Granulomatus inflammatory interstitial nephritis is a necrotizing granulomatus inflammation in infection etiology [1] such as tuberculosis and fungal infection, but non necrotizing granulomatus inflammation in drug induced and sarcoidosis not uncommon [2]. The urinalysis revealed pyuria and esonophiluria and renal biopsy revealed inerstitial nephritis with granuloma [3]. Renal biopsies are critical in establishing this diagnosis and the extent of tubular atrophy and interstitial fibrosis may aid in determining prognosis [4]. Granulomatous Interstitital Nephritis (GIN) is an uncommon form of AIN. Granulomatous interstitial nephritis is a rare cause of renal failure [5]. It is an uncommon histological diagnosis and is seen in <1% of both native and allograft renal biopsies. Caseating granulomas are common in tuberculosis but also found in fungal infections [6].

Dr. Mallick Moniruzzaman of 62 years old man, a diagnosed case of obstructive uropathy, hailing from Khulna Bangladesh. He is diabetic for 10 years. Hypertensive for the same duration and control with medications. He had history of URS+ICPL for left ureteric stone in 2019.TURP for enlarged prostate in 2020.Right sided RIRS for impacted stone in PUJ in June 2021 for that purpose he had H/O 10 kg weight loss in 2021 (march to August). low grade fever, no definite pattern that he went to abroad for treatment purpose (October, 2021). General examination revealed patients is conscious, oriented, Pulse 84/min, Bp 130/75 mm Hg (On medication), temp normal, mildly anaemic, non-icteric, mildly edematus, Lymph nodes not palpable, Bed side   urine   examination   Protein (++),   Urine   output 2.4 litre/day,  Systemic   Examination   revealed   nothing abnormality, fundoscopy normal. Regarding tareatment history: Patient received multiple course of antibiotic even though urine culture was negative., Investigation revealed, urine R/M/E showed, Protein++, RBC 10-15/HPF, Pus cell 8-10/HPF, urine culture: No Growth Hb11.2g% (gm/dl) 110, ESR (mm/1^st hr), WBC 9390 (/cmm) Polymorph-68%, Platelet count(/cmm) 2,50,000, Serium creatinine 1.4 mg/dl, S. electrolyte, Na+ 129 mmol/L, K+ 4.3 mmol/L, CL-100 mmol/L, Tco2 16.1, S. calcium 2.3 mg/dl (corrected), S. PO4 6.7 mg/dl, iPTH 132, S. Albumin 31 gm/L, CRP 8.36 mg/L, RBS 6.0 mmol/L, S.cortisol 415 nmol/L, S Iron 14.1 microgm/dl, TIBC 34 microgm/dl, Transferrin saturation 41%, S Ferritin 2000 ng/l, HBsAg negative, Anti HCV negative, ANA negative ANCAnegative, S. Uric Acid 10.7 mg/dl, 6.0, mmol/l HBA1C 6.5%, FT4 0.61 (miu/L), TSH 0.76 (miu/L), USG revealed left sided mild hydronephrosis Pet Scan, report showed: Increased metabolic activity seen in multiple hypodense areas in cortex of both kidneys likely represents lobar nephronia.

Increased metabolic activity is seen in diffuse wall thickening in urinary bladder, in keeping with cystitis. FDG avid enlarged lymph nodes are in keeping with active disease. Considering Non Diabetic Renal Disease (NDRD) evidenced by absence of retinopathy and neuropathy, urine PCR 3.1, presence of active urinary sediments, renal biopsy was done and biopsy report showed. Glomeruli: Many of the viable glomeruli show ischaemic wrinkling of the periglomerular sclerosis. No segmental sclerosis, thickening/duplication of glomerular basement membrane, spikes the glomerular tuft, proliferation, crescent or necrosis is noted. Tubules/Interstitium: There is severe interstitial fibrosis with atrophy (>50%). The interstitium (sclerosed and non-sclerosed cortex) interstitial inflammation composed of lymphocytes, plasma cells and few non-epithelioid cell granulomas with few Langhaans type of giant cells. Suggestive of tubercular granulomatus interstitial nephrits. Then 3 consecutive morning urine sample for AFB was sent and two urine sample was found positive for AFB. Anti TB drug was initiated from first November 2021 with renal dose adjustment.  This  time  he  was  admitted  to  BSMMU hospital with the complaints of Vomiting for 20 days, Increased frequency of urination., After evaluation he was found to have raised serum creatinine (2.4 mg/) After couple days, that was subsequently resolved spontaneously and he was discharged with stable renal function (Figure 1-2).

Figure 1: Histopathology of Granulomatous Intestinal Nephritis

Figure 2: PET-CT Showed Granulomatous Nephritis

Recurrent sterile pyuria might be considered as the atiology of renal tuberculosis that we have identified in this case. Granulomatus interstitial nephritis is a rare cause of renal failure. TB associated TIN rare but it needed rapid recognition and early intervention to ensure diagnosis of renal involvement of active TB Renal biopsy should be performed as soon as possible. Renal manifestation of tuberculosis include scar manifestation resulting is ureteral stricture and hydronephrosis, chronic cystitis leading on small capacity thimble bladder and secondary amylodosis as well as granulomatus interstitial nephritis [1]. Granulomatus nephritis has various causes including sarcodosis, crystal deposition medication and infection. Cseation granuloma are common in tuberculosis though rare it can be also observed in fungal infection [7]. In this case renal histopathology revealed no evidence of caseation narcosis but interstitium showed lymphocytes plasma cells and few non epitheliod cell granuloma with few lengthens gaint cells suggestive of granulomatous interstitial nephritis. In Asian Sub-Continent tuberculosis is the most common etiology of Granulomatus interstitial nephritis [8]. A medical was arranged along with urologist and nephrologist for a final management protocol. In this case after getting antitubercular drugs renal function was improved. Repeate Kidney biopsy can clarify the degree of improvement in later month. It is a rare presentation in our country in the context of obstructive nephropathy with co-morbidity and several times intervention.

Though rare, tubercular granulomatus interstitial nephritis is a treatable condition, physician should keep in mind to establish its diagnosis particular in context of sterile pyuria.

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2. Shah S. et al. “Granulomatous Interstitial Nephritis.” Clinical Kidney Journal, vol. 8, no. 5, 2015, pp. 516-523.

3. Bijol V. et al. “Granulomatous Interstitial Nephritis: A Clinicopathologic Study of 46 Cases from a Single Institution.” International Journal of Surgical Pathology, vol. 14, no. 1, 2006, pp. 57-63.

4. Nasr S.H. et al. “Granulomatous Interstitial Nephritis.” American Journal of Kidney Diseases, vol. 41, no. 3, 2003, pp. 714-719.

5. Naidu G.D. et al. “Granulomatous Interstitial Nephritis: Our Experience of 14 Patients.” Indian Journal of Nephrology, vol. 23, no. 6, 2013, p. 415.

6. Sampathkumar K. et al. “Granulomatous Interstitial Nephritis Due to Tuberculosis-A Rare Presentation.” Saudi Journal of Kidney Diseases and Transplantation, vol. 20, no. 5, 2009, p. 842.

7. Aleckovic-Halilovic M. et al. “Granulomatous Interstitial Nephritis: A Chameleon in a Globalized World.” Clinical Kidney Journal, vol. 8, no. 5, 2015, pp. 511-515.

8. Manzanera Escribano M.J. et al. “Acute Renal Failure Due to Interstitial Nephritis: A Rare Cause of Acute Kidney Injury.” Clinical and Experimental Nephrology, vol. 11, no. 3, 2007, pp. 238-240.