of water sources. Communitywide outbreaks of rotavirus attributed to fecally contaminated water have been reported but are uncommon (2).

This outbreak underscores the importance of surveillance for rotavirus disease. Rotavirus remains a major cause of diarrheal deaths worldwide (3), many of which might be prevented by aggressive use of ORT (4) and vaccines (5). The investigation of the outbreak in Jamaica suggested that AGE-associated deaths might be attributable to inappropriate case management. Certain children did not receive adequate ORT treatment, nor was home use of ORT emphasized. Certain children received antiemetic and antidiarrheal injections, which are not part of standard diarrhea management. Additional education of physicians, parents, and other caregivers regarding ORT can reduce the severity and mortality from diarrhea during AGE outbreaks (6).


(1.) Dowe G, King SD, Maitland PB, Swaby-Ellis DE. Laboratory investigations on rotavirus in infantile gastroenteritis in Jamaica. Trans R Soc Trop Med Hyg 1988;82:155-9.

(2.) Hopkins RS, Gaspard GB, Williams FP Jr, Karlin RJ, Cukor G, Blacklow NR. A community waterborne gastroenteritis outbreak: evidence for rotavirus as the agent. Am J Public Health 1984;74:263-5.

(3.) Miller MA, McCann L. Policy analysis of the use of hepatitis B, Haemophilus influenzae type b-, Streptococcus pneumoniae-conjugate and rotavirus vaccines in national immunization schedules. Health Econ 2000;9:19-35.

(4.) Santosham M. Oral rehydration therapy: reverse transfer of technology. Arch Pediatr Adolesc Med 2002;156:1177-9.

(5.) Bresee JS, Glass RI, Ivanoff B, Gentsch JR. Current status and future priorities for rotavirus vaccine development, evaluation and implementation in developing countries. Vaccine 1999;17:2207-22.

(6.) Walker GJ, Ashley DE, Hayes RJ. The quality of care is related to death rates: hospital inpatient management of infants with acute gastroenteritis in Jamaica. Am J Public Health 1988;78:149-52.

Reported by: D Ashley, MD, E Hedmann, MD, K Lewis-Bell, MD, E Ward, MD, Jamaican Ministry of Health; J Bryce, MD, National Public Health Laboratory, Kingston, Jamaica. RM Turcios, MD, D Tuller, MA Widdowson, VetMB. JS Bresee, MD, S Adams, S Monroe, PhD, JR Gentsch, PhD, RI Glass, MD, Div of Viral and Rickettsial Diseases, National Center for Infectious Diseases; TK Fischer, MD, EIS Officer, CDC.

COPYRIGHT 2003 U.S. Government Printing Office
COPYRIGHT 2004 Gale Group

Return to Glomerulonephritis
Home Contact Resources Exchange Links ebay