Pneumocystis pneumonia secondary to intensive immunosuppression treatment for anti-GBM disease complicated with IgA nephropathy

Abstract

Rationale:The estimated incidence of anti-glomerular basement membrane (anti-GBM) disease complicated with immunoglobulin A (IgA) nephropathy is minimal, there have only been 15 cases (including this case) reported in the literature, and only 5 (33.33%) of them showed significant improvement in renal function after treatment. Pneumocystis pneumonia is a severe opportunistic pulmonary infection of pneumocystis jiroveci in immunocompromised patients. Here, we report a case of pneumocystis pneumonia secondary to intensive immunosuppression treatment for anti-GBM disease complicated with IgA nephropathy, with no similar reports or studies published before to our knowledge.Patient concerns:The patient was admitted to our hospital with a 1-week diagnosis of crescent glomerulonephritis who had been suffered from hematuria and foamy urine for more than 1 month. Before admission, the patient received pulse dose intravenous methylprednisolone and immunosuppression with rituximab, but the renal function and titer of pathogenic antibody did not improve significantly.Diagnosis:Crescentic glomerulonephritis, anti-glomerular basal membrane disease complicated with IgA nephropathy (Type I+II) was pathologically confirmed by renal biopsy. Secondary pneumocystis pneumonia was diagnosed by acute progressive respiratory failure, chest computed tomography and metagenomic next-generation sequencing of transbronchoscopic bronchoalveolar lavage fluid.Interventions:The key to successful treatment was to make the pathogenic antibody turn negative quickly by combining pulse dose intravenous methylprednisolone, immunosuppression with rituximab, and plasma exchange therapy. Early identification of pneumocystis pneumonia, accurate etiological identification, and active anti-infective treatment were also crucial.Outcomes:The patient was discharged after 16 days of anti-infection with secondary infection controlled and dialysis catheter removed. Up to now, the patient has been followed for a period of 28 weeks, results showed renal function had been repaired even hematuria and proteinuria were basically alleviated.Lessons:Our case provided experience in the treatment of anti-GBM disease complicated with IgA nephropathy, further proposed the potential therapeutic effects of rituximab, also illustrated low dose hormone combined with tacrolimus can be used as sequential therapy after plasma exchange and intensive immunosuppression. Our research also suggested that resulting in severe immune suppression, a high risk of secondary pneumocystis opportunistic infection should be aware of. metagenomic next-generation sequencing might increase the detection rate of the pathogen.

Great prognosis of concurrent anti-GBM disease and IgA nephropathy in a young woman: A case report

“…[8] To better understand the clinical features of concomitant anti-GBM disease with IgA nephropathy, we reviewed and summarized all concurrent anti-GBM disease and IgA nephropathy cases published in PubMed (16 cases in total, including this case), as shown in Table 1. [9][10][11][12][13][14][15][16][17][18][19][20][21][22][23] In these concurrent anti-GBM disease and IgA nephropathy cases, the average age is 40 years, which seems to be consistent with the classic bimodal distribution of anti-GBM disease. [24] Interestingly, the male to female ratio is 1:2, which is inconsistent with the current finding that both anti-GBM disease and IgA nephropathy are highly prevalent in men.…”

“…Interestingly, none of the patients treated with mycophenolate mofetil or rituximab developed dialysis dependence, suggesting that they may have potential in the treatment of concurrent anti-GBM disease and IgA nephropathy. [ 12 , 21 , 23 ] Notably, all patients who eventually depended on dialysis had higher creatinine levels when they started immunosuppressive therapy, the lowest of which was 400.4 μmmol/L. In contrast, all patients with a good prognosis had low serum creatinine levels, below 320 μmmol/L except for 1 case of 481.8 μmmol/L.…”

“…[8] To better understand the clinical features of concomitant anti-GBM disease with IgA nephropathy, we reviewed and summarized all concurrent anti-GBM disease and IgA nephropathy cases published in PubMed (16 cases in total, including this case), as shown in Table 1. [9–23]…”

High-frequency plasma exchange therapy for immunocompromised, type I crescentic glomerulonephritis complicated with IgA nephropathy: A case report and literature review

“…At present, there is no clear guideline or consensus on the treatment of type I crescentic glomerulonephritis and IgA nephropathy. Combined with literature review [3][4][5][6][7][8][9][10][11][12][13] (Table 2), most patients present with extensive glomerular crescent formation, clinically characterized by rapidly progressive GN, due to the acute onset of anti-GBM disease and the severe condition, the treatment should be carried out according to the anti-GBM disease treatment plan first. Standard treatment for anti-GBM disease includes plasmapheresis therapy, which aims to rapidly remove pathogenic autoantibodies; Cyclophosphamide and corticosteroids are also included to inhibit further autoantibody production and improve end-organ inflammation.…”

“…The dosage was reduced to 20 mg at 6 weeks, then gradually reduced until complete cessation at 6 to 9 month. Zhang et al [ 4 ] recently reported pneumocystis pneumonia occurred following intensive immunosuppressive therapy for anti-GBM disease with IgA nephropathy. In the above medical record, the patient was treated with pulsed dose intravenous methylprednisolone, immunosuppression combined with rituximab, and plasmapheresis.…”