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Vol. 28. Issue. 1.February 2008
Pages 1-121
Vol. 28. Issue. 1.February 2008
Pages 1-121
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Acute post-estreptoccocal glomerulonephritis in the elderly
Glomerulonefritis aguda post-estreptocócica en paciente añoso
Rosa Pérez Moralesa, J.. Pérez Martíneza, F.. Llamas Fuentesa, E.. Andrés Mompeana
a Servicio de Nefrología, Complejo Hospitalario Universitario de Albacete, Albacete, Albacete, España,
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To the editor:

Post-streptococcal glomerulonephritis (PSGN) is the prototype of acute glomerulonephritis. It is heralded by a group A b-hemolytic streptococcus infection.1,8 The evolution is benign in children, and poorer with older age2 and in case of renal acute failure.5 Approximately in 95% of the cases renal function is recovers in within 3-4 weeks. The evolution in the elderly is less predictable.1,4,5 Irreversible renal failure occurs in less than 1% of children and in a higher percentage of adults.6,7,9 The treatment consists of antihypertensive drugs, diuretics and antibiotics, and sometimes hemodialysis may be required.1,3,8 Immunosuppressive therapy is indicated in case of glomerulonephritis with crescent formation.5 Steroids appear to be efficacious in adults with PSGN and nephrotic syndrome.3

We present a 78 years old male who was admitted because of cardiac failure of 48 hours and oligo-anuria, together with renal function worsening in the last week. The blood analysis revealed Cr 4.2 mg/dL (former Cr was 1.4 mg/dL), microhematuria and proteinuria of 500 mg/dL. Two weeks ago he had acute pharingotonsillitis and gout, and treatment with NSAIDS and colchicine was prescribed. He had a history of high blood pressure, coronary heart disease and prostatic hyperplasia. On physical exam he was eupneic, had no fever and appeared in good health status. Blood pressure was high, basal crackles were heard in lungs and pitting edemas were evident in both legs. Laboratory findings disclosed glomerular filtration worsening, hyperuricemia, hypoalbuminemia, and mild anemia and leukocytosis. ESR, rheumatoid factor and ASLO values were elevated. The level of C3 was decreased and other immunological parameters were normal. Lipid levels and proteinogram were normal. The Bence Jones selective proteinuria was negative as well as the urine culture. Abdominal ultrasound showed normal looking kidneys, and the echocardiography was also unremarkable. The X-ray film showed pulmonary vascular redistribution. The analysis of pharyngeal exudate disclosed beta-hemolytic Streptococcus.

We initiated treatment with furosemide and antihypertensive drugs and negative balances were achieved. ACE inhibitors and NSAIDS were discontinued. The clinical evolution was favorable, blood pressure was controlled, but renal function did not change. When we received the results of the immunological study we suspect a diagnosis of PSGN and initiated treatment with oral amoxycillina clavulanate for 2 weeks. Renal function further worsened and a renal biopsy was performed on the 20th day of in-hospital stay.

The pathological study revealed diffuse proliferative mesangial and capillary glomerulonephritis (11% glomerular sclerosis, 22% epithelial crescents, diffuse increase of mesangial and endothelial cellularity, and chronic inflammatory infiltrate in the interstitium. Immunofluorescence showed basal membrane and mesangial granular depositions of C3, IgG, IgA, C4, C1q. (fig. 1)

Prednisone (1 mg/kg/day) was initiated, penicillin G sodium was intravenously administered during fourteen days and hemodialysis was required. When the patient was discharged he had lost 6 kg of weight, pharyngeal swab exam was negative, C3 fraction had increased and renal function had improved (Cr 3.1 mg/dL). Steroid treatment was maintained for 17 months and the blood pressure was controlled with 4 drugs. The complement value was normal after two months and the ASLO levels were normal after 6 months. The patient has currently normal blood pressure, good health status and his renal function is stable (Cr. 1.8 mg/dL).

There are few reported cases of PSGN in the elderly, perhaps because the incidence of the disease is very low in this age. For this reason the evolution is not uniformly described, although it is generally accepted that renal biopsy should be performed early, as the clinical picture can be mistaken with other conditions and also because the outcome can be poor. It is indicated to initiate immunosuppressive therapy either with prednisone or with other agents. The decision of the agent and the duration of the therapy should be individualized.

Rodríguez-Iturbe, B. Glomerulonefritis endocapilar aguda. En: Hernando L, Aljama P, Arias M (Ed): Nefrología Clínica 2.ª Edición. Editorial Médica Panamericana. pp. 308-314, Madrid-España, 2004.
Lavjay Butani. Prolonged hypocomplementaemia after post-streptococcal glomerulonephritis. Nephrol Dial Transplant 16: 869, 2001. [Pubmed]
Raff A, Hebert T, Pullman J, Coco M. Crescentic post. streptococcal glomerulonephritis with nephritic syndrome in the adult: is aggressive therapy warranted? Clin Nephrol May; 63 (5): 375-80, 2005.
Hsu YH, Yang AH, Chen TW, Huang TP. Focal segmental glomerulosclerosis after poststreptococcal glomerulonephritis in the elderly: a case report. Zhonghua Yi Xue Za Zhi (Taipei) May; 61 (5): 301-5, 1998.
Vijayakumar M. Acute and crescentic glomerulonephritis. Indian J Pediatr Dec; 69 (12): 1071-5, 2002.
Baldwing DS. Poststreptococcal glomerulonephritis. Am J Med 1077; 62: 1 [Pubmed]
Pinto SW, Sesso R, Vasoncelos E y cols. Follow-up of patients with epidemic poststreptococcal glomerulonephritis. Am J Kidney Dis 38: 249, 2001. [Pubmed]
Couser WG. Glomerulonephritis. The Lancet May (9163): 509-515, 1999.
Melby PC, Musick WD, Luger AM, Khanna R. Poststreptococcal glomerulonephritis in the elderly. Report of a case and review of the literature. Am J Nephrol 7 (3): 235-40, 1987.
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