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Clinical presentation of a patient with cutaneous vasculitis. The upper figures show progressive necrotic lesions on the dorsal feet, mainly on the toes. The lower figures show the amputation of the left fifth toe and the improvement of vasculitic skin lesions following RIPE treatment.
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... 45-year-old woman from Ribeirã o Preto (northeastern region of Sã o Paulo State, Brazil) presented to our clinic with painful necrotic lesions on both feet, mainly on the toes, which had recently increased in number and size. She had a history of headaches and seizures, an ischemic stroke five years earlier (resulting in facial motor sequelae) and five pregnancies, which consisted of four normal deliveries and one abortion at 22 years of age. On examination, there were cervical adenomegalies with bulky and coalescing lymph nodes (the largest measuring 3 cm in diameter) and crusted lesions on the dorsal feet and tips of the toes with purulent exudates and interdigital maceration (Figure 1). The periph- eral sensitivity test yielded normal results. Laboratory tests showed hypochromic anemia with microcytosis (hemoglo- bin: 11.0 g/dL; NR: 12.0-15.5 g/dL), increased inflammatory activity (ESR: 30 mm/1 st hour; NR: ,10 mm/1 st hour; C-reactive protein: 3.46 mg/dL; NR: up to 0.5 mg/dL; alpha1-acid glycoprotein: 156 mg/dL; NR: 50-120 mg/dL), increased levels of immunoglobulins (IgA: 1,070 mg/dL; NR: 134-297 mg/dl; IgG: 1,900 mg/dL; NR: 770-1,510 mg/dl; IgM: 222 mg/dL; NR: 67-208 mg/dl), positive autoantibo- dies (antinucleolar antibody (ANA)-positive 1:100 with nucleolar pattern; lupus anticoagulant (PIL and dRVVT)- positive; anticardiolipin IgG: 14.9 GPL/mL (weak positive); NR: up to 14.0 GPL/ml; p-ANCA-positive), urinary dis- orders (microscopic hematuria: 25-30 RBCs/field; NR: 3- 5 RBCs/field; urinary erythrocytes: 90% total dysmorphic cells, 19% acanthocytes; NR: up 4% acanthocytes; proteinuria: 255 mg/24 h; NR: up to 150 mg/24 h), and intradermal reaction test positive for Tb (PPD: 45 mm with necrosis). Cervical, thoracic and abdominal computed tomographies showed cervical adenomegaly (up to 1.8 cm in length) with central necrosis, a left axillary 2.3-cm lymph node, and several retroperitoneal lymph nodes (up to 0.9 cm in length). A cranial MRI showed a cerebral infarction on the left parietal region and lacunar infarctions in the region of capsular nuclei. Histopathology showed the following: (1) cervical lymph node -chronic granulomatous lymphadenitis with caseous necrosis; (2) fifth left toe -focal granulomatous in addition to leukocytoclastic vasculitis and direct immuno- fluorescence (DIF) strongly positive for anti-fibrinogen serum (3+) on capillary walls; and (3) renal biopsy -focal and segmental sclerosis with mild focal and chronic tubulointer- stitial damage, characterized by mesangial deposition of IgA on DIF, which may correspond to primary IgA nephropathy (Berger's Disease) or Henoch-Schönlein purpura (Figure 2). PCR with DNA that was extracted from paraffin blocks of lymph node and skin biopsies confirmed Mycobacterium sp. only in the lymph node (Figure 3). The final diagnosis consisted of Tb lymphadenitis, CLV, primary IgA nephro- pathy and APS. Ciprofloxacin (500 mg) was prescribed twice per day for ten days, and Fluconazole (150 mg) was prescribed once per week for eight weeks for the secondary infection and interdigital maceration on the feet. Thereafter, aspirin (200 mg daily) and warfarin (for antic- oagulation) were prescribed. The patient was evaluated by physicians in the Departments of Neurology, Ophthalmology, Nephrology and Infectious Diseases. Tb treatment was initiated with RIPE (rifampicin, isoniazid, pyrazinamide and ethambutol). Because an adverse drug reaction to pyrazinamide was observed, administration of this medication was suspended. Because of the worsening necrosis on her toes, the patient's left fifth toe was amputated with no complications. The patient finished the Tb treatment, which was followed by weight recovery, normalization of lymph node size, absence of new vasculitic lesions and significant improvement of previous skin lesions. ANA and PIL were negative, but glomerular hematuria and proteinuria remained ...
