**1. Introduction**

Granulomatous inflammation is a chronic inflammatory reaction, the main feature of which is the cellular transformation of a monocyte into a macrophage—a multinucleate giant epithelioid cell. The most common cause of this transformation is incomplete phagocytosis.

Difficulties in the clinical diagnosis of granulomatous interstitial nephritis (GIN) relate to the lack of a reliable noninvasive diagnostic method. Granulomatous interstitial nephritis is a rare type of kidney disease with a frequency of no more than 1%, according to the data at hand [1]. The precise cause of GIN is not known; due to the rarity of the disease, researchers rely primarily on a series of cases, rather than on the results of multicenter studies. In addition, the etiological structure of GIN can vary in different countries: in more developed countries, GIN is more probably related to drugs and sarcoidosis, whereas in less developed regions, it is likely to be associated with infections [2]. However, the most common causes are drug therapy and infection, and drugs (NSAIDs, antimicrobials, anticonvulsants, diuretics, and allopurinol) [3–5] account for 9–45% [6, 7] up to 55–70% [1], according to different studies.

The main infectious factors in the onset of this pathology, especially in immunocompromised patients, include mycobacteria [7] and fungi [1, 7]. GIN can be associated with HIV infection [8] and the influenza A (H1N1) virus [9]. Patients

with GIN of infectious etiology were stated to have acute kidney damage at onset [6]. In some cases, the etiology of GIN cannot be pinpointed; thus, the disease is considered to be idiopathic [3, 10]. GIN resulting in nephrosclerosis and chronic pathology of the digestive organs, and atopic dermatitis associated with carriage of *Toxocara*, has been reported.

We had a patient born with a body weight of 2.0 kg after an uneventful first pregnancy whose infantile period was unremarkable. When the girl was 1.5 years old, she suffered a common form of atopic dermatitis with periodic exacerbations (treated with topical steroids during exacerbations). At the age of 3 years, she was seen by a gastroenterologist for chronic esophagitis and chronic duodenitis. ELISA revealed contamination with *Toxocara* and *Giardia lamblia*; therapy with albendazole was administrated on an outpatient basis. However, the carriage of Toxocara continued. A repeated course of treatment was conducted in adolescence, but the antibody titer remained. Further courses of therapy were canceled, and *Toxocara* IgG antibody carriage was diagnosed. When the patient was 15, follow-up examination at the gastroenterology department revealed hydronephrosis of the nonfunctioning right kidney. Previously, there were no complaints or clinical manifestations indicating the damage to the urinary organs; urinalysis was unremarkable; blood pressure was normal.

In the course of further examination, urography showed a nonfunctioning right kidney; the excretory function of the left kidney was maintained. Cystography did not reveal any reflux. The patient underwent right nephrectomy.

Findings of the histology exam revealed a kidney with enlarged pelvis cups and the presence of cavities filled with fluid in the medulla and partly in the cortical layer. The capsule of the kidney was thickened by sclerosis. Renal glomeruli demonstrated fibrosis of the capsule with thickening, focal sclerosis of individual glomeruli, and singular glomerular cysts. Multiple, large-sized granulomas with necrosis in the center, surrounded by epithelioid cells and lymphocytes, including Pirogov-Langhans giant cells and eosinophils, were found mainly in the cortical layer (**Figures 1**–**4**).

Smaller granulomas showed fibrosis without central necrosis. Hyaline-droplet dystrophy was noted in the convoluted tubules. Sclerosis was detected in the vessels, diffuse lymphocellular infiltration and foci of fibrosis were observed in the stroma.

