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Acute renal failure in a marathon runner: role of glomerular bleeding intubular injury
BRIEF OBSERVATIONS
Acute Renal Failure in a Marathon Runner: Role of Glomerular Bleeding inTubular Injury Yannick Le Meur, MD, Francois Paraf, MD, Jean Christophe Szelag, MD, Jean Claude Aldigier, MD, Claude Leroux-Robert, MD
H
ematuria is a well recognized and generally benign consequence of sports activity, especially running a marathon (1). A few cases of acute renal failure in long-distance runners have been described due to rhabdomyolysis or less frequently to hemolysis (march hemoglobinuria) (1–3). We report the case of a marathon runner who presented with gross hematuria and anuric renal failure that we considered to be due to tubular injury from glomerular bleeding, similar to that seen in IgA nephropathy (4).
CASE REPORT A 46-year-old man was admitted to the hospital with abdominal pain and distension, and anuria. He was an experienced marathon runner who had been in excellent health. He took no medications, including over-thecounter drugs. He had previously noted several episodes of gross hematuria following long runs. Two days before admission, he had run the 1996 Paris marathon. He received proper hydration throughout the race. In the middle of the race he had an episode of hematuria followed by abdominal pain and diarrhea, but was able to complete the marathon in 3 hours and 50 minutes. Upon finishing the race, his blood pressure was 140/80 mm Hg. The patient’s weight was unchanged when he weighed himself that evening. At the time of admission, the patient was afebrile, with a blood pressure of 150/80 mm Hg. There were no signs of dehydration. The abdomen was diffusely tender to palpation with diminished bowel sounds. Ultrasonography showed normal kidneys. Color doppler sonography confirmed normal flow in the renal arteries. Laboratory tests revealed a serum creatinine level of 12.1 mg/dL, urea nitrogen of 240 mg/dL, potassium of 5.1 mmol/L, calcium of 2.41 mmol/L, phosphate of 2.66 mmol/L, bicarbonate of 21.5 mmol/L, hemoglobin of 13.4 g/dL, white blood cells of 8,500/mL (80% polymorphonuclear cells), haptoglobin of 2.6 g/L (normal), serum glutamic oxaloacetic q1998 by Excerpta Medica, Inc. All rights reserved.
Figure 1. (A) Renal biopsy (Masson’s trichrome, 320x): tubular necrosis with numerous necrotic casts in the tubular lumen. (B) Renal biopsy (HES, 500x): erythrocyte casts in the tubular lumen.
transaminase of 10 IU/L, and a creatine phosphokinase (CPK) of 233 UI/L. The day following admission he passed 180 mL of dark urine, and the next day he passed 250 mL with a red blood cell count of 4 x 106/mL. A test for myoglobinuria was negative; hemoglobinuria was slightly positive for a few days. A renal biopsy was performed. The glomeruli and ves-
Figure 2. Renal biopsy (Prussian blue reaction, 400x): large deposits of hemosiderin within the cytoplasm of the tubular cells. 0002-9343/98/$19.00 251 PII S0002-9343(98)00241-1
Brief Observation
sels were normal. Lesions of acute tubular necrosis were present with numerous erythrocytes and necrotic casts in the tubular lumens (Figure 1). The Prussian blue reaction revealed large deposits of hemosiderin within the cytoplasm of the tubular cells (Figure 2). Immunofluorescence study was negative for immunoglobulin and complement. The patient required three sessions of hemodialysis before his renal function gradually improved. Complete recovery occurred in 2 months. The hematuria disappeared in 15 days. Six months later the patient was authorized to run short distances. After a 5-km race, the hematuria reappeared.