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Citations
... Among antibiotics, IgAV cases were reported for beta-lactams, fluoroquinolones, and macrolides. The median time from drug initiation and the onset of vasculitis was 10 days for antibiotics [6]. It has been suggested that immune complexes are formed in active tuberculosis and that this may be related to the mechanism of vasculitis [7,8]. ...
... Thereafter, we only included the cases with simultaneous involvement of the skin and renal tissues reported between 1990 and 2020. Totally, 7 cases including our case met these inclusion criteria [2,[7][8][9][10]. The characteristics of all cases are summarized in Table 1. ...
... The time interval for these cases seems to have a wide range (range between 1 week and 5 months). Despite laboratory evidence of renal involvement (hematuria and proteinuria), renal biopsy was performed only in 4 out of 7 [2,8,9]. Among those, crescent formation was present in 3, which steroid was administered only in 2. Interestingly, the caseous necrosis, which is a characteristic feature of TB infection, was demonstrated in one case [2]. ...
... Therefore, in such conditions, the addition of steroid and/or other immunosuppressive agents might play a vital importance in terms of prognosis [31]. In this review, administration of anti-TB drugs (quadruple regimen including INH, RIF, ETA, PRZ) is by far the most common preferred treatment modality [2,[7][8][9][10]. We also found that most of the cases seemed well-responded to anti-TB regimen despite renal involvement [2,7,9,10]. ...
Immunoglobulin (Ig) A vasculitis (IgAV), formerly known as Henoch–Schonlein purpura (HSP), is a relatively uncommon form of vasculitis primarily targeting the skin, gastrointestinal system, and the kidneys. Although the pathogenesis has not yet been well identified, several triggering factors, such as infections, drugs, have been implicated in the development of IgAV. Tuberculosis (TB), albeit rare, may precipitate IgAV. Herein, we have presented a case manifested by purpuric skin rash and proteinuria 6 weeks following diagnosis of pulmonary tuberculosis while receiving anti-TB drugs. The case was diagnosed as having active tuberculosis and TB-related IgA vasculitis with multi-organ involvement. In this case-based review, we recruited cases with TB-related Ig A vasculitis from the literature and discussed the features of tuberculosis that mimic vasculitides and vice versa. We also discussed the difficulties in diagnosis and the therapeutic approach in the light of the literature.
... Amongst these, 280 were excluded as they were deemed irrelevant, with the remaining 28 cases reporting glomerulonephritis in the context of extra-renal TB infection. Ten of these showed renal histology consistent with IgA nephropathy (IgA-N) [5][6][7][8], while 18 cases showed non-IgA glomerulonephritis on renal biopsy [2,7,[9][10][11][12][13][14][15][16][17]. Of the patients presenting with non-IgA glomerulonephritis, only 3 previous cases were reported to have MCGN, as seen in this case [7,12,13]. ...
... Seventeen previously reported cases report a tubercular focus that is pulmonary or pleuro-pulmonary [7-12, 16, 17], while 4 cases presented with disseminated TB [7], and another with miliary TB [2]. Of the remaining cases of glomerulonephritis with extra-renal TB, 2 were reported following lumbar vertebral TB [7,13], and 1 each following TB lymphadenitis [5], peritonitis [15], pancreatic TB [14], and lupus vulgaris [6]. While the index case presented developed nephrotic syndrome (NS) over the 2 weeks following diagnosis and treatment of pulmonary TB, 17 previously reported cases showed evidence of renal disease on initial presentation (hypertension, haematuria, significant proteinuria, fluid retention, oliguria) [2,7,9,12,13,15,16]. ...
... Of the remaining fully recovered patients, four received steroid treatment, two received renal replacement therapy in the form of haemodialysis, and one each received cyclophosphamide, diuretics, ramipril, and non-steroidal anti-inflammatory drugs [2,7,13,17]. Of those patients who failed to recover completely, two exhibited persistent proteinuria and haematuria, one patient died, and two patients developed end-stage renal failure, one in spite of treatment with anti-tubercular therapy, steroids and mycophenolate mofetil, and in another who was not treated with anti-tubercular drugs [5,7,9,12]. In our case, although renal function was never impaired, proteinuria persisted despite anti-tubercular therapy, prednisolone and enalapril treatment. ...
