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Proliferative “crescentic” glomerulonephritis in a burned patient
Burns 29 (2003) 381–384
Case report
Proliferative “crescentic” glomerulonephritis in a burned patient Mustafa Deveci a,∗ , Mehmet Bozkurt a , Önder Öngürü b , Mustafa Sengezer a a
Department of Plastic and Reconstructive Surgery and Burn Centre, Gülhane Military Medical Academy, 06018 Etlik, Ankara, Turkey b Department of Pathology, Gülhane Military Medical Academy, Ankara, Turkey Accepted 2 December 2002
Abstract Acute renal failure is one of the major complications of burn and it is accompanied by a high mortality rate. However, acute glomerulonephritis due to major burn have not been reported in burn literature. We report a case of crescentic glomerulonephritis which began at 27 days postburn. In this case glomerulonephritis may be due to infection probably pseudomonas or enterococus sepsis. We also felt that imipenem may be contributed the formation of glomerulonephritis. © 2003 Elsevier Science Ltd and ISBI. All rights reserved.
1. Introduction
2. Case report
Extensive cutaneous burn produces local changes which may cause general effects involving each system of the body [1]. Changes in blood volume, fluid exchanges and drug interactions may result in renal damage [1–3]. Usually acute renal failure is one of the major complications of burn and it is accompanied by a high mortality rate. The incidence of acute renal failure (ARF) in severely burned patients ranges from 1.3 to 38% and this complication has always been associated with high mortality rate, which is between 73 and 100% [2].The pathophysiologic mechanism may be related to filtration failure or tubular dysfunction. However, acute glomerulonephritis due to major burn have not been reported in burn literature. Necrotizing (crescentic) glomerulonephritis is a histological type that has been recognised for over 50 years [4]. It is associated with many clinical conditions such as polyarteritis nodosa, infective endocarditis, Wegener’s granulomatosis, idiopathic pulmonary hemorrhage (Goodpasture syndrome), the Churg–Strauss syndrome and relapsing polychondritis. It has been regarded as a severe progressive form of renal disease with an extremely poor prognosis [4]. Herein, we report a case of crescentic glomerulonephritis which began at 27 days postburn and the possible mechanisms are also discussed.
A 22-year-old man who was injured by flame burn was admitted to our burn centre. Physical examination revealed full-thickness burn injury involving 46% of TBSA and 32% was full thickness burn. On admission central catheter was inserted via femoral vein (the groin not being burned). A foley catheter was inserted, and urine output was maintained at >75 ml/h. He sustained full-thickness burn to anterior part of neck, anterior chest, both forearms and to both legs. From admission, he remained haemodynamically stable and he did not have any renal problems. Excision was delayed because the patients general condition was poor and admitted at 5 day postburn. Prior surgery second generation sefalosporin was stared. After the patients general condition had been improved excision and auto-homografting was performed to 32% full thickness burn surface at 7 days postburn. He was normotensive and did not have any urinary abnormalities. At 12 days postburn, the patient developed fever 39.5 ◦ C. Swab culture, blood, urine cultures were taken. Central line was withdrawn and the tip catheter was sent to microbiology laboratory for analysis. Blood culture revealed staphylococcus (coagulase negative) and was sensitive to ciprofloksasin and amikacin hence they were started. The patient responded and within 3 days his temperature returned to a baseline level of 37.2 ◦ C. Amikacin and ciprofloksasin were ceased at 19 days postburn and blood samples sent to microbiology laboratory for analysis and blood culture was negative. At 21 days postburn the patient’s general condition deteriorated and developed high spiking fever of 38.7 ◦ C with the increase in his neutrophilic leucocytosis. Swab, blood
∗ Corresponding author. Tel.: +90-312-304-5401; fax: +90-312-304-5412. E-mail address: [email protected] (M. Deveci).