**Figure 1.**

*Medium-sized granuloma and peripheral lymphocytic infiltration. Renal glomeruli with edema of the mesangium are seen in the upper part.*

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**Figure 4.**

*chronic inflammation).*

*Granulomatous Interstitial Nephritis in Children Resulting from Wegener's Granulomatosis…*

*A giant multinucleated cell in the center. To the left and to the right, there are renal glomeruli with edema,* 

*The giant granuloma; two glomeruli with marked mesangial edema are on top. Renal tissue with pronounced* 

*Granuloma with surrounding infiltration. A granuloma with a necrotic focus in the center. On the periphery, there is a proliferation of connective tissue fibers with mildly expressed lymphocytic infiltration (a marker of* 

*tubules with dystrophic changes, and the stroma replete with lymphoid infiltration.*

*DOI: http://dx.doi.org/10.5772/intechopen.84491*

**Figure 2.**

**Figure 3.**

*lymphoid infiltration.*

*Granulomatous Interstitial Nephritis in Children Resulting from Wegener's Granulomatosis… DOI: http://dx.doi.org/10.5772/intechopen.84491*

#### **Figure 2.**

*Sarcoidosis and Granulomatosis - Diagnosis and Management*

*Toxocara*, has been reported.

pressure was normal.

layer (**Figures 1**–**4**).

nephrectomy.

with GIN of infectious etiology were stated to have acute kidney damage at onset [6]. In some cases, the etiology of GIN cannot be pinpointed; thus, the disease is considered to be idiopathic [3, 10]. GIN resulting in nephrosclerosis and chronic pathology of the digestive organs, and atopic dermatitis associated with carriage of

We had a patient born with a body weight of 2.0 kg after an uneventful first pregnancy whose infantile period was unremarkable. When the girl was 1.5 years old, she suffered a common form of atopic dermatitis with periodic exacerbations (treated with topical steroids during exacerbations). At the age of 3 years, she was seen by a gastroenterologist for chronic esophagitis and chronic duodenitis. ELISA revealed contamination with *Toxocara* and *Giardia lamblia*; therapy with albendazole was administrated on an outpatient basis. However, the carriage of Toxocara continued. A repeated course of treatment was conducted in adolescence, but the antibody titer remained. Further courses of therapy were canceled, and *Toxocara* IgG antibody carriage was diagnosed. When the patient was 15, follow-up examination at the gastroenterology department revealed hydronephrosis of the nonfunctioning right kidney. Previously, there were no complaints or clinical manifestations indicating the damage to the urinary organs; urinalysis was unremarkable; blood

In the course of further examination, urography showed a nonfunctioning right kidney; the excretory function of the left kidney was maintained. Cystography did not reveal any reflux. The patient underwent right

the presence of cavities filled with fluid in the medulla and partly in the cortical layer. The capsule of the kidney was thickened by sclerosis. Renal glomeruli demonstrated fibrosis of the capsule with thickening, focal sclerosis of individual glomeruli, and singular glomerular cysts. Multiple, large-sized granulomas with necrosis in the center, surrounded by epithelioid cells and lymphocytes, including Pirogov-Langhans giant cells and eosinophils, were found mainly in the cortical

Findings of the histology exam revealed a kidney with enlarged pelvis cups and

Smaller granulomas showed fibrosis without central necrosis. Hyaline-droplet dystrophy was noted in the convoluted tubules. Sclerosis was detected in the vessels, diffuse lymphocellular infiltration and foci of fibrosis were observed in the stroma.

*Medium-sized granuloma and peripheral lymphocytic infiltration. Renal glomeruli with edema of the* 

**102**

**Figure 1.**

*mesangium are seen in the upper part.*

*A giant multinucleated cell in the center. To the left and to the right, there are renal glomeruli with edema, tubules with dystrophic changes, and the stroma replete with lymphoid infiltration.*

#### **Figure 3.**

*The giant granuloma; two glomeruli with marked mesangial edema are on top. Renal tissue with pronounced lymphoid infiltration.*

#### **Figure 4.**

*Granuloma with surrounding infiltration. A granuloma with a necrotic focus in the center. On the periphery, there is a proliferation of connective tissue fibers with mildly expressed lymphocytic infiltration (a marker of chronic inflammation).*
