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Saudi Journal of Kidney Diseases and Transplantation
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Table of Contents   
CASE REPORT  
Year : 2014  |  Volume : 25  |  Issue : 4  |  Page : 872-875
Rapidly progressive glomerulonephritis in tuberculosis


1 Department of Nephrology, Jawaharlal Nehru Institute of Medical Sciences, Porompat Imphal, India
2 Department of Nephrology, Institute of Post-Graduate Medical Education and Research, Kolkata, India

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Date of Web Publication24-Jun-2014
 

   Abstract 

Renal involvement in tuberculosis occurs due to lympho-hematogenous dissemi­nation. However, glomerular involvement is an uncommon event. Crescentic nephritis compli­cating tuberculosis is a therapeutic dilemma and weighs the risk of worsening the infection after immunosuppressive therapy. We present here a case of miliary tuberculosis with immune com­plex crescentic nephritis with advanced renal injury requiring renal replacement therapy. A diagnosis of miliary tuberculosis was made on the basis of positive sputum AFB, lymph node biopsy showing caseating granulomas and urinary polymerase chain reaction being positive for mycobacterial antigens. The patient recovered renal function with anti-tuberculous therapy with­out requiring immunosuppressive therapy.

How to cite this article:
Waikhom R, Sarkar D, Bennikal M, Pandey R. Rapidly progressive glomerulonephritis in tuberculosis. Saudi J Kidney Dis Transpl 2014;25:872-5

How to cite this URL:
Waikhom R, Sarkar D, Bennikal M, Pandey R. Rapidly progressive glomerulonephritis in tuberculosis. Saudi J Kidney Dis Transpl [serial online] 2014 [cited 2019 May 21];25:872-5. Available from: http://www.sjkdt.org/text.asp?2014/25/4/872/135187

   Introduction Top


Glomerular involvement in tuberculosis pre­senting as rapidly progressive glomeruloneph-ritis is a rare entity. We present here a young boy who had disseminated tuberculosis with crescentic nephritis and was successfully treated with anti-tubercular therapy.


   Case Report Top


A 12-year-old boy presented to us with a swel­ling of the lower limbs one week prior to admission. He gave a history of fever two weeks before the onset of the swelling, which was treated with antipyretics. He started passing smoky colored urine and noted decreased urine output two days after the onset of the swelling. There was no history of sore throat/joint pain/ skin rash/oral ulcers/photosensitivity. He had not taken any medications prior to the onset of his symptoms and gave no history of any subs­tance abuse. Family history and past history were not significant. He received his treatment first from a primary physician, and was given acetaminophen for his fever at onset.

On examination, he had pedal edema and his blood pressure was 150/100 mm Hg. There were multiple lymph nodes in the left cervical region. Systemic examination was unremar­kable, except for decreased breath sounds and crepitations in the right lung. There were no hepatosplenomegaly or ascites. The neurological examination was also unremarkable. The labo­ratory findings are as shown in [Table 1]. Cervical lymph node biopsy showed caseating granuloma with features of tuberculous (TB) lymphadenitis. Renal biopsy was performed that showed cellular crescents involving eight of 12 glomeruli. Endocapillary proliferative changes with partial obliteration of the capil­lary lumina were observed in all the glomeruli. The basement membrane was irregularly thickened. There were RBC casts within the tubules, and some of the tubular epithelial cell showed protein resorption droplets. Interstitial edema and mild inflammatory infiltrates were also present. No granuloma was seen. Immuno-fluorescence microscopy showed intense staining for C3 and IgG. Urinary polymerase chain reaction (PCR) was positive for Mycobac-terium tuberculosis. The patient received five sessions of hemodialysis. The patient was started on anti-tuberculosis drugs (ATD) cate­gory 1 as per the Revised National Tuberculosis Control Programme. He did not receive methyl prednisolone or cyclophosphamide or any immunosuppressive medications. Urine output improved six days after the initiation of ATD and serum creatinine began to decline. At the last follow-up (6 months), his serum creatinine was 0.91 mg/dL and his 24-h urine protein was 310 mg.
Table 1: Laboratory parameters before admission, at admission and at the 6-month follow-up.