0305-4179/03/$30.00 © 2003 Elsevier Science Ltd and ISBI. All rights reserved. doi:10.1016/S0305-4179(03)00012-3
382
M. Deveci et al. / Burns 29 (2003) 381–384
culture and urine cultures were taken again. Blood culture revealed pseudomonas suppurativa and methicilline resistant staphyloccus aureus. Microbiology results revealed Staphylococcus was sensitive to vancomycin and pseudomonas to imipenem so they were stared. The patient responded well to the treatment but at the 27 days postburn there was a deterioration in renal function (Table 1) and antibiotherapy was ceases. Hematuria, proteinuria, and rapidly decreasing renal function, without hypertension presenting acute nephritic syndrome was observed. Blood samples were taken and send for microbiology laboratory at 27 days postburn which were negative. As the renal function abnormalities persisted a week, a renal percutaneous biopsy was performed which revealed a
Table 1 Evolution of renal failure with serum creatinine, urinary protein
severe crescentic glomerulonephritis with the crescents involving 60% of the glomeruli (Fig. 1). A mild focal infiltrate of lymphocytes, histiocytes and eosinophils were also present in interstitum (Fig. 2). The infiltrate was closely centred on the tubular basement membranes which were disrupted in many areas with degenerative changes in the overlying tubular epithelial cells. No vasculitis were evident. By immunofluorescence IgG, IgM, IgA, fibrinogen and complement were not present within the glomeruli. As glomerulonephritis was diagnosed antibiotherapy was not stared. The progression of the nephritic syndrome was quite rapid. The patient required dialysis within 2 weeks and renal deterioration returned to normal after 6 weeks.
M. Deveci et al. / Burns 29 (2003) 381–384
383
Fig. 1. Four glomeruli showing crescent formation.
Fig. 2. High power view of the glomerulus. Crescent (thin arrow) formed by proliferation of parietal cells obliterates Bowman space and compresses the glomerular tuft (thick arrow).
3. Discussion Firstly, the classic description of ‘crescentic glomerulonephritis’ appeared in the literature. It was referred to as extracapillary proliferation. Later, the term ‘rapidly progressive glomerulonephritis type I for patients with nephritis who developed renal failure within weeks or months was introduced. At present, crescentic nephritis is categorised us-
ing a variety of clinical, morphological, immunohistological, and serological criteria. Three broad groups of cresenteric nephritis can be distinguished [4,5]: 1. Anti GBM (glomerular basement membrane) disease. 2. Renal microscopic vasculitis characterised by scanty deposits of immunoglobin and circulating antineutrophil cytoplasmic antibodies (ANCA).
384
M. Deveci et al. / Burns 29 (2003) 381–384
3. Heterogenous group in which crescent formation complicates an identifiable form of nephritis, usually proliferative in type. In group 3, most of the patients fall into one of the following three subgroups: (a) Those with infection. (b) Those with systemic immune complex. (c) Those with pre-existing nephritis [5]. Our patient may be placed in the first or third subgroup. Cresenteric nephritis have been reported during the course of a number of viral and bacterial infections. These include Rose river virus, hepatitis B, legionella, mycoplasma, syphilis and leprosy [5–8]. Cresenteric nephritis has also been attributed to rifampicin during treatment for tuberculosis and to tuberculosis itself [9,10]. However, crescentic glomerulonephritis have not been reported in burn literature. Many drugs may cause nephrotoxicity. In the presented case vancomycin, ciprofloksasin, amikacin and imipenem were administered. The drugs most commonly implicated in causing or exacerbating acute renal failure are the aminoglycoside antibiotics and one of these aminoglycoside is amikacin. In a review of 144 studies of aminoglycoside nephrotoxicity, it was reported that 9.4% of the courses of the treatment with amikacin were associated with nephrotoxicity. In those that developed nephrotoxicity, typical clinical picture is relatively mild with tubular proteinuria and impairment of urinary concentrating ability of urinary concentrating ability and damage involves the proksimal tubular brush border [4]. It may be considered that in the presented case amikasin did not cause nephrotoxicity. Since amikacin and ciprofloksasin were ceased at 19 day postburn. Imipenem is a carbapenem and is a new broad-spectrum antibiotic. It is combined with cilastatin to confer protection against renal toxicity. The nephrotoxic beta-lactam antibiotic imipenem causes acute proximal tubular necrosis and significant renal toxicity. Mechanisms of injury include: (1) transport into the tubular cell, mainly through the antilu-
minal organic anion secretory carrier; (2) acylation of target proteins, causing respiratory toxicity by inactivation of mitochondrial anionic substrate carriers; and (3) lipid peroxidation. Imipenem probably cause nephrotoxicity in the presented case. In conclusion, we have presented a case of crescentic glomerulonephritis in a burned patient developed at 27 days postburn. In this case glomerulonephritis may be due to infection probably pseudomonas or enterococus sepsis. To our best knowledge, there is no report which presents a patient with crescentic glomerulonephritis due major cutaneous burn in the literature. We also felt that imipenem may have contributed the formation of glomerulonephritis.