DISCUSSION
REFERENCES 1. Abarbanel J, Benet A, Lask D, Kimche D. Sports hematuria. J Urol. 1990:143:887– 890. 2. MacSearraigh M, Kallmeyer J, Schiff H. Acute renal failure in marathon runners. Nephron. 1979;24:236 –240. 3. Pollard T, Weiss I. Acute renal necrosis in patient with march hemoglobinuria. NEJM. 1970;283:15–16. 4. Fogassi GB, Imbasciati E, Moroni G, et al. Reversible acute renal failure from gross hematuria due to glomerulonephritis: not only in IgA nephropathy and not associated with intratubular obstruction. Nephrol Dial Transplant. 1995;10:624 – 629. September 1998
From the Service de Ne´phrologie et d’Anatomie-Pathologique, Hoˆpital Universitaire, Dupuytren, Limoges, France. Requests for reprints should be addressed to Y. Le Meur, Service de Ne´phrologie, Hoˆpital Dupuytren, 87042 Limoges Cedex France. Manuscript submitted November 5, 1997 and accepted in revised form May 26, 1998.
Cardiac Tamponade in Hereditary Hemorrhagic Telangiectasia Liliane Kopel, MD, Silvia G. Lage, MD
This patient presented with anuric acute renal failure shortly after running a marathon. During the race he developed gross hematuria. Rhabdomyolysis and severe hemoglobinuria were not observed. There was no evidence of a toxic cause and no sign of dehydration. A renal biopsy revealed no glomerular or vascular lesions that could account for the renal failure. A dramatic decrease in urine volume related to decreased renal blood flow is well known in marathon runners and may have contributed to this patient’s renal failure (3). Nevertheless, we believe that the principal cause of the acute renal failure was hematuria of glomerular origin caused by the prolonged and intense effort. This may have led to intraluminal obstruction. Alternatively, there may have been a toxic effect of hemoglobin on tubular cells, as has previously been described in acute renal failure due to IgA nephropathy with glomerular bleeding (4). There may be direct toxicity of heme pigments or nitric oxide inhibition that causes intrarenal vasoconstriction (5). Sports hematuria is usually considered to be a benign phenomenon of renal or bladder origin (1). In our patient the presence of erythrocyte casts in the tubular lumens and the deposits of hemosiderin within the tubular cells proved that the bleeding was of glomerular origin. We believe that glomerular bleeding may cause acute renal failure following very strenuous exercise.
252
5. Heyman SN, Brezis M. Acute renal failure in glomerular bleeding: a puzzling phenomenon. Nephrol Dial Transplant. 1995;10:591–593.
THE AMERICAN JOURNAL OF MEDICINEt
H
ereditary hemorrhagic telangiectasia, also known as Osler-Weber-Rendu disease, is an inherited autosomal dominant disorder characterized by widespread vascular malformations that may rupture spontaneously (1). Epistaxis and telangiectases of the skin and mucosal surfaces are the most frequent clinical manifestations. Involvement of the gut, lungs, and liver have been reported. We report a patient with hereditary hemorrhagic telangiectasia who developed a large pericardial effusion with cardiac tamponade, and provide data demonstrating vascular involvement of the pericardium.
CASE REPORT A 37-year-old-woman was admitted to the hospital because of progressively increasing exertional dyspnea and lower extremity edema for 15 days. Her symptoms had persisted despite treatment for presumed congestive heart failure with digoxin, diuretics and vasodilator drugs. Her medical history included cutaneous telangiectases and polycythemia that had been observed 3 months earlier with no final diagnosis. There was no family or personal history of bleeding episodes. During her hospital stay the patient had one episode of epistaxis. On physical examination, her blood pressure was 120/75 mm Hg, pulse 100 beats/min and regular, respiratory rate 26/min. Multiple telangiectases were present over the chest, upper abdominal wall and arms. She had jugular venous distension, cyanosis, and clubbing of the nails. Fine rales in both lung bases and a mitral regurgitation murmur were heard. Admission laboratory studies revealed a hemoglobin level of 13.7 g/dL and a hematocrit of 42%. Arterial blood gas levels while the patient was breathing room air were a pH of 7.45, a pCO2 of 33 mm Hg, and a pO2 of 51 mm Hg. A chest radiograph showed cardiomegaly and
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Acute Renal Failure in a Marathon Runner: Role of Glomerular Bleeding inTubular Injury Yannick Le Meur, MD, Francois Paraf, MD, Jean Christophe Szelag, MD, Jean Claude Aldigier, MD, Claude Leroux-Robert, MD
H
ematuria is a well recognized and generally benign consequence of sports activity, especially running a marathon (1). A few cases of acute renal failure in long-distance runners have been described due to rhabdomyolysis or less frequently to hemolysis (march hemoglobinuria) (1–3). We report the case of a marathon runner who presented with gross hematuria and anuric renal failure that we considered to be due to tubular injury from glomerular bleeding, similar to that seen in IgA nephropathy (4).
