Recurrent Acute Glomerulonephritis

CASE REPORTS

Recurrent Acute Glomerulonephritis Denis Glotz, MD, Marie-Helene Jouvin, MD, Dominique Nochy, MD, Philippe Druet, MD, and Jean Bariety, MD • Biopsy-proven recurrent acute glomerulonephritis (AGN) Is extremely rare and is usually seen In children with acute, well-defined streptococcal infections. We present here a patient with recurrent AGN In the absence of chronic bacterial infection. The subject, an 80-year-old man, had eight episodes of acute nephritic syndrome following upper respiratory tract infection. No abnormalities were detected during remissions. Renal biopsies during two of those episodes showed typical postinfectlous acute exsudative endocaplllary glomerulonephritis, while results of another biopsy performed during remission were normal. © 1991 by the National Kidney Foundation, Inc. INDEX WORDS: Acute glomerulonephritis; acute renal failure; recurrence.

~STINFECTIOUS acute glomerulonephritis

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(AGN) is a well-defined clinical and pathological entity, most commonly seen in children and young adults, 1 and is associated with a good prognosis. Recurrence of postinfectious AGN is a rare event, only described in children in association with well-defined bacterial infections.2-4 AGN in the elderly population is infrequent5 and may be associated with a poorer outcome. 6 We report here the case of an elderly man with eight episodes of AGN, with complete histological healing between episodes. The clinical symptoms and the histopathological findings are typical of poststreptococcal AGN. To the best of our knowledge, no such recurrence in this age group has been reported. CASE REPORT

An 80-year-old man was first admitted to our renal unit in December 1985 for an acute nephritic syndrome marked by oliguria, renal failure, heavy proteinuria, and gross hematuria. A week earlier, he had cough, fever, and anorexia. Hematuria was noted on the second day, together with oliguria. According to the patient, this was the fifth episode of this kind, starting in 1980, always occurring during the winter season. Physical examination on admission showed the subject to be healthy but asthenic; arterial blood pressure was 160/100 mm Hg, edema was noted on the lower limbs , and body temperature was 37.8 °C. Laboratory data showed hyperleukocytosis (white blood cell count, 12,800/mL), elevated erythrocyte sedimentation rate (70 mm), renal failure (serum creatinine, 481 JtmollL [4.4 mg/dL]; blood urea nitrogen [BUN], 16.5 mmol/L [93

From the Service de Nephrologie et INSERM Unite 28, Hopital Broussais, Paris, France. Address reprint requests to Denis Glotz , MD, Service de Nephrologie, Hopital Broussais, 96 rue Didot, 75014 Paris, France. © 1991 by the National Kidney Foundation, Inc. 0272-6386/91/1702-0024$3.00/0 228

mg/dL]) . Urinalysis showed gross hematuria with significant proteinuria . Blood and throat swab cultures were negative. CHso was depressed «20%). Serum levels of IgG and IgM were mildly depressed (lgG, 7.3 gIL [730 mg/dL]; IgM, 0.87 giL [87 mg/dL]), but IgA level was low (0.43 gIL [43 mg/dL]) without any monoclonal component on immunoelectrophoresis. There were no circulating immune complexes, cryoglobulinemia, or autoantibodies (antinuclear antibodies [ANA], rheumatoid factor (RF), or antitissue). A first percutaneous renal biopsy was performed (serum creatinine, 395 mmollL [3.6 mg/dL]). On light microscopy, all 10 glomeruli showed diffuse, major endocapillary proliferation associated with numerous polymorphonuclear cells, without any humps . Two glomeruli had focal necrosis without crescent formation. Interstitium and vessels were normal. By immunofluorescenCe, all glomeruli showed granular deposits of C3, IgG, and C Iq in the mesangiocapillary areas without any deposition of IgA (Fig lA and B). Two weeks later, renal function was normal (serum creatinine, 85 JtIDollL [0.77 mg/dL]) and urinalysis showed mild proteinuria. Six months later, blood pressure, renal function, urinalysis, and CHso were normal. Serum IgM and IgG levels were normal, but serum IgA stayed low at 0.5 gIL (50 mg/dL). Similar episodes occurred in March 1986 and October 1987 (Fig 2). On each occasion, identical prodromes were noted, but no infectious agent could be demonstrated by blood and tissue cultures or serologic studies for Streptococcus, Staphylococcus, herpes simplex virus, hepatitis B virus, cytomegalovirus, rickettsia, chlamydia, oruithosis, psittacosis, or Epstein-Barr virus. ENT and ondotologic examinations were normal, and a scintiscanning with autologous-labeled granulocytes showed no abnormal fixation. In October 1987, serum immunoelectrophoresis showed a faint monoclonal component of the IgG, x type. In February 1988, renal function was normal, a mild proteinuria (0.3 g/d composed of 90% albumin and 10% light chains of the x isotype by immunofixation) was present without hematuria, and the patient agreed to undergo another renal biopsy in the absence of any clinical illness (serum creatinine, 96 JtmollL [0.87 mg/dL]) . By light microscopy, 12 glomeruli were seen. two of which were obsolescent, the others being normal. No deposits were seen by immunofluorescence, even using antisera specific for>. and k light chains (Fig IC and D). In June 1988, an eighth episode occurred, and a third renal biopsy was performed (serum creatinine, 650 JtmollL [5.9 mg/dL]). The histological findings were similar to

