Limits...
Etiological diagnosis of granulomatous tubulointerstitial nephritis in the tropics.

Agrawal V, Kaul A, Prasad N, Sharma K, Agarwal V - Clin Kidney J (2015)

Bottom Line: We studied the etiology of GIN and compared the clinical and histological features and outcome in different etiologies at a tertiary care center in North India.Necrosis in granuloma, demonstration of acid fast bacilli, blood interferon gamma release assay and urine culture is not sensitive for the diagnosis of tuberculosis in GIN.Our findings suggest that tissue PCR for tuberculosis performed in an appropriate clinical setting is useful in the diagnostic evaluation of GIN.

View Article: PubMed Central - PubMed

Affiliation: Department of Pathology , Sanjay Gandhi Post Graduate Institute of Medical Sciences , Lucknow, Uttar Pradesh , India.

ABSTRACT

Background: Granulomatous tubulointerstitial nephritis (GIN) is common due to infections, drugs or sarcoidosis. However, the cause is often difficult to establish and the studies are limited. We studied the etiology of GIN and compared the clinical and histological features and outcome in different etiologies at a tertiary care center in North India.

Methods: Renaö biopsies from GIN cases diagnosed from January 2004 to April 2014 were retrieved. Stain for acid fast bacilli was performed in all biopsies. Etiological diagnosis was based on clinical features, extra-renal manifestations, radiology, history of drug intake and demonstration of infective agent. Tissue PCR for tubercular DNA was performed in seven biopsies.

Results: Seventeen GIN patients [mean age 35 ± 15 years; males 11] were identified. Tuberculosis was the commonest etiology followed by idiopathic, sarcoidosis and fungal. Both tuberculosis and sarcoidosis patients presented with subnephrotic proteinuria and raised serum creatinine. Acid fast bacilli were demonstrated in 1/9 and necrosis was demonstrated in 3/9 granulomas in tuberculosis. Tissue PCR for tubercular DNA was positive in six TB patients and negative in one sarcoidosis patient. Patients responded well to appropriate therapy.

Conclusion: Etiological diagnosis of GIN is essential for timely and appropriate therapy. Tuberculosis is the commonest etiology (53%) in the tropics. Necrosis in granuloma, demonstration of acid fast bacilli, blood interferon gamma release assay and urine culture is not sensitive for the diagnosis of tuberculosis in GIN. Our findings suggest that tissue PCR for tuberculosis performed in an appropriate clinical setting is useful in the diagnostic evaluation of GIN.

No MeSH data available.


Related in: MedlinePlus

Renal biopsy showing interstitial granuloma composed of epithelioid histiocytes and occasional giant cells associated with variable inflammatory cell infiltrate. Necrosis (asterisk) seen occasionally in tubercular granuloma (A), is not a feature of sarcoidosis (B) and idiopathic granulomatous interstitial nephritis (arrow, C). Fungal granuloma showing aseptate hyphae within giant cells (arrow, D). [A—Hematoxylin and eosin ×400; B, C—hematoxylin and eosin ×200; D—silver methenamine ×400].
© Copyright Policy - creative-commons
Related In: Results  -  Collection

License
getmorefigures.php?uid=PMC4581389&req=5

SFV071F3: Renal biopsy showing interstitial granuloma composed of epithelioid histiocytes and occasional giant cells associated with variable inflammatory cell infiltrate. Necrosis (asterisk) seen occasionally in tubercular granuloma (A), is not a feature of sarcoidosis (B) and idiopathic granulomatous interstitial nephritis (arrow, C). Fungal granuloma showing aseptate hyphae within giant cells (arrow, D). [A—Hematoxylin and eosin ×400; B, C—hematoxylin and eosin ×200; D—silver methenamine ×400].

Mentions: Renal biopsies showed interstitial granulomas associated with variable mononuclear to mixed inflammatory cell infiltrate, tubular atrophy and interstitial fibrosis (Table 2). The mixed inflammatory infiltrate was composed of lymphocytes, plasma cells, histiocytes, neutrophils and eosinophils. Acid fast bacilli (n = 1) and caseous necrosis (n = 3) were found only in biopsies with tuberculosis-associated GIN (Figure 3). None of the other histological features were useful in reaching an etiological diagnosis in GIN (Table 2). Well-circumscribed discrete ‘naked’ granulomas as typically described in sarcoidosis were not seen on renal biopsies (Figure 3).Fig. 3.


