Intraglomerular crescentic metastases of malignant melanoma

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Human Pathology (2011) 42, 2025–2028

www.elsevier.com/locate/humpath

Case study

Intraglomerular crescentic metastases of malignant melanoma Yasemin Ozluk MD a,⁎, Isin Kilicaslan MD a , Rumeyza Kazancioglu MD b , Cuyan Demirkesen MD c , Duygu Derin MD d , Nil Molinas Mandel MD d a

Istanbul University, Istanbul Faculty of Medicine, Department of Pathology, 34098 Istanbul, Turkey VKV American Hospital, Department of Nephrology, 34365 Istanbul, Turkey c Istanbul University, Cerrahpasa Faculty of Medicine, Department of Pathology, 34098 Istanbul, Turkey d VKV American Hospital, Department of Medical Oncology, 34365 Istanbul, Turkey b

Received 24 February 2010; revised 4 May 2010; accepted 21 May 2010

Keywords: Intraglomerular metastasis; Crescent; Malignant melanoma; Kidney

Summary We describe here a patient with a metastatic malignant melanoma displaying crescentic lesions in the glomeruli. A 64-year-old woman was referred to our hospital because of a sudden increase of serum creatinine. Clinical diagnosis suggested rapidly progressive glomerulonephritis. Renal biopsy revealed diffuse crescentic lesions containing metastatic melanoma cells. These cells were also seen in the glomerular capillary lumina and tubules, and a few scattered tumor cells were also present in the interstitium. Glomerular metastasis is a very rare entity. To the best of our knowledge, this patient is the first to be described in the English language literature showing intraglomerular metastasis of malignant melanoma as demonstrated by needle biopsy and is only the second patient with intraglomerular metastasis presenting with acute renal failure. © 2011 Elsevier Inc. All rights reserved.

1. Introduction Intraglomerular metastasis (IGM) is a very rare entity, with very few cases reported in the literature despite the large amount of blood circulating through the kidneys [1-6]. Although not well documented, IGM has been reported in 6% to 10% of secondary renal malignancies [1,6,7] and in 3% of all disseminated malignancies [1]. The exact incidence of IGM may be higher because renal biopsies are not routinely performed in patients with disseminated malignancies. The mechanism underlying the etiology of IGM is not well understood, and no relationship of IGM to clinical symptoms or primary tumor type is known.

⁎ Corresponding author. Yasemin Ozluk, MD, Istanbul Tip Fakultesi, Temel Tip Bilimleri Binasi, Patoloji AD, 34390 Capa-Topkapi, Istanbul/Turkey. E-mail address: [email protected] (Y. Ozluk). 0046-8177/$ – see front matter © 2011 Elsevier Inc. All rights reserved. doi:10.1016/j.humpath.2010.05.032

We describe here a patient with a histologically diagnosed IGM from malignant melanoma, who presented with acute renal failure and was evaluated by renal needle biopsy.

2. Case report A 64-year-old woman presented to our nephrology outpatient clinic with a 1-month history of epigastric pain and dysuria. She had undergone a hysterectomy and bilateral oophorectomy 11 years earlier and had quit smoking 10 years previously. One week earlier, a 1 × 1-cm cutaneous pigmented lesion had been removed from the medial lower quadrant of her right breast. This lesion was diagnosed histologically as a malignant melanoma with a Breslow thickness of 2.03 mm and a Clark level of IV. On physical examination, the patient appeared anemic and there was a small incisional scar on her right breast. Her blood

2026 pressure was 140/70 mm Hg; her physical parameters were otherwise normal. Her initial laboratory tests showed elevated concentrations of blood urea (56 mg/dL; reference range, 10-50 mg/ dL), creatinine (2.8 mg/dL; reference range, 0.6-1.2 mg/dL), phosphorus (4.27 mg/dL; reference range, 2.8-4 mg/dL), and complement C4 (3 mg/dL; reference range, 10-40 mg/dL); along with a low hemoglobin level (11.3%; reference range, 11.7%-16%) and hematocrit (32.1%; reference range, 35%47%). Complement C3 was within normal limits (123 mg/ dL; reference range, 90-180 mg/dL). Urinalysis revealed 4 to 5 erythrocytes and hyaline casts per high-power field. Renal ultrasound showed a renal parenchyma of normal size and thickness. Both kidneys were of grade I echogenicity; and there was no evidence of calculus, mass, or pelvicaliceal ectasia. A 24-hour urine collection revealed proteinuria of 3.1 g/d and creatinine clearance of 19.9 mL/min. Based on her history of malignancy and the presence of metastatic sentinel axillary lymph nodes, she underwent a thoracoabdominal computed tomographic scan, which

Y. Ozluk et al. revealed calcified paratracheal lymph nodes and millimetric bilateral calcified nodules on both lungs. An abdominal examination was within normal limits. She was presumptively diagnosed with rapidly progressive glomerulonephritis, and a percutaneous renal needle biopsy was performed. Renal needle biopsy cores were stained with hematoxylineosin (HE), periodic acid-Schiff (PAS), periodic acidmethenamine silver (PAMS), Masson's trichrome, and Congo red and assessed by light microscopy. Cores were also incubated with fluorescently labeled antibodies against immunoglobulin (Ig) G, IgA, IgM, fibrinogen, C3, and C1q and examined by fluorescence microscopy.