Glomerulonephritis in tuberculosis may be a direct manifestation of renal infection or a result of immune-complex deposition complicating extra-renal infection, such as in pulmonary tuberculosis. A 17-year-old adolescent boy from Somalia was found to have pulmonary tuberculosis during routine health screening performed on entering Malta, with computed tomography of the chest showing scarring and calcification of the left upper lobe, left lower lobe consolidation, and a small left-sided pleural effusion. Five days after starting anti-tuberculous therapy, he developed lower limb and sacral oedema: urinary albumin: creatinine ratio was > 400 µg albumin/mg creatinine, and 24-h urinary protein showed nephrotic-range proteinuria of 4.963 g/day. In view of worsening lower limb, sacral and periorbital oedema and ascites, he was started on oral prednisolone, omeprazole and penicillin V prophylaxis. As heavy proteinuria persisted, a renal biopsy was performed after 8 days of prednisolone treatment, which confirmed the presence of mesangiocapillary glomerulonephritis (MCGN), with electron microscopy showing effacement of the podocytes, with hypercellularity and subendothelial immune deposits, confirming an immune-mediated pathophysiology. Ziehl–Neelsen staining did not reveal acid-fast organisms. The patient received a total of 3 weeks of oral prednisolone with subsequent tailing doses, 2 months of pyrazinamide and ethambutol and 6 months of rifampicin and isoniazid with complete resolution of his clinical and radiological signs, though heavy proteinuria persisted, so he was commenced on oral enalapril. This case highlights the potential association of MCGN with tuberculosis in adolescence. Timely recognition and treatment can prevent progression to chronic kidney disease.
... Released cytokines (IL-1, TNF, and IL12) favor the expression of E-selectin on endothelial vascular growth factor and on skin lymphocyte antigen expression, with amplification of initial skin inflammation and creating favorable conditions for microbial colonization and infection (7). The common denominator in dermatitis and TB are the circulating immune complexes (up to 56% of TB cases), which are formed by the interaction between an antibody and bacterial antigen (8), which was in this case evidenced by increased levels of IgA and IgG. ...
Introduction
People with Tuberculosis (TB) infection may present with glomerulonephritis (GN). The range of presentations, renal pathologies, and clinical outcomes are uncertain. Whether clinical features that establish if GN etiology is medication or TB related, and possible benefits of immunosuppression remain uncertain.
Methods
A scoping review was completed, searching MEDLINE, EMBASE, Cochrane Central Register of Controlled Trials, Web of Science and Conference Abstracts from Inception to December, 2023. The study population included patients with TB infection who developed GN and underwent renal biopsy. All data regarding presentation, patient characteristics, renal pathology, management of TB and GN, and outcomes were summarized.
Results
There were 62 studies identified, with 130 patients. These cases included a spectrum of presentations including acute kidney injury, nephrotic syndrome and hypertension, and a range of 10 different renal pathology diagnoses. Cases that included immunosuppression and outcomes ranged from complete remission to long-term dialysis dependence. The presence of granulomas (4/4, 100%), anti-GBM disease (3/3, 100%), amyloidosis (75/76, 98.7%), and FSGS (2/2, 100%) were specific for GN being TB-infection related. On the other hand, minimal change disease was specific for anti-TB therapy related (7/7, 100%). While patients with more aggressive forms of GN commonly were prescribed immunosuppression, this study was unable to confirm efficacy. Only rifampin or isoniazid were implicated in drug-associated GN.
Discussion
This study provides a clear rationale for renal biopsy in patients with TB and GN, and outlines predictors for the GN etiology. Thus, this study establishes key criteria to optimize diagnosis and management of patients with TB and GN.
We report a case of IgA vasculitis that developed during the treatment of tuberculosis. Patients with tuberculosis who are on antituberculosis treatment can be administered steroids for severe disease or complications.
A 27-year-old man without any medical history presented concomitantly a pulmonary and urinary tuberculosis and a nephrotic syndrome with hematuria and renal failure. The renal biopsy showed increased mesangial matrix, few focal segmental lesions, and IgA deposits confirming the diagnosis of IgA nephropathy. Nephrotic syndrome remission occurred quickly after antituberculous treatment. The association between tuberculosis and IgA nephropathy has been previously reported in 9 patients. Renal outcome was always favorable with antituberculous treatment. No relapse occurred, with a maximal follow-up of 42 months. Here, we discuss this singular association and previous similar cases.
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