Is Minimal Change Disease Associated with Prostate Cancer or Is Age Just a Number?

Abstract

Background: Prostate cancer is the most common malignancy in men. Secondary nephrotic syndrome, a feature of paraneoplastic syndrome, occurs in 11% of cases and is mainly caused by membranous glomerulopathy. The association between minimal change disease and prostate cancer is rare. Only one cause has been described in the available literature.

Case presentation: We present the case of a 77-year-old patient who was admitted to our department with stage 3 acute kidney injury and with nephrotic syndrome with anasarca (creatinine: 168 µmol/L, eGFR: 33 mL/min/1.73 m², albumin: 18.5 g/L, total cholesterol: 6.86 mmol/L, urine albumin creatinine ratio: 812.7 mg/mmol). In the differential diagnosis of nephrotic syndrome, looking for a secondary cause is essential, so the parainfectious causes of nephrotic syndrome were excluded. An elevated prostate-specific antigen (10.69 ng/L) was found when screening for oncological causes, and prostate adenocarcinoma was identified on biopsy. A renal biopsy was then performed with a finding of minimal change disease. Despite the generally accepted guidelines of prostate carcinoma in that stage and age of the patient being watchful waiting, antiandrogen therapy was started with the cooperation of a urologist. There was a significant improvement in renal parameters in the patient (creatinine: 87 µmol/L, eGFR: 73 mL/min/1.73 m², albumin: 33.4 g/L, urine albumin creatinine ratio: 27.6 mg/mmol).

Conclusion: This case shows the importance of multidisciplinary cooperation in the treatment of secondary causes of nephrotic syndrome. In the case of proven paraneoplastic syndrome, it is necessary to start treating the malignancy; however, in general, a conservative approach without treatment is recommended.

Keywords: minimal change disease; nephrotic syndrome; prostate cancer.

Figure 1

Histological examination of renal biopsy. (a) Light microscopy with periodic acid-methenamine silver staining (magnification ×100): no changes in the glomerular basal membrane; (b) light microscopy with haematoxylin eosin staining (magnification ×400): no changes are observed in the glomeruli; (c) electron microscopy (magnification ×5000): extensive foot processes effacement (red arrows), no electron dense deposits or segmental sclerosis, and normal glomerular basement membrane thickness.

Figure 2

Histological examination of prostate biopsy. (a) H&E staining (magnification ×100): adenocarcinoma formed by a mixture of glands with a preserved lumen (Gleason growth pattern 3) and glands with an indistinct, minimally marked lumen (Gleason growth pattern 4). (b) H&E staining (magnification ×100): adenocarcinoma formed by the predominance of Gleason growth pattern 3 with minimal involvement of growth pattern 4: Gleason score 7 (3 + 4).

Figure 3

Clinical course before and after LHRH agonist and oral glucocorticoids administration; UACR—urine albumin/creatine ratio, LHRH—luteinising hormone-releasing hormone, CSs—corticosteroids.

Figure 4

The development of a prostate-specific antigen after LHRH agonist administrations; PSA—prostate-specific antigens, LHRH—luteinising hormone-releasing hormone.