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Saudi Journal of Kidney Diseases and Transplantation
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CASE REPORT Table of Contents   
Year : 2009  |  Volume : 20  |  Issue : 5  |  Page : 842-845
Granulomatous interstitial nephritis due to tuberculosis-a rare presentation

1 Department of Nephrology, Meenakshi Mission Hospital and Research Centre, Lake Area, Melur Road, Madurai, Tamil Nadu, India
2 Department of Pathology, Amrita Institute of Medical Sciences, Amrita Lane, Elamakkara Post, Kochi, Kerala, India
3 Department of Molecular Biology, Amrita Institute of Medical Sciences, Amrita Lane, Elamakkara Post, Kochi, Kerala, India

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Date of Web Publication2-Sep-2009


Granulomatous interstitial nephritis (GIN) is an uncommon form of acute interstitial nephritis. We report a young male who presented to us with a rapidly progressing renal failure and massive proteinuria. A renal biopsy revealed GIN, and we were able to demonstrate the presence of tuberculous DNA in the biopsy specimen. The patient was started on anti-tuberculous therapy and steroids besides 11 sessions of hemodialysis. He recovered and is currently doing well. This case highlights an uncommon manifestation of renal tuberculosis, namely massive proteinuria, acute renal failure, and granulomatous interstitial lesions.

How to cite this article:
Sampathkumar K, Sooraj YS, Mahaldar AR, Ramakrishnan M, Rajappannair A, Nalumakkal SV, Erode E. Granulomatous interstitial nephritis due to tuberculosis-a rare presentation. Saudi J Kidney Dis Transpl 2009;20:842-5

How to cite this URL:
Sampathkumar K, Sooraj YS, Mahaldar AR, Ramakrishnan M, Rajappannair A, Nalumakkal SV, Erode E. Granulomatous interstitial nephritis due to tuberculosis-a rare presentation. Saudi J Kidney Dis Transpl [serial online] 2009 [cited 2022 May 17];20:842-5. Available from: https://www.sjkdt.org/text.asp?2009/20/5/842/55374

   Introduction Top

Acute interstitial nephritis (AIN) is most com­monly encountered due to drugs such as non­steroidal anti-inflammatory agents or antibiotics, infections (Leptospirosis, Legionella, streptoco­ccus) or immunological diseases (Sjogren's syn­drome). Granulomatous interstitital nephritis (GIN) is an uncommon form of AIN. [1],[2] We report an unusual case of renal tuberculosis pre­senting as GIN.

   Case History Top

A 17 year old male presented to our outpatient department with a history of nausea, vomiting and fatigue for 2 weeks. There was no facial puffiness, swelling of legs, hematuria, dysuria, rashes, or joint pains. Two months earlier, he had developed an ulcer with a serous discharge in his left axilla, which was associated with a low grade fever. There was no past history of tuberculosis, chronic drug intake, or sexual ex­posure.

Physical examination revealed a moderately nourished male who was afebrile. His blood pressure was 110/70 mmHg. A 2 cm healed scar was observed in his left axilla. However, the systemic examination was non contributory.

Laboratory investigations showed: 10.8 g/dL, Total leucocyte count: 9000/cumm, Differential leucocyte count: polys 68, Lym 29, Eos: 3, ESR: 32 mm/hr, blood urea nitrogen: 156 mg/dL and serum creatinine: 10.7 mg/dL, and liver func­tion tests and electrolytes were within normal limits. Urinalysis revealed 2+ albuminuria and 5-6 pus cells/hpf and spot urine protein crea­tinine ratio was 2.8. An ultrasonogram of the abdomen showed normal sized kidneys (Right kidney - 10.2 × 5.1 cm, Left kidney - 11.5 × 5.1 cm) with normal cortical echoes and cortico­medullary differentiation. A chest x-ray was normal. Urine culture did not reveal any growth. Rapidly progressive glomerulonephritis was diag­nosed, and the patient was initiated on hemo­dialysis through a right internal jugular double lumen catheter. After adequately dialyzing him, a renal biopsy was performed.

