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Post Streptococcal Glomerulonephritis Case Study

A 13-year-old female presents with malaise, facial edema and decreased urinary output. Prior history is positive for strep throat, previously treated. Her work-up revealed severe abnormal lab values. Her final diagnosis is Post Streptococcal Glomerulonephritis.

Post streptococcal glomerulonephritis (PSGN) is a type of immune-mediated glomerulonephritis that arises after infection with a particular strains of group A streptococcus bacteria. PSGN can express itself in a variety of clinical symptoms, and laboratory values are crucial in identifying and treating this illness (Alhamoud et al., 2021; Havrda, 2022).

Serum creatinine is one of the key laboratory measures that may be abnormal in PSGN. PSGN is a form of acute kidney injury (AKI) that can cause kidney function to decline. Serum creatinine levels are a standard measure for assessing renal function, and increased values in PSGN would indicate compromised kidney function. Renal dysfunction is also frequently related with high blood urea nitrogen levels (BUN). Urinalysis results can also give critical diagnostic information. PSGN is characterized by hematuria, which is caused by inflammation and injury to the glomeruli in the kidneys (Alhamoud et al., 2021; Havrda, 2022). Dysmorphic red cells are likely to be found in urine since PGSN is primarily a nephritic syndrome. Additionally, lower serum albumin levels may be noted in PSGN due to albumin loss in the urine because of glomerular filtration barrier impairment. If the streptococcal infection has not been addressed, leukocytosis and neutrophilia are common, indicating an active bacterial infection. Serum C-reactive protein (CRP), a typical inflammatory marker, will also be elevated. Serologic tests may detect hypocomplementemia as well (Havrda, 2022).

A positive streptococcal infection, as evidenced by high anti-streptolysin O (ASO) titers, is crucial in the setting of PSGN because it serves as proof of the underlying streptococcal infection that initiated the immune response that resulted in glomerulonephritis. PSGN is frequently associated with Group A streptococcus, which is known to cause strep throat and skin infections. The presence of a positive streptococcal infection assists in determining the origin of PSGN and directs proper therapy, which may include antibiotics to clear the infection and anti-inflammatory medications to regulate the immune response (Alhamoud et al., 2021).

It is critical to distinguish between acute and chronic glomerulonephritis. Acute glomerulonephritis usually manifests itself rapidly, with symptoms such as hematuria, proteinuria, hypertension, and reduced kidney function. PSGN is a kind of acute glomerulonephritis that, with proper treatment, is frequently self-limiting, and most patients recover completely without long-term consequences. Other conditions that may generate features typical of acute glomerulonephritis include lupus, Goodpasture’s syndrome, Wegener’s disease, and polyarteritis nodosa (Sethi et al., 2022). Chronic glomerulonephritis, on the other hand, develops slowly over time and may not manifest with noticeable symptoms until the later stages. Chronic glomerulonephritis can result from unresolved acute glomerulonephritis, but it is also frequently associated with long-term illnesses such as diabetes, hypertension, or autoimmune disorders (Oda & Yoshizawa, 2021). It is frequently irreversible and can proceed to end-stage renal disease (ESRD), which necessitates long-term renal replacement therapy such as dialysis or kidney transplantation.

In contrast to the chronic form, acute glomerulonephritis often resolves, depending on a variety of factors such as the underlying etiology, degree of renal impairment, and the promptness and success of therapeutic interventions. Addressing the underlying cause of the problem, such as infections, immune-mediated disorders, or other contributing factors, is critical to promoting resolution. For example, in situations of PSGN, antibiotics may be used to treat the infection and reduce immune-mediated damage to the renal tissue. Supportive treatments, in addition to addressing the underlying cause, are critical in the management of acute glomerulonephritis and promoting resolution. Uncontrolled hypertension can worsen kidney damage; therefore, optimal blood pressure control is critical (Sethi et al., 2022). To control fluid overload and edema, medications such as diuretics may be used, while dietary changes such as limiting salt and protein intake may be helpful to reducing the stress on the kidneys.

Regular monitoring and thorough follow-up are essential in determining the resolution and course of acute glomerulonephritis. Serial evaluation of relevant laboratory results, urine analysis, and blood pressure readings can help determine the success of the treatment plan and identify any potential problems. Furthermore, imaging techniques, such as renal ultrasonography, may be used to examine the size and shape of the kidneys, providing vital information on the response to treatment and the overall prognosis of the condition.

Risk factor for PSGN includes but not limited to age greater than 60 years of age, and children ages 5 to 12 and more frequent in males as in females. It is also the most common of glomerulonephritis in children (Sethi et al., 2022).  For our 13-year-old, as stated above, close monitoring, proper treatment, and supportive care will be vital in her recovery. 

References

Alhamoud, M. A., Salloot, I. Z., Mohiuddin, S. S., AlHarbi, T. M., Batouq, F., Alfrayyan, N. Y., 

Alhashem, A. I., & Alaskar, M. (2021). A Comprehensive Review Study on Glomerulonephritis. Associated With Post-streptococcal Infection. Cureus, 13(12), e20212. https://doi.org/10.7759/cureus.20212

Havrda M. (2022). Glomerulonephritides associated with infections. Glomerulonefritidy 

asociované s infekcemi. Vnitrni lekarstvi, 68(7), 432–437. https://doi.org/10.36290/vnl.2022.091

Oda, T., & Yoshizawa, N. (2021). Factors Affecting the Progression of Infection-Related 

Glomerulonephritis to Chronic Kidney Disease. International journal of molecular sciences, 22(2), 905. https://doi.org/10.3390/ijms22020905

Sethi, S., De Vriese, A. S., & Fervenza, F. C. (2022). Acute glomerulonephritis. Lancet (London, 

           England), 399(10335), 1646–1663. https://doi.org/10.1016/S0140-6736(22)00461-5