A Rare Sequela of Untreated Streptococcus Pharyngitis: A Case Report

Abstract

Pharyngitis is commonly caused by the gram positive bacteria, streptococcus. Given the potential morbid complications of untreated streptococcal pharyngitis, antibiotics are critical. One of the rarer complications is pulmonary‐renal syndrome (PRS), defined as rapidly progressive glomerulonephritis and diffuse alveolar hemorrhage. PRS is associated with high rates of morbidity and mortality, making swift diagnosis and treatment imperative for survival. More common causes of PRS are tied to autoimmune diseases. This case describes a novel progression of PRS caused by streptococcus.

A 26‐year‐old male with no significant medical history presented to our emergency department with streptococcal group A‐positive sore throat. After discontinuing amoxicillin due to pruritus, the patient returned one month later with persisting hematuria and dysuria, diagnosed with post‐streptococcal glomerulonephritis. Despite receiving another antibiotic prescription, it was not filled. He returned six days later with worsening symptoms, leading to ICU admission due to hemoptysis requiring subsequent intubation. Diffuse alveolar hemorrhage was confirmed with bronchial washings. Negative autoimmune laboratory results and clinical symptoms suggest streptococcal pharyngitis induced pulmonary‐renal syndrome.

Although only the sixth case of streptococcal induced PRS, it is imperative to consider when treating patients with diffuse alveolar hemorrhage, due to its possible mortality. Prompt recognition and treatment with pulse steroids and plasmapheresis is crucial for PRS resolution. Laryngoscope, 135:1940–1942, 2025

Pharyngitis caused by streptococcus can lead to severe complications if left untreated like pulmonary‐renal syndrome (PRS), characterized by diffuse alveolar hemorrhage and rapidly progressive glomerulonephritis. This case report describes a 26‐year‐old male who developed PRS following streptococcal pharyngitis due to nonadherence to antibiotic treatment. Prompt recognition and treatment with pulse dose steroids and plasmapheresis are essential for reducing morbidity and mortality rates associated with PRS.

INTRODUCTION

Streptococcus is a common bacterium that causes pharyngitis. Timely antibiotic treatment is critically important to prevent severe complications. One of the rarest complications of untreated streptococcal pharyngitis is pulmonary‐renal syndrome (PRS), defined by rapidly progressive glomerulonephritis (PGN) and diffuse alveolar hemorrhage (DAH). ¹ PGN is a swiftly worsening form of kidney inflammation within the glomeruli, causing a reduction in the kidney's ability to filter waste. ² This presents with edema, hematuria, and hypertension which leads to kidney failure if not treated promptly. ³ DAH presents with hemoptysis and respiratory distress due to small capillaries bleeding into the alveolar spaces of the lungs. ¹ The accumulation of blood impairs gas exchange, leading to rapidly developing respiratory failure, often requiring mechanical ventilation. ¹

Together these conditions form PRS, a condition with high rates of morbidity and mortality, requiring urgent medical intervention. ⁴ Although PRS is more commonly associated with autoimmune disorders, post‐streptococcal PRS is exceedingly rare, highlighting the need for early recognition and treatment. ⁴ The goal of this case report is to raise awareness of an extremely rare complication of untreated streptococcal pharyngitis: pulmonary‐renal syndrome. This case emphasizes the importance of early antibiotic adherence and guiding providers on the swift diagnosis and management of PRS to improve patient outcomes.

CASE REPORT

A 26‐year‐old male with no significant past medical history presented to the emergency department (ED) with a 1‐day history of sore throat. He endorsed recent exposure to a relative diagnosed with streptococcal pharyngitis. In the ED, a rapid streptococcal Group A nucleic acid amplification test was positive. The patient was prescribed a 10‐day course of amoxicillin and was discharged.

One month later, the patient returned to the ED with persisting sore throat, new cough, and hematuria, having only taken one dose of amoxicillin due to pruritus. He was febrile at 100.5 °F with another positive rapid streptococcal test. Urinalysis revealed significant hematuria, pyuria, proteinuria, and positive nitrites. Complete blood count showed an elevated white blood cell count of 20 K/mcL and a slightly elevated creatine phosphokinase. Based on the lab work and clinical picture, he was diagnosed with post‐streptococcal glomerulonephritis (PSGN). He received cefdinir for better tolerance and steroids. The patient was discharged with a 10‐day course of cefdinir and instructed to follow up at the PCP clinic.

