A Tale of Two Lesions: Tuberculosis Presenting as Granulomatous Interstitial Nephritis with Collapsing Glomerulopathy

Introduction: Sarcoidosis can present with acute renal failure (ARF) due to granulomatous interstitial nephritis (GIN). We report the case of granulomatous acute renal failure (ARF) revealing multisystemic sarcoidosis in the nephrology department of the Aristide Le Dantec hospital in Dakar. Observation: Mrs. kD aged 54 with a past history of high blood pressure for 22 years, a multi nodular euthyroid goiter, referred to the nephrology department for impaired renal function. The clinical examination revealed at entry, deterioration in the general condition with weight loss and non-selective anorexia. Clinical anemia was also noted. The clinical examination also revealed Cushingoid syndrome and dry mouth syndrome. On biology, the blood count showed bicytopenia with anemia at 10.9 g/dl and leukopenia at 2620/mm3. There was an impairment of renal function with creatinine at 139.2 mg/l and blood urea at 1.76 g/l. The renal ultrasound became normal. Cervical ultrasound showed an aspect of abscessed thyroiditis of the right lobe. Chest computed tomography (CT) showed bilateral hilar adenomegaly and a band of bilateral basal linear atelectasis. The renal biopsy showed glomeruli of subnormal structure, the interstitium is riddled with tuberculoid follicles formed of epithelioid and multinucleated histiocytes of the Langhans type. The diagnosis of granulomatous acute interstitial nephritis revealing multisystemic sarcoidosis was kept. The evolution was favorable after 1 month of treatment with corticosteroid therapy with a clear improvement in renal function. Conclusion: Renal manifestations during sarcoidosis are rare. They can be indicative of the disease as in our patient. Renal biopsy is essential in any patient presenting with impaired renal function with extra-renal signs.

South Africa continues to be burdened by human immunodeficiency virus (HIV) and tuberculosis (TB). In Cape Town, the epidemic of HIV-TB co-infection is as high as 70%. Granulomatous interstitial nephritis (GIN) has increased in frequency on renal biopsy. This study aimed to determine GIN prevalence and causes in HIV-positive patients as well as renal outcomes, patient survival and associated factors. This observational cohort study reviewed HIV-positive renal biopsies for GIN from 2005 to 2012. Causes of GIN (medications, TB, fungal and other), and baseline characteristics were analysed. A comparison of baseline data, renal function and survival was made between GIN and non-GIN cohorts. There were 45/316 biopsies demonstrating GIN. TB was the likely cause of GIN in 27 (60%) and 9 (20%) were due to a drug. Low estimated glomerular filtration rate was a statistically significant factor associated with mortality in both GIN (P = 0.045) and non-GIN cohorts (P < 0.000). In the GIN group, there were 12 (26.7%) deaths. Mortality for all patients was greatest in the first 6 months (P = 0.057). TB co-infection in both cohorts was associated with a higher mortality. The multivariate logistic regression demonstrated that a higher urine protein/creatinine ratio (uPCR) and lower estimated glomerular filtration rate were statistically associated with death. GIN is common in HIV-positive renal biopsies in Cape Town. TB-GIN was the commonest cause and associated with a high early mortality. GIN should be considered in HIV-positive patients with acute kidney injury, its presence conveys a survival benefit. There is a need for improved diagnostic accuracy and treatment strategies of TB-GIN.

Background: Granulomatous interstitial nephritis (GIN) is uncommon in native kidneys, and descriptions in allografts are few. We report clinical and pathologic findings in 22 allograft recipients with GIN identified in renal allograft biopsies and nephrectomies.Methods: Renal allografts with GIN were retrieved from the pathology files of two academic medical centers. Available clinical and pathologic data were compiled retrospectively for a 23-year period.Results: GIN was present in 23 specimens from 22 patients (15 males and 7 females) with allograft dysfunction [serum creatinine averaged 3.3 mg/dL (range 1.4–7.8)], at a mean age of 48 years (range 22–77). GIN was identified in 0.3% of biopsies at a mean of 552 days post transplantation (range 10–5898). GIN was due to viral (5), bacterial (5) and fungal (2) infections in 12 (54.5%), and drug exposure was the likely cause in 5 cases (22.7%). One had recurrent granulomatosis with polyangiitis. In 4 cases, no firm etiology of GIN was established. Of 18 patients with follow up data, 33.3% had a complete response to therapy, 44.5% had a partial response and 22.2% developed graft loss due to fungal and E. coli infections. All responders had graft survival for more than 1 year after diagnosis of GIN.Conclusions: Allograft GIN is associated with a spectrum of etiologic agents and was identified in 0.3% of biopsies. Graft failure occurred in 22% of this series, due to fungal and bacterial GIN; however, most had complete or partial dysfunction reversal and long–term graft survival after appropriate therapy.