References [1] Sevitt S. Renalh function after burning. J Clin Path 1965;18:572–8. [2] Schiavon M, Landro D, Baldo M, DeSilvestro G, Chiarelli A. A study of renal damage in seriously burned patients. Burns 1988;14(2):107– 14. [3] Eklund J. Studies on renal function in burns. Acta Chir Scand 1970;136:735–40. [4] Furlong TJ, Ibels LS, Eckstein RP. The clinical spectrum of nectrotizing glomerulonephritis. Medicine 1987;66(3):192–201. [5] Davison AM, Cameron JS, Granfeld JP, Kerr DNS, Ritz E, Winearls CG. Textbook of clinical nephrology, vol. 1–3. 2nd ed. Oxford, 1998. [6] Lai FM, Li PK, Suen MW, Lui SF, Lai KM. Cresentic glomerulenephritis related to related to hepatitis B virus. Mod Pathol 1992;5(3):262–7. [7] Wegmüller E, Hess T, Reubi FC. Rapidly progressive glomerulonephritis accompanying legionnaires disease. Arch Intern Med 1985;145:1711–3. [8] Davies DJ, Warwick G, Boulton-Jones M, Mclay A, Jackson B, Stevenson RD. Rapidly progressive glomerulonephritis and nephrotic syndrome associated with myocoplasma pneumonia pneumonia. Nephrol Dialysis Transplant 1991;6:518–20. [9] Hirsch DJ, Bia FJ, Kasharigan M, Bia MJ. Rapidly progressive glomerulonephiritis during antituberculous therapy. Am J Nephrol 1983;3:7–10. [10] Murray AN, Cassidy MJD, Templecamp C. Rapidly progressive glomerulonephritis associated with rifampicin therapy for pulmonary tuberculosis. Nephron 1987;46:373–6.
Case report
Proliferative “crescentic” glomerulonephritis in a burned patient Mustafa Deveci a,∗ , Mehmet Bozkurt a , Önder Öngürü b , Mustafa Sengezer a a
Department of Plastic and Reconstructive Surgery and Burn Centre, Gülhane Military Medical Academy, 06018 Etlik, Ankara, Turkey b Department of Pathology, Gülhane Military Medical Academy, Ankara, Turkey Accepted 2 December 2002
Abstract Acute renal failure is one of the major complications of burn and it is accompanied by a high mortality rate. However, acute glomerulonephritis due to major burn have not been reported in burn literature. We report a case of crescentic glomerulonephritis which began at 27 days postburn. In this case glomerulonephritis may be due to infection probably pseudomonas or enterococus sepsis. We also felt that imipenem may be contributed the formation of glomerulonephritis. © 2003 Elsevier Science Ltd and ISBI. All rights reserved.
1. Introduction
2. Case report
Extensive cutaneous burn produces local changes which may cause general effects involving each system of the body [1]. Changes in blood volume, fluid exchanges and drug interactions may result in renal damage [1–3]. Usually acute renal failure is one of the major complications of burn and it is accompanied by a high mortality rate. The incidence of acute renal failure (ARF) in severely burned patients ranges from 1.3 to 38% and this complication has always been associated with high mortality rate, which is between 73 and 100% [2].The pathophysiologic mechanism may be related to filtration failure or tubular dysfunction. However, acute glomerulonephritis due to major burn have not been reported in burn literature. Necrotizing (crescentic) glomerulonephritis is a histological type that has been recognised for over 50 years [4]. It is associated with many clinical conditions such as polyarteritis nodosa, infective endocarditis, Wegener’s granulomatosis, idiopathic pulmonary hemorrhage (Goodpasture syndrome), the Churg–Strauss syndrome and relapsing polychondritis. It has been regarded as a severe progressive form of renal disease with an extremely poor prognosis [4]. Herein, we report a case of crescentic glomerulonephritis which began at 27 days postburn and the possible mechanisms are also discussed.