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   Discussion Top


Genito-urinary tuberculosis can occur in 10- 15% of pulmonary tuberculosis due to hema-togenous dissemination. [1] Usually, the manifes­tation is in the form of sterile pyuria, voiding symptoms, resistant urinary tract infection, obstructive nephropathy or interstitial neph­ritis. Glomerular involvement is uncommon in tuberculosis, and is seen as a manifestation of secondary amyloidosis or glomerulonephritis with varying histopathological pictures. Cre-scentic nephritis complicating tuberculosis is considered as a rare condition, with only two previous case reports on the literature search. [2],[3] We present here a young boy with active disse­minated tuberculosis who presented with ra­pidly progressive glomerulonephritis and ad­vanced renal failure. The occurrence of tuber­culosis and acute kidney injury simultaneously with isolation of the organism from the urine culture, the histopathological finding and im­provement on antitubercular therapy proves that the relationship is causal. Similar presen­tations were previously reported by Sopena et al and Wen et al. [2],[3] Both the patients had mi-liary tuberculosis and advanced kidney injury requiring hemodialysis. Renal biopsy showed endocapillary proliferative nephritis with cre­scents and immune complex deposits, not un­like our patient.

Patients with crescentic nephritis are usually treated with immunosuppressive agents in the form of pulse steroids in combination with cyclophosphamide. Plasmapheresis also has some beneficial role in those who present with advanced renal failure. Our patient presented with advanced renal failure requiring hemo-dialysis support. Immunosuppressive agents were not used considering that he had features of active tuberculosis. Early initiation of ATD was possible in this case following the urinary PCR report without having to wait for the culture. Urine output improved within one week of initiation of ATD. Whether the reco­very was spontaneous or whether ATD had any bearing on the recovery of renal function is not known. However, similar improvement in renal function following institution of ATD was noted in a previous case report as well. [3]

Circulating immune complexes have been demonstrated in patients with miliary tuber­culosis and immune complex nephritis, sug­gesting that the pathogenesis probably in­volves deposition of circulating immune depo­sits. In this context, antitubercular drugs, by decreasing the mycobacterial load from circu­lation, may decrease the antigen load and con­sequently immune complex formation, thereby allowing the kidney to clear the deposited complexes without any further deposition. This could possibly lead to enhanced recovery of renal function. Shribman earlier suggested T lymphocyte suppression with a negative Man-toux test as a prerequisite for immune complex nephritis. [4] Subsequently, however, it was shown that immune complex nephritis can occur in patients with a positive Mantoux test. [5] Our pa­tient also had a strong positive Mantoux test, suggesting that T lymphocyte suppression is not always required to cause immune complex nephritis.

In conclusion, immune complex crescentic nephritis can present in patients with active disseminated tuberculosis and complete renal recovery may be possible if ATD is instituted early, thereby avoiding the need for immuno-suppressive and cytotoxic agents.

 
   References Top

1.Wise GJ, Shteynshlyuger A. An update on lower urinary tract tuberculosis. Curr Urol Rep 2008;9:305-13.  Back to cited text no. 1
    
2.Sopena B, Sobrado J, Javier Perez A, et al. Rapidly progressive glomerulonephritis and pulmonary tuberculosis. Nephron 1991;57251-2.  Back to cited text no. 2
    
3.Wen YK, Chen ML. Crescentic glomerulonephritis associated with military tuberculosis. Clin Nephrol 2009;71:310-3.   Back to cited text no. 3
    
4.Shribman JH, Eastwood JB, Uff J. Immune complex nephritis complicating military tuber­culosis. BMJ 1983;287:1594.   Back to cited text no. 4
    
5.O'Brien AA, Kelly P, Gaffney EF, Clancy L, Keogh JA. Immune complex glomerulo-neph-ritis secondary to Tuberculosis. Ir J Med Sci 1990;159:187.  Back to cited text no. 5
    

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Correspondence Address:
Rajesh Waikhom
Department of Nephrology, Jawaharlal Nehru Institute of Medical Sciences, Porompat Imphal
India
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DOI: 10.4103/1319-2442.135187

PMID: 24969205

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