Brouwer, R.L.M.

Gerding, M.N.

Groen, J. (Jan)

Jordans, J.G.M.

Osterhaus, A.D.M.E. (Albert)

Gerding, MN

Groen, J

Brouwer, RLM

Jordans, JGM

Osterhaus, Ab

EUR Research Repository

Correspondence Acute Renal Failure due to Leptospirosis grippotyphosa Introduction In a minority of previously healthy patients presenting with acute renal failure, infectious agents are responsible for renal deterio- ration. Isolation of microorganisms is often unsuccessful and therefore a nosological diagnosis difficult. We describe two pa- tients with reversible acute renal failure, which by serological methods proved to be due to infection with Leptospira grippo- typhosa. It is considered unusual for this microorganism to raise severe symptoms in humans. Case I: A 71-year-old farmer was admitted to our hospital be- cause of a high fever (39.5°C) for 3 days. The patient was in stable health until 5 days before admission, when fever developed. Two weeks before he had supervised the cleaning of ditches on his farmland. On examination he appeared moderately ill. Body temperature was 39.4-C, pulse 78 bpm and blood pressure 110/70 mmHg. No rash or lymphadenopathy was noted. He had a mild conjunctivitis and was not icteric. Examination of lungs, heart, abdomen and neurological examination was normal. Laboratory data showed renal failure (blood urea 41 mmol/1, creatinine 787 Ixmol/1). Bilirubin was normal and liver enzymes were only marginally elevated (ASAT 31 U/l, A L A T  38 U/l, nor- mal both < 30 U/l). Proteinuria of 5.6 g/1 was found. The sediment contained no cylinders or leucocytes and only a few red cells were seen. An  ultrasound examination of the abdomen was nor- mal. X-ray films of the chest were also normal. Blood and urine cultures were negative. On the first hospital day the patient be- came anuric. The anuria did not respond to intravenous infusion of 3 litres of saline 0.9%. A Swan-Ganz pulmonary artery cathe- ter was inserted and adequate left ventricular filling pressures were found. On the second hospital day haemodialysis was start- ed. At  the fourth hospital day he became polyuric (>6 1/24h) and dialysis was discontinued. During the following days renal func- tion improved. After  12 days he was discharged from the hospi- tal with serum creatinine of 159 t~mol/l. Renal function gradual- ly reverted to normal in the following weeks. Serum antibodies against L. grippotyphosa were demonstrated on the 15th day af- ter hospitalisation (IgM 1:320, IgG 1:1,280), and on day 21 after hospitalisation IgM antibodies were negative, while IgG titre amounted to 1:5,120. Leptospira antibodies were detected at the K.I.T. Reference Laboratory for Leptospirosis, Amsterdam, The Netherlands (using ELISA for IgM antibodies, combined with a micro-agglutination test for specific IgG antibodies). Serum an- tibodies against hantaviruses remained negative. Case 2: A 47-year-old gardener was admitted to our hospital be- cause of suspected pyelonephritis. He was previously in good health until 4 days before admission When abrupt high fever of 40.5°C developed. Cold chills and bilateral flank pain occurred. On examination he was ill, blood pressure 140/80 mmHg, pulse 100 bpm, temperature 39.6°C. Examination of the chest and ab- domen were normal except for renal lodge pain bilateral on pal- pation. There was no edema. Laboratory data: urea 18.5 mmol/1, creatinine 418 ixmol/t, K 4.7 mmol/1, Na 135 mmol/1, Ca 2.13 retool/l, P 1.33 mmol/1, bilirubin <17 retool/l, direct <5 mmot/1, A F  47 U/l, ASAT 14 U/l, A L A T  19 U/l, LDH 303 U/l, gammaGT • 30 U/l, CK 140 U/l, albumin 40 g/1. Urinalysis: 0-10 erythro- cytes/ixl, no leucocytes, no cell cylinders. Proteinuria: 6.9 g/24 h. X-ray of thorax and ECG and ultrasonography showed no ab- normalities. The patient