IntroductionRenal injury due to sarcoidosis develops in less than a quarter of patients with this systemic disease. In most cases, granulomatous tissue alters the production of vitamin D, which leads to hypercalciuria, nephrocalcinosis, and nephrolithiasis. Granulomatous interstitial nephritis is another well-recognized pathological process associated with sarcoidosis. However, a glomerular pathology is very rarely noted, and only a few cases are reported to have cellular crescentic glomerulonephritis.Case presentationWe describe the case of a 26-year-old African American woman with systemic sarcoidosis, with a unique constellation of renal lesions, including noncaseating epithelioid granulomatous necrotizing interstitial nephritis, cellular crescent formation, and necrotizing vasculitis. Immunosuppressive therapy was helpful for alleviating her nephrotic syndrome and maintaining the stability of her renal function over a 30-month period.ConclusionGlomerular involvement of sarcoidosis needs to be considered in the differential diagnosis in cases of rapidly progressive glomerular nephritis.

209: Granulomatous Interstitial Nephritis Secondary to Carbamazepine Causing Acute Renal Failure

Crohn’s Disease With Progressive Renal Impairment

Sarcoidosis affects multiple organs including lung, heart and kidney. Sarcoidosis causes hypercalcemia, hypergammaglobulinemia, and rarely, granulomatous interstitial nephritis, resulting in renal stromal damage. Granulomatous interstitial nephritis is characterized as interstitial nephritis with noncaseating epithelioid granulomas. Diagnosing granulomatous interstitial nephritis before patient's death is challenging; hence, only few cases proven by renal biopsy have been reported till date. We present a case of acute kidney injury caused by granulomatous interstitial nephritis as a renal manifestation of sarcoidosis proven by renal biopsy, which can be confirmed by 18F-fluorodeoxyglucose positron emission tomography/computed tomography. Glucocorticoid therapy was helpful for improving and maintaining her renal function over a 6-year period.

Granulomatous interstitial nephritis is a rare finding in renal biopsy caused by drugs, infections, and inflammatory or autoimmune diseases. Idiopathic cases account for 18% of granulomatous interstitial nephritis in native kidneys. Sarcoidosis and drugs are the most common causes of granulomatous interstitial nephritis in Western countries, while in India tuberculosis prevails. Few cases of renal sarcoidosis without extrarenal involvement, that is, isolated renal sarcoidosis, have been reported. The diagnostic criteria of isolated renal sarcoidosis remain, however, unclear. Extrarenal sarcoidosis and other etiologies of granulomatous interstitial nephritis, in particular drug-related, have to be excluded. Some of these patients may develop extrarenal manifestations during follow-up. Changes in calcium and vitamin D metabolism are frequently observed in renal sarcoidosis and support its diagnosis. While non-necrotizing granulomas are a feature of sarcoidosis and drug-induced granulomatous interstitial nephritis, they also prevail in tuberculosis-associated granulomatous interstitial nephritis. Granulomatous interstitial nephritis caused by sarcoidosis and drugs usually responds to steroid therapy. A poor response to steroids may indicate an infectious etiology such as tuberculosis and should lead to a review of the initial diagnosis. This article gives an overview of the various etiologies of granulomatous interstitial nephritis, their frequency and histopathological characteristics, as well as potential biomarkers associated with renal sarcoidosis.