2.1. Light microscopy findings A total of 24 glomeruli were seen, 2 of which were globally sclerotic. All nonsclerotic glomeruli contained both intracapillary and crescentlike extracapillary tumor cells (Fig. 1A-B), with a high nuclear/cytoplasm ratio and

Fig. 1 A, Intraglomerular tumor cells displaying both intracapillary and extracapillary proliferation (PAS ×100). B, Tumor cells in the capillary, Bowman space, and proximal tubular lumina (PAS ×100). C, Intracapillary tumor thrombi and crescentlike tumor cell proliferation in the Bowman space, with prominent necrosis (HE ×200). D, Brown granular pigment in the cytoplasm of tumor cells in the Bowman space (HE ×200).

Intraglomerular crescentic metastases of malignant melanoma

2027

positivity for melanocytic markers; S-100 (clone 4C4.9, 1/ 200 dilution, 1-hour incubation, NeoMarkers, Thermo Fischer Scientific, Fremont, CA, USA) (Fig. 2), MART-1/ Melan-A (clones M2-7C10 + M2-9E3, 1/100 dilution, 1-hour incubation, NeoMarkers), and HMB45 (clones HMB45 +HMB50, 1/100 dilution, 1-hour incubation, NeoMarkers). Immunohistochemistry also detected a few scattered tumor cells in the interstitium, which were not observed on HE stains (Fig. 2).

2.2. Immunofluorescence microscopy findings Seven glomeruli were evaluated, but no immune deposits were detected. Fig. 2 Strong S-100 immunopositivity of melanoma cells in the glomeruli and rare tumor cells in the interstitium (anti-S-100 antibody, ×100).

prominent nucleoli, along with a brown intracytoplasmic granular pigment and numerous mitotic figures. Some of the crescentlike infiltrations contained foci of necrosis (Fig. 1C-D). Metastatic tumor cells were also observed within the capillaries, forming luminal tumor thrombi. Glomerular basement membrane disruption was seen in some of the metastatic glomeruli that displayed crescentic lesions. The extracapillary crescentlike tumor foci were continuous with those of the proximal tubules (Fig. 1B). Some tubular crosssections were full of tumor cells, even replacing the tubular epithelium. Melanin pigment was demonstrated by MassonFontana staining. Immunohistochemistry revealed strong

Table 1

3. Discussion Although the kidneys receive as much as 20% to 30% of cardiac output, IGM is exceedingly rare [1-6,8,9]. For example, one study found IGM in only 7 of 100 extrarenal tumors [6], whereas another study reported that the incidence of IGM was 10% among all secondary neoplasms of the kidney and 3% of all disseminated malignancies [1]. The real incidence of IGM is likely to be higher than reported because renal needle biopsies are not routinely performed in patients with disseminated malignancies and fewer autopsies have been performed in recent years. Various types of malignancies displaying IGM have been described, most of which were lung carcinomas [1,3,10,11]. We reviewed the literature on IGM and summarize our findings in Table 1. Intraglomerular metastasis has been

Summary of reports on intraglomerular metastases

Source

n

Glomerular morphology

Primary tumor

Diagnostic method

Galloway and Ray, 1964 [8] Ross, 1966 [3] Wagle et al, 1975 [7] Datta, 1978 [9] Belghiti et al, 1984 [2]

1 1 5 1 2

Iskandar et al, 1985 [13] Toth, 1987 [6] Sarma and Simmons, 1989 [12] Yang et al, 1991 [14] Melato et al, 1991 [11] Carr et al, 1994 [5] Nomura et al, 1995 [10] Sridevi et al, 1999 [1]

1 2 1 1 1 1 1 4

IC IC and EC N/A IC IC IC and EC IC IC and EC IC IC IC IC IC IC; IC and EC

Autopsy Autopsy Autopsy N/A Needle biopsy Autopsy N/A Autopsy N/A Needle biopsy N/A Nephrectomy Autopsy Autopsy

Yokoi et al, 2001 [4]

1

IC

Renal cell ca Lung (SCC) N/A N/A N/A Ovary Lymphoma Pancreas (ACA) Thyroid (Papillary ca) Lymphoma Lung Renal cell ca Lung (ACA) Lung (SCC) Pancreas (ACA) Hematologic Mesothelioma Pancreas

Needle biopsy

Abbreviations: IC indicates intracapillary; EC, extracapillary; N/A, not available; SCC, squamous cell carcinoma; ACA, adenocarcinoma; ca, carcinoma.