Etiological diagnosis of granulomatous tubulointerstitial nephritis in the tropics.

Agrawal V, Kaul A, Prasad N, Sharma K, Agarwal V - Clin Kidney J (2015)

Renal biopsy showing interstitial granuloma composed of epithelioid histiocytes and occasional giant cells associated with variable inflammatory cell infiltrate. Necrosis (asterisk) seen occasionally in tubercular granuloma (A), is not a feature of sarcoidosis (B) and idiopathic granulomatous interstitial nephritis (arrow, C). Fungal granuloma showing aseptate hyphae within giant cells (arrow, D). [A—Hematoxylin and eosin ×400; B, C—hematoxylin and eosin ×200; D—silver methenamine ×400].
© Copyright Policy - creative-commons
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4581389&req=5

SFV071F3: Renal biopsy showing interstitial granuloma composed of epithelioid histiocytes and occasional giant cells associated with variable inflammatory cell infiltrate. Necrosis (asterisk) seen occasionally in tubercular granuloma (A), is not a feature of sarcoidosis (B) and idiopathic granulomatous interstitial nephritis (arrow, C). Fungal granuloma showing aseptate hyphae within giant cells (arrow, D). [A—Hematoxylin and eosin ×400; B, C—hematoxylin and eosin ×200; D—silver methenamine ×400].
Mentions: Renal biopsies showed interstitial granulomas associated with variable mononuclear to mixed inflammatory cell infiltrate, tubular atrophy and interstitial fibrosis (Table 2). The mixed inflammatory infiltrate was composed of lymphocytes, plasma cells, histiocytes, neutrophils and eosinophils. Acid fast bacilli (n = 1) and caseous necrosis (n = 3) were found only in biopsies with tuberculosis-associated GIN (Figure 3). None of the other histological features were useful in reaching an etiological diagnosis in GIN (Table 2). Well-circumscribed discrete ‘naked’ granulomas as typically described in sarcoidosis were not seen on renal biopsies (Figure 3).Fig. 3.

Bottom Line: We studied the etiology of GIN and compared the clinical and histological features and outcome in different etiologies at a tertiary care center in North India.Necrosis in granuloma, demonstration of acid fast bacilli, blood interferon gamma release assay and urine culture is not sensitive for the diagnosis of tuberculosis in GIN.Our findings suggest that tissue PCR for tuberculosis performed in an appropriate clinical setting is useful in the diagnostic evaluation of GIN.

View Article: PubMed Central - PubMed

Affiliation: Department of Pathology , Sanjay Gandhi Post Graduate Institute of Medical Sciences , Lucknow, Uttar Pradesh , India.

ABSTRACT

Background: Granulomatous tubulointerstitial nephritis (GIN) is common due to infections, drugs or sarcoidosis. However, the cause is often difficult to establish and the studies are limited. We studied the etiology of GIN and compared the clinical and histological features and outcome in different etiologies at a tertiary care center in North India.

Methods: Renaö biopsies from GIN cases diagnosed from January 2004 to April 2014 were retrieved. Stain for acid fast bacilli was performed in all biopsies. Etiological diagnosis was based on clinical features, extra-renal manifestations, radiology, history of drug intake and demonstration of infective agent. Tissue PCR for tubercular DNA was performed in seven biopsies.

Results: Seventeen GIN patients [mean age 35 ± 15 years; males 11] were identified. Tuberculosis was the commonest etiology followed by idiopathic, sarcoidosis and fungal. Both tuberculosis and sarcoidosis patients presented with subnephrotic proteinuria and raised serum creatinine. Acid fast bacilli were demonstrated in 1/9 and necrosis was demonstrated in 3/9 granulomas in tuberculosis. Tissue PCR for tubercular DNA was positive in six TB patients and negative in one sarcoidosis patient. Patients responded well to appropriate therapy.

Conclusion: Etiological diagnosis of GIN is essential for timely and appropriate therapy. Tuberculosis is the commonest etiology (53%) in the tropics. Necrosis in granuloma, demonstration of acid fast bacilli, blood interferon gamma release assay and urine culture is not sensitive for the diagnosis of tuberculosis in GIN. Our findings suggest that tissue PCR for tuberculosis performed in an appropriate clinical setting is useful in the diagnostic evaluation of GIN.

No MeSH data available.


Related in: MedlinePlus