Background: Sarcoidosis is a multi-system disorder characterized by noncaseating epitheloid granuloma in multiple organs. However, granulomatous interstitial nephritis in the absence of extrarenal renal lesions is very rare. Case presentation: A 64-year-old male presented with a weight loss of 10 kg and an increase in serum creatinine from 1.1 to 4.8 mg/dl over a 1-year period. At admission, no proteinuria or hematuria was found, although serum creatinine was 5.1 mg/dl and was associated with slight increases in serum angiotensin converting enzyme and calcium levels. Renal biopsy revealed granulomatous interstitial nephritis with noncaseating epitheloid cells. The patient was diagnosed with sarcoidosis, although no extrarenal sarcoid lesion was found. Oral prednisolone was effective, with normalization of serum creatinine levels 2 weeks later. A review of the literature showed that isolated granulomatous renal sarcoidsosis preferentially affected elderly males, and their serum angiotensin converting enzyme levels were normal or mildly increased in many cases. Conclusions: This paper describes a rare case of isolated renal sarcoidosis with acute granulomatous interstitial nephritis. This case and a relevant review of the literature demonstrate that sarcoid granulomatous interstitial nephritis should be considered as one of differential diagnoses in elderly male patients with suspected tubulointerstitial nephritis irrespective of angiotensin converting enzyme levels.

We present a case of granulomatous interstitial nephritis (GIN) associated with chronic lymphocytic leukaemia (CLL). GIN is a rare pathological finding noted in renal biopsy specimens. Furthermore, CLL does not usually cause GIN. In this case, acute renal injury probably resulted from GIN, and urgent dialysis was required, despite sufficient chemotherapy. Immunohistochemical analyses of a biopsy specimen revealed invasion of CD20( +) CLL cells, surrounded by reactive T cells, and granuloma formation. Thus, CLL may induce secondary interstitial nephritis as a granulomatous reaction.

Granulomatous interstitial nephritis (GIN) is a rare histologic diagnosis in renal allografts. We report three cases with GIN. Case 1: a 37-yr-old woman received a kidney from her mother. On follow-up 15 months later, serum creatinine was increased and a graft biopsy showed epithelioid granuloma in the center of massive mononuclear cell infiltration. She had presented with refractory urinary tract infection treated with antibiotics before biopsy. The case was presumed to be GIN associated with UTI or hypersensitivity to medication. Case 2: a 47-yr-old woman received a second graft from a non-heart-beating donor. A protocol graft biopsy was performed six months after transplantation and showed several granulomatous nodules. She was followed closely without therapy. Case 3: a 27-yr-old woman received an ABO-incompatible kidney from her father. A protocol graft biopsy was performed three months after transplantation and showed granulomatous reaction with severe mononuclear cell infiltration. She received steroid pulse therapy. The two latter patients had no obvious factor contributing to GIN. Therefore, they were presumed to have idiopathic GIN. Infection is considered to be the main causative factor of GIN in renal allografts. This paper describes rare cases of GIN that had no infectious episode in the renal allografts.

Granulomatous interstitial nephritis secondary to chronic lymphocytic leukemia/small lymphocytic lymphoma.

Granulomatoses rénales : étude rétrospective de 44 observations

Granulomatous interstitial nephritis is a rare cause of renal failure in both native and allograft renal biopsies. Drugs and sarcoidosis are the commonest causes of granulomatous interstitial nephritis as reported in Western countries. Unlike the west, tuberculosis is the commonest cause of granulomatous interstitial nephritis in Indian subcontinent. The etiological factors, clinical course, glomerular and tubulointerstitial changes associated with granulomatous interstitial nephritis have been analyzed in the present study along with the outcome in patients with granulomatous interstitial nephritis.

Granulomatous interstitial nephritis has been observed in <1% of native renal biopsies. Here, we describe two patients with granulomatous interstitial nephritis in relation to Crohn's disease. Circulating helper and cytotoxic T cells were highly activated, and both cell types predominated in the interstitial infiltrate, indicating a cellular autoimmune response. After immunosuppressive treatment, renal function either improved or stabilized in both patients. In conclusion, granulomatous interstitial nephritis is a genuine extraintestinal manifestation of Crohn's disease, the treatment of which should include immunosuppressive agents.