American Journal of Kidney Diseases, Vol XVII, No 2 (February). 1991: pp 228-230

RECURRENT GLOMERULONEPHRITIS

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Fig 1. First renal biopsy showing (A) an increase in endocapillary cellularity with moderate numbers of polymorphs (Masson's trichrome, original magnification x 400, and (B) granular deposits along the glomerular capillary walls (anti-C 3 , original magnification x 200); second renal biopsy showing (C) a normal glomerular aspect (Masson's trichrome, original magnification x 400) and (D) a granular staining of the arteriolar walls without staining of the glomerulus (g) (anti-C3 , original magnification x 200); (E and F) third renal biopsy essentially identical to the first one.

lonephritis. The precession of AGN by upper respiratory tract symptoms, as well as the depressed levels of IgA, strongly supports an infectious origin. However, we were unable at any time to demonstrate the presence of any bacterial or viral pathogen. Moreover, only 2 to 3 days separated the respiratory tract symptoms from the clinical onset of AGN, as often seen in IgA nephropathy. This case is reminiscent, by some aspects, of the cases of asymptomatic AGN following nonstreptococcal respiratory infection described by Smith et aJ.7 In fact, the first four episodes in our patient have not been investigated, due to the rapid resolu-

the first biopsy, showing intense exudative endocapillary proliferation in all 10 glomeruli, but without any area of necrosis (Fig IE and F) . The patient recovered uneventfully as usual. Serum immunoelectrophoresis still showed a minor monoclonal IgG-x component, with a normal level of IgG and IgM, and depressed but stable level of IgA. Mild proteinuria (0.35 g/ d) composed of albumin and x light chains is still present, without hematuria.

DISCUSSION

The renal biopsy showing complete histological healing between episodes proves that this patient presented recurrent episodes of AGN, as opposed to clinical exacerbations of chronic glomeru-

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GLOTZ ET AL

tion of the symptoms. Complement was normal between episodes, thus ruling out any complement component deficit. T-cell function, as assessed by intradermal testing with various antigens (Nultitest, Nerieux, Lyon, France), was normal. A mild, but definite decrease in IgA was present, but, to our knowledge, such a decrease has never been associated with AGN. Moreover, serologic studies showed normal responses to usual pathogens, thus ruling out an immune deficiency. An interesting possibility could be an impairment in the ability of the reticuloendothelial system to

clear up immune complexes. This could explain the transient localization of immune material within the glomerulus, as demonstrated in mice. 8 Last, a relationship between the monoclonal gammopathy and the glomerulonephritis cannot be ruled out, but seems unlikely. The appearance of such gammopathy in an 80-year-old man is not unusual, and the reported cases of glomerulonephritis with gammopathies are marked by chronic renal failure associated with heavy histological damage. 9 . 10

REFERENCES Kassirer IP, Schwartz WB: Acute glomerulonephritis. N Engl I Med 265:686-692, 1961 2. Roy S III, Wall HP, Etteldorf IN: Second attacks of acute glomerulonephritis. I Pediatr 75:758-767, 1969 3. Rosenberg HG, Donoso PL, Vial SU, et al: Clinical and morphological recovery between two episodes of acute glomerulonephritis: A light and electron microscopic study with immunofluorescence. Clin Nephrol 21:350-354, 1984 4. Velhote V, Saldanha LB, Malheiro PS, et al: Acute glomerulonephritis: Three episodes demonstrated by light and electron microscopy and immunofluorescence studies-A case report. Clin Nephrol 26:307-310, 1986 5. Lee A, Stirling G, Sharpstone P: Acute glomerulonephritis in middle-aged and elderly patients. Br 'Med 2:1361-1363, 1966

6. Nesson HR, Robbins SL: Glomerulonephritis in older age groups. Arch Intern Med 105:47-56, 1960 7. Smith MC, Cooke IH, Zimmerman DM, et al:· Asymptomatic glomerulonephritis after nonstreptococcal upper respiratory infections. Ann Intern Med 91:697-702, 1979 8. Sato M, Ideura T, Koshikawa S: Experimental IgA nephropathy in mice. Lab Invest 54:377-384, 1986 9. Avasthi PS, Erickson DG, Williams RC, et al: Benign monoclonal gammaglobulinemia and glomerulonephritis. Am I Med 62:324-329, 1977 10. Kebler R, Kithier K, McDonald FD, et al: Rapidly progressive glomerulonephritis and monoclonal gammopathy. Am I Med 78: 133-138, 1985