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Updated: Jun 19, 2026

Analyses of Proteinuria, Renal Infiltration of Leukocytes, and Renal Deposition of Proteins in Lupus-prone MRL/lpr Mice

Analyses of Proteinuria, Renal Infiltration of Leukocytes, and Renal Deposition of Proteins in Lupus-prone MRL/lpr Mice

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ACUTE INTERSTITIAL NEPHRITIS.

W T Councilman¹

¹Sears Pathological Laboratory of Harvard University.

The Journal of Experimental Medicine

|October 30, 2009

Summary

This summary is machine-generated.

Acute interstitial nephritis in children involves plasma cell infiltration in the kidneys, often linked to infections like diphtheria and scarlet fever. The focal nature of these kidney lesions remains unexplained.

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Last Updated: Jun 19, 2026

Analyses of Proteinuria, Renal Infiltration of Leukocytes, and Renal Deposition of Proteins in Lupus-prone MRL/lpr Mice

Analyses of Proteinuria, Renal Infiltration of Leukocytes, and Renal Deposition of Proteins in Lupus-prone MRL/lpr Mice

Published on: June 8, 2022

Area of Science:

Pediatric Nephrology
Infectious Diseases
Renal Pathology

Background:

Acute interstitial nephritis is observed in various childhood infectious diseases, notably diphtheria and scarlet fever.
The condition is histologically characterized by interstitial kidney infiltration with plasma cells.
Focal accumulation of plasma and lymphoid cells in renal blood vessels precedes interstitial infiltration.

Purpose of the Study:

To describe the cellular characteristics and distribution of acute interstitial nephritis in infectious diseases.
To investigate the origin and migration of plasma cells in renal interstitial tissue.
To explore potential explanations for the focal nature of kidney lesions.

Main Methods:

Histopathological examination of kidney tissue from children with infectious diseases.
Identification and characterization of infiltrating cells, particularly plasma cells and lymphoid cells.
Correlation of cellular infiltration patterns with specific infectious agents and clinical presentations.

Main Results:

Plasma cells, originating from lymphoid cells, infiltrate the kidney interstitium, often in focal patterns within the boundary zone, sub-capsular cortex, and around glomeruli.
Cellular infiltration originates from emigration from blood vessels and subsequent mitotic division.
While plasma cells are found in infectious nephritis, their exact role and the cause of focal distribution are not fully elucidated; bacterial presence is not consistently linked to these foci.

Conclusions:

Acute interstitial nephritis in children is associated with plasma cell infiltration, frequently seen in conjunction with infections like diphtheria and scarlet fever.
The precise mechanisms driving the focal accumulation of plasma cells in the kidney remain unclear, with circulation dynamics and potential chemotactic factors suggested.
Further research is needed to fully understand the pathogenesis of focal interstitial nephritis and the role of plasma cells in infectious kidney diseases.