CASE REPORT A 46-year-old man was admitted to the hospital with abdominal pain and distension, and anuria. He was an experienced marathon runner who had been in excellent health. He took no medications, including over-thecounter drugs. He had previously noted several episodes of gross hematuria following long runs. Two days before admission, he had run the 1996 Paris marathon. He received proper hydration throughout the race. In the middle of the race he had an episode of hematuria followed by abdominal pain and diarrhea, but was able to complete the marathon in 3 hours and 50 minutes. Upon finishing the race, his blood pressure was 140/80 mm Hg. The patient’s weight was unchanged when he weighed himself that evening. At the time of admission, the patient was afebrile, with a blood pressure of 150/80 mm Hg. There were no signs of dehydration. The abdomen was diffusely tender to palpation with diminished bowel sounds. Ultrasonography showed normal kidneys. Color doppler sonography confirmed normal flow in the renal arteries. Laboratory tests revealed a serum creatinine level of 12.1 mg/dL, urea nitrogen of 240 mg/dL, potassium of 5.1 mmol/L, calcium of 2.41 mmol/L, phosphate of 2.66 mmol/L, bicarbonate of 21.5 mmol/L, hemoglobin of 13.4 g/dL, white blood cells of 8,500/mL (80% polymorphonuclear cells), haptoglobin of 2.6 g/L (normal), serum glutamic oxaloacetic q1998 by Excerpta Medica, Inc. All rights reserved.
Figure 1. (A) Renal biopsy (Masson’s trichrome, 320x): tubular necrosis with numerous necrotic casts in the tubular lumen. (B) Renal biopsy (HES, 500x): erythrocyte casts in the tubular lumen.
transaminase of 10 IU/L, and a creatine phosphokinase (CPK) of 233 UI/L. The day following admission he passed 180 mL of dark urine, and the next day he passed 250 mL with a red blood cell count of 4 x 106/mL. A test for myoglobinuria was negative; hemoglobinuria was slightly positive for a few days. A renal biopsy was performed. The glomeruli and ves-
Figure 2. Renal biopsy (Prussian blue reaction, 400x): large deposits of hemosiderin within the cytoplasm of the tubular cells. 0002-9343/98/$19.00 251 PII S0002-9343(98)00241-1
Brief Observation
sels were normal. Lesions of acute tubular necrosis were present with numerous erythrocytes and necrotic casts in the tubular lumens (Figure 1). The Prussian blue reaction revealed large deposits of hemosiderin within the cytoplasm of the tubular cells (Figure 2). Immunofluorescence study was negative for immunoglobulin and complement. The patient required three sessions of hemodialysis before his renal function gradually improved. Complete recovery occurred in 2 months. The hematuria disappeared in 15 days. Six months later the patient was authorized to run short distances. After a 5-km race, the hematuria reappeared.