The patient returned 6 days after his most recent ED visit with continued sore throat, a new rash, burning urination, and brown urine. He had not filled his cefdinir prescription. His urinalysis was consistent with previous results, showing hematuria, pyuria, proteinuria, and positive nitrites. He had a negative urine culture and elevated creatinine of 1.32 mg/dL (previously 1.08 mg/dL). The patient was admitted for worsening streptococcal glomerulonephritis, and treated with ciprofloxacin and azithromycin. ENT consultation confirmed appropriate treatment for worsening streptococcal pharyngitis and PSGN, with no further intervention needed.

That evening, ENT evaluated the patient for hemoptysis via nasopharyngoscopy, but could not locate the source of bleeding. Due to the profuse bleeding and airway concerns, the patient was intubated and admitted to the intensive care unit (ICU). Blood work revealed a hemoglobin of 7.7 g/dL (previously was 11.4 g/dL) and an increased creatinine level of 1.56 mg/dL. Chest CT showed diffuse bilateral infiltrates (Fig. 1), and bronchoscopy revealed three consecutive bloody washings (Fig. 2), confirming the diagnosis of DAH. Autoimmune testing was negative for common and more likely causes of PRS, but was positive for an elevated antistreptolysin O (ASLO) titre (2374 IU/mL) with a low complement C3 (63 mg/dL) and normal C4. The patient was promptly started on the appropriate PRS treatment regimen, including pulse dose steroids (1 mg/kg) for 5 days and plasmapheresis for 3 days. The patient was extubated after 8 days without further issue and made a complete recovery.

Fig. 1.

Chest computed tomography (CT), a noninvasive medical procedure that uses X‐rays to create cross‐sectional images of the body showing evidence of diffuse bilateral infiltrates. This imaging description is consistent with the radiological manifestation of diffuse alveolar hemorrhage (DAH) because this condition involves bilateral and widespread bleeding into the alveoli, leading to increased lung opacities. This results in the characteristic appearance of ground glass opacities or infiltrates on chest X‐rays or CT scans as shown in this case.

Fig. 2.

Bronchial washings completed during bronchoscopy. The presence of blood in bronchial washings is confirmatory for diffuse alveolar hemorrhage (DAH) because it indicates active bleeding within the alveoli. Unlike other conditions, DAH shows persistent blood across consecutive samples, indicating diffuse bleeding from the small capillaries within the lungs, more specifically within the alveolar spaces.

The lab findings in this case were crucial for diagnosing PRS. ⁴ Urinalysis revealed hematuria and significant proteinuria, indicating glomerular damage, whereas leukocytosis reflected ongoing inflammation and infection. The rising creatinine level signaled worsening renal function. Elevated antistreptolysin O (ASLO) titre indicated a recent streptococcal infection, along with a low complement C3 level and normal C4 levels, supporting the diagnosis of PGN. ³ The patient's intense hemoptysis, combined with chest CT findings of diffuse bilateral infiltrates and bloody bronchial washes, confirmed DAH. ³ This clinical picture was sufficient for PRS diagnosis. ¹

DISCUSSION

This case highlights an extremely rare complication of untreated streptococcal pharyngitis: pulmonary‐renal syndrome, with fewer than 10 post‐streptococcal PRS cases reported. ² Although PSGN is a known complication of streptococcal infections, the development of DAH is not. ⁴ PSGN typically emerges 10 days after streptococcal pharyngitis or 2 weeks after impetigo. ³ Our patient's presentation closely mirrored those reported by Sung ³ and Shettigar, ² with symptom onset 2–4 weeks post‐streptococcal pharyngitis, and was comparable to the Shimokawa ⁴ case of impetigo with acute hemoptysis and PSGN.

The pathogenesis of streptococcal mediated PRS remains poorly understood. ³ Nephritogenic antigens, such as streptococcus pyrogenic exotoxin B and nephritis‐associated plasmin receptors, are believed to play a role in the pathogenesis of PSGN. ⁴ These same antigens have the capacity to accumulate in the glomeruli, activate plasmin, and progressively degrade the glomerular basement membrane. ⁴ Degradation triggers an immune response, activating complement and generating circulating antibodies, leading to immune complex formation. ⁴ These complexes infiltrate the damaged glomerular basement and deposit in the subepithelial space. ³ In the setting of profound hemoptysis of PRS, it is hypothesized that these complexes have the capacity to infiltrate and damage the alveolar membrane, causing DAH. ⁴

This case underscores the importance of expanding the differential diagnosis for PRS to include post‐streptococcal PRS, as early recognition is critical for reducing high mortality risk. Given that this case resulted from antibiotic nonadherence, it highlights the need for stricter patient follow‐up to prevent similar complications in the future. Advocating for improved adherence can be lifesaving in cases like this one.

CONCLUSION

In conclusion, PRS can occur as a rare complication of untreated streptococcal pharyngitis. Early recognition and prompt treatment with pulse steroids and plasmapheresis are crucial for PRS resolution.