Academic Writing in Nursing and Anatomy

A Case Analysis of Post-Streptococcal Glomerulonephritis Etiology and Epidemiology

Post Strep glomerulonephritis is commonly caused by untreated group A streptococcal infections, most often streptococcal pharyngitis or "strep throat", leading to the formation of immune complexes that deposit in the glomeruli. This condition is most prevalent in children between 5-15 years old, as seen in the presented case of a 28-year old nursery school teacher who developed signs of post-streptococcal glomerulonephritis such as hematuria and elevated creatinine, one week after contracting impetigo from a student, fitting with the typical etiology and epidemiology (Rogers, 2023). PSGN results from an immune-mediated process following streptococcal infection, where antibodies produced in response cross-react with antigens in the glomerular basement membrane. The immune complexes activate the complement system, resulting in inflammation and endothelial injury in the glomeruli (Alhamoud et al., 2021). Early antibiotic treatment can reduce the risk of developing PSGN, though 15% may still be affected by nephritogenic streptococcal strains. While most common in children, this case demonstrates adults can also be affected, especially those in professions with frequent exposure to children, highlighting the importance of proper treatment of streptococcal infections.

Underlying Pathophysiology

PSGN occurs due to an immune complex-mediated glomerulonephritis that develops one to three weeks following a streptococcal infection, most commonly of the skin (Rogers, 2023). The underlying pathophysiology involves the deposition of circulating immune complexes containing streptococcal antigens and antibodies within the glomerular basement membrane, triggering an inflammatory response cascading downstream. This leads to glomerulonephritis, characterized by glomerular inflammation and endothelial cell activation. This in turn can cause hematuria, proteinuria, edema and hypertension, as clinically manifested in the presented case. Certain streptococcal antigens like nephritis-associated plasmin receptor (NAPlr) and streptococcal pyrogenic exotoxin B (SPEB) have plasmin binding capabilities that facilitate immune complex deposition within the glomeruli. This activation of innate immune pathways results in glomerular injury underlying the systemic signs of PSGN (Rodríguez-Iturbe & Batsford, 2007). In this particular case, the pathophysiological mechanisms of immune complex mediated injury explain the clinical laboratory findings consistent with PSGN.

Signs, Symptoms and Diagnostic Tests

Post-streptococcal glomerulonephritis results from the deposition of immune complexes containing streptococcal antigens in the glomerular basement membrane, triggering an inflammatory response and glomerular injury. This pathophysiological process clinically manifests as hematuria, proteinuria, and potentially edema and hypertension if the glomerulonephritis is severe. As seen in the case, patients may report changes in urine color to cola-colored or tea-colored urine, as well as peripheral edema and headaches (Rogers, 2023). On physical examination, findings may include elevated blood pressure and signs of a previous streptococcal infection like impetigo. Laboratory testing reveals hematuria, red blood cell casts, and proteinuria on urinalysis, as well as elevated serum creatinine levels. Low complement levels (C3, C4, CH50) provide supportive evidence for the immune complex-mediated mechanism. Diagnosis of poststreptococcal glomerulonephritis relies on compatible symptoms occurring 1-6 weeks after a streptococcal infection, along with abnormal urinalysis demonstrating hematuria, proteinuria, and cellular casts, with low complement levels and renal impairment confirming glomerular inflammation and injury from immune complex deposition triggered by the preceding infection (Alhamoud et al., 2021). Definitive diagnosis requires ruling out other causes through a comprehensive history, physical exam, urinalysis and complement level assessment as performed for the nurse in this case.

Latest Advances on Diagnosis, Treatment and Implications to Practice

Diagnosis of PSGN has improved with advances in urinary and laboratory testing. Detection of nephritogenic streptococcal antigens like NAPlr and SPEB through urine ELISA provides a more sensitive and specific method for confirming a preceding strep infection compared to antistreptolysin O titers alone. Measurement of complement levels like C3 and C4 help establish alternative pathway activation as the underlying mechanism. Newer duplex ultrasound techniques allow assessment of renal size, echogenicity, and blood flow to evaluate severity and guide management. Combined with clinical history, physical exam, and urinalysis findings, these improved diagnostic modalities allow for more rapid diagnosis.

Current treatment focuses on supportive care and controlling complications like fluid overload and hypertension. While antibiotics do not prevent PSGN once established, prompt treatment of antecedent infections helps reduce recurrence risk. Angiotensin converting enzyme inhibitors and angiotensin receptor blockers now serve as first-line agents for hypertension based on their renal protective effects. For severe presentations with crescentic glomerulonephritis or progressive renal failure, eculizumab represents a novel therapy option based on its effect of blocking terminal complement activation (Chehade et al., 2021). Studies also suggest corticosteroids may benefit the rare patients presenting with crescentic glomerulonephritis or failing to respond to standard care, though larger trials are still needed (Yang et al., 2018). In my practice, I would incorporate the latest diagnostic tests to expedite confirmation and rule out alternative etiologies. For the attached case, obtaining SPEB and C3/C4 levels would help establish the diagnosis. I would educate patients on follow-up strep treatments and lifestyle modifications like salt restriction to control her elevated blood pressure and reduce long-term sequelae risk like chronic kidney disease.

References

*Alhamoud, M. A., Salloot, I. Z., Mohiuddin, S. S., AlHarbi, T. M., Batouq, F., Alfrayyan, N., Alhashem, A. I., & Alaskar, M. (2021). A comprehensive review study on Glomerulonephritis associated with post-streptococcal infection. Cureus. 

https://doi.org/10.7759/cureus.20212

*Chehade, H., Guzzo, G., Cachat, F., Rotman, S., Teta, D., Pantaleo, G., Sadallah, S., Sharma, A., Rosales, I. A., Tolkoff-Rubin, N., & Pascual, M. (2021). Eculizumab as a new treatment for severe acute post-infectious Glomerulonephritis: Two case reports. Frontiers in Medicine, 8. 

https://doi.org/10.3389/fmed.2021.663258

*Rodríguez-Iturbe, B., & Batsford, S. (2007). Pathogenesis of poststreptococcal glomerulonephritis a century after Clemens von Pirquet. Kidney International, 71(11), 1094 1104. 

https://doi.org/10.1038/sj.ki.5002169

Rogers, J. L. (2023). Alterations of renal and urinary tract function in children: glomerulonephritis. In J. L. Rogers (Ed.), McCance & Huether’s pathophysiology: The biologic basis for disease in adults and children (9th ed., pp. 1274-1276). Elsevier. 

*Yang, T. J., Shah, H., Olagunju, A., Novak, M., & Difilippo, W. (2018). Role of steroids in post streptococcal Glomerulonephritis without crescents on renal biopsy. Cureus. 

https://doi.org/10.7759/cureus.3150