A 22-year-old man who was injured by flame burn was admitted to our burn centre. Physical examination revealed full-thickness burn injury involving 46% of TBSA and 32% was full thickness burn. On admission central catheter was inserted via femoral vein (the groin not being burned). A foley catheter was inserted, and urine output was maintained at >75 ml/h. He sustained full-thickness burn to anterior part of neck, anterior chest, both forearms and to both legs. From admission, he remained haemodynamically stable and he did not have any renal problems. Excision was delayed because the patients general condition was poor and admitted at 5 day postburn. Prior surgery second generation sefalosporin was stared. After the patients general condition had been improved excision and auto-homografting was performed to 32% full thickness burn surface at 7 days postburn. He was normotensive and did not have any urinary abnormalities. At 12 days postburn, the patient developed fever 39.5 ◦ C. Swab culture, blood, urine cultures were taken. Central line was withdrawn and the tip catheter was sent to microbiology laboratory for analysis. Blood culture revealed staphylococcus (coagulase negative) and was sensitive to ciprofloksasin and amikacin hence they were started. The patient responded and within 3 days his temperature returned to a baseline level of 37.2 ◦ C. Amikacin and ciprofloksasin were ceased at 19 days postburn and blood samples sent to microbiology laboratory for analysis and blood culture was negative. At 21 days postburn the patient’s general condition deteriorated and developed high spiking fever of 38.7 ◦ C with the increase in his neutrophilic leucocytosis. Swab, blood
∗ Corresponding author. Tel.: +90-312-304-5401; fax: +90-312-304-5412. E-mail address: [email protected] (M. Deveci).
0305-4179/03/$30.00 © 2003 Elsevier Science Ltd and ISBI. All rights reserved. doi:10.1016/S0305-4179(03)00012-3
382
M. Deveci et al. / Burns 29 (2003) 381–384
culture and urine cultures were taken again. Blood culture revealed pseudomonas suppurativa and methicilline resistant staphyloccus aureus. Microbiology results revealed Staphylococcus was sensitive to vancomycin and pseudomonas to imipenem so they were stared. The patient responded well to the treatment but at the 27 days postburn there was a deterioration in renal function (Table 1) and antibiotherapy was ceases. Hematuria, proteinuria, and rapidly decreasing renal function, without hypertension presenting acute nephritic syndrome was observed. Blood samples were taken and send for microbiology laboratory at 27 days postburn which were negative. As the renal function abnormalities persisted a week, a renal percutaneous biopsy was performed which revealed a
Table 1 Evolution of renal failure with serum creatinine, urinary protein
severe crescentic glomerulonephritis with the crescents involving 60% of the glomeruli (Fig. 1). A mild focal infiltrate of lymphocytes, histiocytes and eosinophils were also present in interstitum (Fig. 2). The infiltrate was closely centred on the tubular basement membranes which were disrupted in many areas with degenerative changes in the overlying tubular epithelial cells. No vasculitis were evident. By immunofluorescence IgG, IgM, IgA, fibrinogen and complement were not present within the glomeruli. As glomerulonephritis was diagnosed antibiotherapy was not stared. The progression of the nephritic syndrome was quite rapid. The patient required dialysis within 2 weeks and renal deterioration returned to normal after 6 weeks.
M. Deveci et al. / Burns 29 (2003) 381–384
383
Fig. 1. Four glomeruli showing crescent formation.
Fig. 2. High power view of the glomerulus. Crescent (thin arrow) formed by proliferation of parietal cells obliterates Bowman space and compresses the glomerular tuft (thick arrow).
3. Discussion Firstly, the classic description of ‘crescentic glomerulonephritis’ appeared in the literature. It was referred to as extracapillary proliferation. Later, the term ‘rapidly progressive glomerulonephritis type I for patients with nephritis who developed renal failure within weeks or months was introduced. At present, crescentic nephritis is categorised us-
ing a variety of clinical, morphological, immunohistological, and serological criteria. Three broad groups of cresenteric nephritis can be distinguished [4,5]: 1. Anti GBM (glomerular basement membrane) disease. 2. Renal microscopic vasculitis characterised by scanty deposits of immunoglobin and circulating antineutrophil cytoplasmic antibodies (ANCA).