On histopathology, the specimen revealed 21 glomeruli; one was obsolescent, and the rest were normal in size with focal mild mesangial hyper-cellularity. There was no endocapillary proliferation or crescents. Tubules showed focal lymphocytic infiltration of the epithelium. The tubular lumina showed hyaline casts, granular debris and a neutrophilic collection. The inters­titium appeared edematous with multiple granu­lomas composed of epitheloid histiocytes and few Langhan's type giant cells. One of the gra­nulomas showed caseous necrosis. The rest of the interstitium showed a mixed inflammatory infiltrate composed of lymphocytes, plasma cells, eosinophils, and neutrophils [Figure 1]a and [Figure 1]b. Immunofluoresence showed 1+ mesangial C3 and minimum to 1+ IgA, while IgG, IgM and C1q staining were negative.

The differential diagnosis of GIN was consi­dered. Work-up for  Brucella More Details and parasites were negative. His serum calcium and uric acid were within normal limits. There was no evidence of vasculitis or uveitis. Mantoux test was per­formed which was strongly positive (21 mm at 48 hours). The DNA from the renal biopsy was isolated using a nucleic acid purification kit (Roche Applied Science, Germany). [3] Polyme­rase chain reaction (PCR) was performed using primers specific for rpoB gene of Mycobacte­rium tuberculosis. The DNA from the patient was found to be positive [Figure 2]. This is one of the rare instances in which the DNA of the Mycobacterium tuberculosis has been isolated from a patient with GIN causing rapidly pro­gressive renal failure.

The patient underwent a total of 11 hemodia­lysis sessions. He was started on steroids and anti-tuberculous drugs including rifampicin, iso­niazid, pyrazinamide and ethambutol. He also received prednisolone 1 mg/kg/day for 4 weeks. His renal parameters started improving by day 10 and hemodialysis was discontinued. The cli­nical course is depicted in [Figure 3].

The patient completed a full course of anti-tu­berculous treatment with normal renal parameters.

   Discussion Top

Many features in this case are unusual. A ne­phrotic range proteinuria with the tubuloin­terstitial nephritis is usually encountered with NSAIDs and Methicillin. [4] Tuberculosis produ­cing such presentation has not ever been re­ported. The presentation of our patient with se­vere acute renal failure requiring dialysis is also rare in acute interstitial nephritis except in cases induced by rifampicin therapy. There was no eosinophilia, fever or skin rash. In fact, our pre biopsy diagnosis was compatible with a rapidly progressive glomerulonephritis.

Infections account for only a small percentage of cases with GIN. In a study of 46 patients with GIN, 44.7% were classified as drug-induced, 28.9% as renal sarcoidosis, and 15.9% as a list of rare cases including Wegener's granulo­matosis, foreign body giant cell reaction, GIN secondary to intravesical bacillus Calmette Guerin therapy for bladder cancer, and xanthogranulo­matous pyelonephritis. [1] Mignon et al reported 3 cases with GIN secondary to tuberculosis. [2] Tu­berculous granuloma in the renal allograft have been described in the medical literature. [5],[6]

Tuberculosis most often affects the lungs, and the commonest sites of the extrapulmonary tu­berculosis are the lymph nodes and the genito­urinary tract, which accounts for 27% (range 14 to 41%) of nonpulmonary cases. [7] The kidney is usually affected by hematogenous spread of ba­cilli from a focus of infection in the lung. In most cases, at the time of presentation, there is no evidence for an active pulmonary disease. There may be a clinical or radiological evidence of past infection, and renal involvement usually occurs after a period of dormancy. [7] Mallinson et al described 3 patients who had advanced re­nal failure with normal sized kidneys, [8] and their renal biopsies revealed interstitial granulomas with caseation in two of them; acid fast bacilli were demonstrated by conventional stains in two patients; chest x-ray showed evidence of tuber­culosis in two patients, whereas one patient had evidence of tubercular peritonitis.