DISCUSSION
REFERENCES 1. Abarbanel J, Benet A, Lask D, Kimche D. Sports hematuria. J Urol. 1990:143:887– 890. 2. MacSearraigh M, Kallmeyer J, Schiff H. Acute renal failure in marathon runners. Nephron. 1979;24:236 –240. 3. Pollard T, Weiss I. Acute renal necrosis in patient with march hemoglobinuria. NEJM. 1970;283:15–16. 4. Fogassi GB, Imbasciati E, Moroni G, et al. Reversible acute renal failure from gross hematuria due to glomerulonephritis: not only in IgA nephropathy and not associated with intratubular obstruction. Nephrol Dial Transplant. 1995;10:624 – 629. September 1998
From the Service de Ne´phrologie et d’Anatomie-Pathologique, Hoˆpital Universitaire, Dupuytren, Limoges, France. Requests for reprints should be addressed to Y. Le Meur, Service de Ne´phrologie, Hoˆpital Dupuytren, 87042 Limoges Cedex France. Manuscript submitted November 5, 1997 and accepted in revised form May 26, 1998.
Cardiac Tamponade in Hereditary Hemorrhagic Telangiectasia Liliane Kopel, MD, Silvia G. Lage, MD
This patient presented with anuric acute renal failure shortly after running a marathon. During the race he developed gross hematuria. Rhabdomyolysis and severe hemoglobinuria were not observed. There was no evidence of a toxic cause and no sign of dehydration. A renal biopsy revealed no glomerular or vascular lesions that could account for the renal failure. A dramatic decrease in urine volume related to decreased renal blood flow is well known in marathon runners and may have contributed to this patient’s renal failure (3). Nevertheless, we believe that the principal cause of the acute renal failure was hematuria of glomerular origin caused by the prolonged and intense effort. This may have led to intraluminal obstruction. Alternatively, there may have been a toxic effect of hemoglobin on tubular cells, as has previously been described in acute renal failure due to IgA nephropathy with glomerular bleeding (4). There may be direct toxicity of heme pigments or nitric oxide inhibition that causes intrarenal vasoconstriction (5). Sports hematuria is usually considered to be a benign phenomenon of renal or bladder origin (1). In our patient the presence of erythrocyte casts in the tubular lumens and the deposits of hemosiderin within the tubular cells proved that the bleeding was of glomerular origin. We believe that glomerular bleeding may cause acute renal failure following very strenuous exercise.
252
5. Heyman SN, Brezis M. Acute renal failure in glomerular bleeding: a puzzling phenomenon. Nephrol Dial Transplant. 1995;10:591–593.
THE AMERICAN JOURNAL OF MEDICINEt
H
ereditary hemorrhagic telangiectasia, also known as Osler-Weber-Rendu disease, is an inherited autosomal dominant disorder characterized by widespread vascular malformations that may rupture spontaneously (1). Epistaxis and telangiectases of the skin and mucosal surfaces are the most frequent clinical manifestations. Involvement of the gut, lungs, and liver have been reported. We report a patient with hereditary hemorrhagic telangiectasia who developed a large pericardial effusion with cardiac tamponade, and provide data demonstrating vascular involvement of the pericardium.
CASE REPORT A 37-year-old-woman was admitted to the hospital because of progressively increasing exertional dyspnea and lower extremity edema for 15 days. Her symptoms had persisted despite treatment for presumed congestive heart failure with digoxin, diuretics and vasodilator drugs. Her medical history included cutaneous telangiectases and polycythemia that had been observed 3 months earlier with no final diagnosis. There was no family or personal history of bleeding episodes. During her hospital stay the patient had one episode of epistaxis. On physical examination, her blood pressure was 120/75 mm Hg, pulse 100 beats/min and regular, respiratory rate 26/min. Multiple telangiectases were present over the chest, upper abdominal wall and arms. She had jugular venous distension, cyanosis, and clubbing of the nails. Fine rales in both lung bases and a mitral regurgitation murmur were heard. Admission laboratory studies revealed a hemoglobin level of 13.7 g/dL and a hematocrit of 42%. Arterial blood gas levels while the patient was breathing room air were a pH of 7.45, a pCO2 of 33 mm Hg, and a pO2 of 51 mm Hg. A chest radiograph showed cardiomegaly and
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