2028 observed in both intracapillary [11-14] and extracapillary [1,6,15] forms. Most previously reported patients were diagnosed at autopsy, although one was diagnosed from a nephrectomy specimen [5] and 3 were diagnosed from core biopsies [2,4,14]. Intraglomerular metastasis, along with disseminated disease, is associated with poor prognosis. Proteinuria and hematuria were the most common kidneyrelated clinical findings in patients with IGM [2,4,7,10]. Acute renal failure is very rare and has been previously reported in only one patient [8]. The pathogenesis of IGM remains unclear. Several factors are required to induce and maintain metastasis. Tumor cell interposition has been observed in the glomerular basement membrane zone, suggesting that IGM is associated with extravasation of tumor cells [10]. The proliferation of tumor cells in capillary lumina has been shown to be the first step in the process of metastasis [4,10]. As our patient presented with both intracapillary and extracapillary proliferation of tumor cells, along with intratubular distribution, the pathway of tumor cells may be the same as that of the urinary stream, from filtration to actual urine production. The detection of glomerular basement membrane disruption in some glomeruli suggests that intracapillary tumor cells are the first to arrive as the metastatic process commences. Moreover, crescentic lesions may be composed of both tumor and epithelial cells of Bowman capsule, the latter of which are activated by disruption of basement membranes. Furthermore, obstruction of the tubular lumina and/or renovascular hemodynamic changes caused by capillary blockage may have precipitated the acute renal failure observed in our patient. In conclusion, intraglomerular metastasis is an extremely rare condition in patients with disseminated malignancies. The pathogenetic mechanism of this condition is currently unknown, and more patients must be studied. Although very rare, this condition should be kept in mind in the differential diagnosis of glomerular pathologies, including proteinuria,

Y. Ozluk et al. hematuria, and (less frequently) renal failure, observed in patients with malignancies.

References [1] Sridevi D, Jain D, Vasishta RK, Joshi K. Intraglomerular metastasis: a necropsy study. J Clin Pathol 1999;52:307-9. [2] Belghiti D, Hirbec G, Bernaudin JF, Pariente EA, Martin N. Intraglomerular metastases. Report of two cases. Cancer 1984;54: 2309-12. [3] Ross L. Bronchogenic squamous cell carcinoma metastasizing to Bowman's capsule. J Clin Pathol 1966;19:375-7. [4] Yokoi H, Nakata M, Sawai K, et al. Intraglomerular metastasis from pancreatic cancer. Am J Kidney Dis 2001;37:1299-303. [5] Carr RA, Yoong AK, Newman J. Intracapillary glomerular metastases in a nephrectomy specimen removed for ipsilateral renal cell carcinoma. J Clin Pathol 1994;47:558-9. [6] Toth T. Extracapillary tumourous metastatic crescents in glomeruli of the kidney. Pathol Res Pract 1987;182:240-3. [7] Wagle DG, Moore RH, Murphy GP. Secondary carcinomas of the kidney. J Urol 1975;114:30-2. [8] Galloway CN, Ray CT. Diffuse glomerular metastasis from hypernephroma. Arch Intern Med 1964;114:803-5. [9] Datta BN. Case report: intraglomerular metastasis. Indian J Pathol Microbiol 1978;21:184-5. [10] Nomura S, Takeda M, Manabe T, et al. Case report: intraglomerular metastasis with neoplastic cell interposition. Am J Med Sci 1995;309: 179-82. [11] Melato M, Laurino L, Bianchi P, Faccini L. Intraglomerular metastases. A possibly maldiagnosed entity. Zentralbl Pathol 1991;137:90-2. [12] Sarma DP, Simmons GT. Intraglomerular metastases from papillary carcinoma of the thyroid. J La State Med Soc 1989;141:26-8. [13] Iskandar SS, Jennette JC, Weis LS. Primary cerebral lymphoma with glomerular renal involvement. Arch Pathol Lab Med 1985;109:524-8. [14] Yang KH, Lee KY, Gang SJ, Kim BK, Shim SI, Kim SM. Intraglomerular malignant lymphomatosis: a report of a case. J Korean Cancer 1991;23:443-50. [15] Fer MF, McKinney TD, Richardson RL, Hande KR, Oldham RD, Greco FA. Cancer and the kidney: renal complications of neoplasms. Am J Med 1981;71:704-18.

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