Instances of acute GIN with acute renal failure have been reported in cases of intravesical che­motherapy with bacilli Calmette-Guerin (BCG) for superficial transitional cell carcinoma of the bladder. [9] Hematogenous dissemination via a trau­matic instillation of BCG and/or an immune­complex mechanism may contribute to the renal damage.

Detection of tuberculous interstitial nephritis is not easy. Three urine cultures considered to be the "gold standard" for diagnosis of renal tu­berculosis, are often negative.10 PCR for tuber­culosis has been shown to have an overall sensitivity, specificity, positive predictive value and negative predictive value of 97.87%, 100%, 100%, and 94.73%, respectively. In our case PCR was positive and we were able to reach a diagnosis. [10]

Modern short course anti-tuberculous drug re­gimens (ATT) are effective in the treatment of tuberculous GIN. This includes 2 months of in­tensive therapy consisting of isoniazid, rifam­picin, ethambutol and pyrazinamide followed by 4 months of isoniazid and rifampicin. Reduc­tion in dosage is not required for these drugs in renal failure except ethambutol whose dose has to be reduced as there is a risk of irreversible optic neuritis. [7] Our patient received anti tuber­culosis therapy and he recovered.

We conclude that our case highlights an uncommon manifestation of renal tuberculosis, namely massive proteinuria, acute renal failure and granulomatous interstitial lesions.

   References Top

1.Bijol V, Mendez GP, Nose V, Rennke HG. Granulomatous interstitial nephritis: A clinico­pathologic study of 46 cases from a single institution. Int J Surg Pathol 2006;14:57-63.  Back to cited text no. 1    
2.Mignon F, Mery JP, Mougenot B, Ronco P, Roland J, Morel-Maroger L. Granulomatous Interstitial Nephritis. Adv Nephrol Necker Hosp 1984;13:219-45.  Back to cited text no. 2    
3.Whelen AC, Felmlee TA, Hunt JM, et al. Direct genotype detection of Mycobacterium tubercu­losis rifampicin resistance in clinical specimens by using single-tube heminested PCR. J Clin Microbiol 1995;33:556-61.  Back to cited text no. 3  [PUBMED]  [FULLTEXT]
4.Nolan CM, Abernathy RS. Nephropathy asso­ciated with methicillin therapy. Prevalence and determinants in patients with staphylococcal bac­teremia. Arch Intern Med 1977;137(8):997-1000.  Back to cited text no. 4    
5.Ozdemir BH, Sar A, Uyar P, Suren D. Post­transplant tubulointerstitial nephritis: clinico­pathological correlation. Transplant Proc 2006; 38(2):466-9.  Back to cited text no. 5    
6.Meehan SM, Josephson MA, Haas M. Granu­lomatous tubulointerstitial nephritis in the renal allograft. Am J Kidney Dis 2000;36(4):E27.  Back to cited text no. 6    
7.Eastwood JB, Corbishley CM, Grange JM. Tuberculosis of the kidney. J Am Soc Nephrol 2001;12:1307-14.  Back to cited text no. 7  [PUBMED]  [FULLTEXT]
8.Mallinson WJ, Fuller RW, Levinson DA, Baker LR, Cattell WR. Diffuse interstitial tuberculosis an unusual cause of renal failure. Q J Med 1981; 57:31-5.  Back to cited text no. 8    
9.Modesto A, Marty L, Suc JM, et al. Renal complications of intravesical bacillus Calmette Guerin therapy. Am J Nephrol 1991;11(6):501-4.  Back to cited text no. 9    
10.Manzanera Escribano MJ, Morales Ruiz E, Odriozola Grijalba M, et al. Acute renal failure due to interstitial nephritis after intravesical instillation of BCG. Clin Exp Nephrol 2007;11 (3):238-40.  Back to cited text no. 10    

Correspondence Address:
Krishnaswamy Sampathkumar
Department of Nephrology, Meenakshi Mission Hospital and Research Centre, Lake Area, Melur Road, Madurai, TamilNadu - 625 107
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Source of Support: None, Conflict of Interest: None

PMID: 19736486

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  [Figure 1], [Figure 2], [Figure 3]

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