384
M. Deveci et al. / Burns 29 (2003) 381–384
3. Heterogenous group in which crescent formation complicates an identifiable form of nephritis, usually proliferative in type. In group 3, most of the patients fall into one of the following three subgroups: (a) Those with infection. (b) Those with systemic immune complex. (c) Those with pre-existing nephritis [5]. Our patient may be placed in the first or third subgroup. Cresenteric nephritis have been reported during the course of a number of viral and bacterial infections. These include Rose river virus, hepatitis B, legionella, mycoplasma, syphilis and leprosy [5–8]. Cresenteric nephritis has also been attributed to rifampicin during treatment for tuberculosis and to tuberculosis itself [9,10]. However, crescentic glomerulonephritis have not been reported in burn literature. Many drugs may cause nephrotoxicity. In the presented case vancomycin, ciprofloksasin, amikacin and imipenem were administered. The drugs most commonly implicated in causing or exacerbating acute renal failure are the aminoglycoside antibiotics and one of these aminoglycoside is amikacin. In a review of 144 studies of aminoglycoside nephrotoxicity, it was reported that 9.4% of the courses of the treatment with amikacin were associated with nephrotoxicity. In those that developed nephrotoxicity, typical clinical picture is relatively mild with tubular proteinuria and impairment of urinary concentrating ability of urinary concentrating ability and damage involves the proksimal tubular brush border [4]. It may be considered that in the presented case amikasin did not cause nephrotoxicity. Since amikacin and ciprofloksasin were ceased at 19 day postburn. Imipenem is a carbapenem and is a new broad-spectrum antibiotic. It is combined with cilastatin to confer protection against renal toxicity. The nephrotoxic beta-lactam antibiotic imipenem causes acute proximal tubular necrosis and significant renal toxicity. Mechanisms of injury include: (1) transport into the tubular cell, mainly through the antilu-
minal organic anion secretory carrier; (2) acylation of target proteins, causing respiratory toxicity by inactivation of mitochondrial anionic substrate carriers; and (3) lipid peroxidation. Imipenem probably cause nephrotoxicity in the presented case. In conclusion, we have presented a case of crescentic glomerulonephritis in a burned patient developed at 27 days postburn. In this case glomerulonephritis may be due to infection probably pseudomonas or enterococus sepsis. To our best knowledge, there is no report which presents a patient with crescentic glomerulonephritis due major cutaneous burn in the literature. We also felt that imipenem may have contributed the formation of glomerulonephritis.
References [1] Sevitt S. Renalh function after burning. J Clin Path 1965;18:572–8. [2] Schiavon M, Landro D, Baldo M, DeSilvestro G, Chiarelli A. A study of renal damage in seriously burned patients. Burns 1988;14(2):107– 14. [3] Eklund J. Studies on renal function in burns. Acta Chir Scand 1970;136:735–40. [4] Furlong TJ, Ibels LS, Eckstein RP. The clinical spectrum of nectrotizing glomerulonephritis. Medicine 1987;66(3):192–201. [5] Davison AM, Cameron JS, Granfeld JP, Kerr DNS, Ritz E, Winearls CG. Textbook of clinical nephrology, vol. 1–3. 2nd ed. Oxford, 1998. [6] Lai FM, Li PK, Suen MW, Lui SF, Lai KM. Cresentic glomerulenephritis related to related to hepatitis B virus. Mod Pathol 1992;5(3):262–7. [7] Wegmüller E, Hess T, Reubi FC. Rapidly progressive glomerulonephritis accompanying legionnaires disease. Arch Intern Med 1985;145:1711–3. [8] Davies DJ, Warwick G, Boulton-Jones M, Mclay A, Jackson B, Stevenson RD. Rapidly progressive glomerulonephritis and nephrotic syndrome associated with myocoplasma pneumonia pneumonia. Nephrol Dialysis Transplant 1991;6:518–20. [9] Hirsch DJ, Bia FJ, Kasharigan M, Bia MJ. Rapidly progressive glomerulonephiritis during antituberculous therapy. Am J Nephrol 1983;3:7–10. [10] Murray AN, Cassidy MJD, Templecamp C. Rapidly progressive glomerulonephritis associated with rifampicin therapy for pulmonary tuberculosis. Nephron 1987;46:373–6.