ACUTE NEPHRITIC SYNDROME AND POLYMYALGIA RHEUMATICA: COINCIDENTAL OR ASSOCIATED?

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NEPHROLOGY 2007; 12, 625

doi:10.1111/j.1440-1797.2007.00842.x

Instructive Case

ACUTE NEPHRITIC SYNDROME AND POLYMYALGIA RHEUMATICA: COINCIDENTAL OR ASSOCIATED? A 70-year-old Japanese woman was admitted because of severe general myalgia, systemic oedema and renal dysfunction. She had no medical history including urinary abnormalities and renal dysfunction. Three weeks previous to admission, she had noticed general myalgia and minimal fever; her symptoms had worsened, and ultimately she could not move because of severe systemic myalgia. One week later therefore she was admitted to a local hospital, and laboratory examination revealed marked inflammatory signs without any renal dysfunction or urinary abnormalities. During hospitalization, however, renal dysfunction, urinary abnormalities and systemic oedema had suddenly developed; thus, she was referred to our hospital. She had not reported pharyngitis, skin infections or diarrhoea during this episode. On admission, urinalysis showed proteinuria (2.4 g/ day) and haematuria with active nephritic sediments. Full blood count revealed mild anaemia with normal peripheral blood smear and coagulation screen. She showed mild hypoproteinaemia, normal liver biochemistry including creatine kinase, and progressive renal dysfunction (blood urea nitrogen, 33.2 mmol/L; creatinine, 343.9 mmol/L) with marked inflammatory signs and hypocomplementaemia (C3, 0.39 g/L and C4, 0.08 g/L). Further laboratory tests (i.e. blood/urine cultures, antistreptolysin O, hepatitis B/C antigen/antibodies, parvovirus B 19 IgM antibodies, rheumatoid factor, antinuclear antibodies, antidouble-strandedDNA antibodies, cryoglobulin, antineutrophil cytoplasmic antibodies, and antibasement membrane antibodies) showed negative/normal results. As oliguria developed, we initiated intermittent haemodialysis on day 3. Further, the patient complained of marked systemic myalgia; thus, we also initiated prednisolone at 20 mg/day. These treatments dramatically improved her oliguria, severe myalgia, renal dysfunction and inflammatory signs; thus, haemodialysis could be stopped on day 7. On day 12, percutaneous renal biopsy was carried out. On light microscopic examination, all glomeruli showed diffuse mesangial and endocapillary proliferation without segmental tuft necrosis, fibrous/cellular crescents or global duplication of the capillary loops. Glomerular endocapillary proliferation consisted of an infiltration of polymorphonuclear cells and mononuclear cells. Immunofluorescence microscopic examination showed diffuse granular deposition of C4, but no deposition of IgG, IgA, IgM, C3 or C1q in the glomeruli. The dose of corticosteroids was tapered to prednisolone at 5 mg/day on day 20; however, myalgia, gross

© 2007 The Authors Journal compilation © 2007 Asian Pacific Society of Nephrology

haematuria, oliguria and inflammatory signs reappeared; thus, the dose of prednisolone was increased to 15 mg/day. This increased dose rapidly improved her manifestations, indicating that her clinical and renal manifestations were sensitive to the low-dose corticosteroids. One month after admission, her clinical and laboratory abnormalities were completely improved with prednisolone at 15 mg/day. Two years later, her clinical manifestations were absent without corticosteroid therapy. Our patient showed acute nephritic syndrome, endocapillary proliferative glomerulonephritis and hypocomplementaemia, suggesting that she might have acute post-infectious glomerulonephritis; however, no clinical and laboratory evidence of preceding infections could be found.1 Our patient’s myalgia was typical for polymyalgia rheumatica and her myalgia and renal manifestations were sensitive to the lowdose corticosteroids; thus, polymyalgia might be closely linked with acute nephritic syndrome in our case. As systemic small-vessel vasculitis can cause polymyalgia rheumatica-like symptoms,2 systemic small-vessel vasculitis may have caused her manifestations; however, no pathological evidence of vasculitis was found in her renal biopsy. There is another possibility that unidentified viral infections may have caused her clinical symptoms. Therefore, the question remains whether polymyalgia rheumatica was a real association, a simple coincidence or a precipitating factor of our patient’s acute nephritic syndrome. TOSHIRO SUGIMOTO,1 YUKI TANAKA,1 KEIZO KANASAKI,1 KEIJI ISSHIKI,2 UZU TAKASHI,1 DAISUKE KOYA3 and ATSUNORI KASHIWAGI1 1 Department of Internal Medicine and 2Hemodialysis Unit, Shiga University of Medical Science, Otsu, Shiga, and 3 Division of Endocrinology and Metabolism, Kanazawa Medical University, Ishikawa, Japan Accepted for publication 25 June 2007.

REFERENCES 1. Nadasdy T, Silvia FG. Acute postinfectious glomerulonephritis and glomerulonephritis caused by persistent bacterial infection. In: Jennette JC, Olson JL, Schwartz MM, Silva FG (eds). Heptinstall’s Pathology of the Kidney, 6th edn. Philadelphia, PA: LippincottWilliam & Wilkins, 2007; 322–96. 2. Little MA, Nazar L, Farrington K. Polymyalgia rheumatica preceding small-vessel vasculitis: Changed spots or misdiagnosis? Q. J. Med. 2004; 97: 289–92.

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