recovered completely and renal rune- tion was restored, while proteinuria disappeared after 3 days. Serologic data for L. grippotyphosa antibodies: 8 days after hos- pitalization, no antibodies could be detected, after 18 days IgM titre was 1:320 and IgG titre 1:1,280. Fifty days after hospitaliza- tion IgM titre amounted to 1:80, while IgG titre rose to 1:5,120. Serum antibodies against hantaviruses remained negative. Discussion Both patients presented with acute renal failure due to L. grip- potyphosa. No signs of Well 's  syndrome were present in our pa- tients (clinical syndrome of jaundice, thrombopenia and acute renal failure after infection with leptospirae). Anicteric lepto- spirosis is considered to be mild and without concurrent mortal- ity [1], however, our two patients presented with severe acute re- nal failure. Both patients presented with symptoms and signs of acute renal failure suggestive for hantavirus infection (serotype Puumala). It has been encountered several times in our region of the country and also in Germany, in Northrhine-Westphalia, which apparently forms a continuum with the Twente area [2]. In fact, our first impression of the clinical picture was hantavirus nephropathy and therefore we did not perform renal biopsy. In L. grippotyphosa field-mice are the main reservoir and inhala- tion of aerosols, or direct contact with urine, probably causes in- fection. Diagnosis is primarily serologic; however, diagnosis can also be made by recently developed PCR assays in body secre- tions [3, 4]. Acute renal failure in leptospirosis may be oliguric or non-oliguric [5]. Acute tubular necrosis is also described, either caused by hypoxemia or as a direct toxic effect of leptospirae. In- flammatory changes in the kidney may be seen in the later stag- es, and in one patient deposition of complement components and electron dense bodies in glomeruli, suggesting immune complex glomerulonephritis, are described [6]. The mechanisms of dete- rioration of renal function and transient proteinuria have not been elucidated [7]. In this report  we present two patients with symptoms and clinical course compatible with hantavirus infec- tion, who were found to be infected by L. grippotyphosa. Zoo- logic field studies may be needed in the future to investigate ro- dent reservoirs of leptospirae and hantaviruses, as severe renal failure can occur in humans. M. N. Gerding, J. Groen, R. L. M. Brouwer, J. G. M. Jordans, A. D. M. E. Osterhaus References Kennedy, N. D., Rainford, D. J., Pusey, C. D., Higginson, A.: Lep- tospirosis and acute renal failure - clinical experiences and a review of the literature. Postgrad, Med. J. 55 (1979) 176--179. Received: 24 June 1997/Revision accepted: 15 September 1997 M. N. Gerding, M. D., R. L. M. Brouwer, M. D., J. G. M. Jordans, M. D., Medical Spectrum Twente, Dept. of Internal Medicine, P. O. Box 50000, NL-7500 KA Enschede; J. Groen, Ph. D., Center for Exotic Virus Infec- tions, Dept. of Clinical Virology, University Hospital Rotterdam: A. D. M. E. Osterhaus, Ph.D., Center for Exotic Virus Infections, Dept. of Clinical Virology, University Hospital Rotterdam and Institute of Virol- ogy, Erasmus University Rotterdam, The Netherlands. Correspondence to: M. N. Gerding, M. D., Academic Medical Center, FS-171, Meibergdreef 9, NL-1105 AZ Amsterdam, The Netherlands. Infection 25 (1997) No. 6 © MMV Medizin Verlag GmbH Mtinchen, M0nchen 1997 3 7 9 / 5 5  M. N. Gerding et al.: A Serious Zoonic Infection 2. Gerding, M. N., Groen, J., Jordans, J. G. M., Osterhaus, A. D. M. E.: Hantavirus nephropathy in the Netherlands: clinical, histopatholog- ical and epidemiological findings. Neth. J. Med. 47 (1995) 106-112. 3. Terpstra, W. J.: Serodiagnosis of bacterial diseases: problems and de- velopments. Scand. J. Immunol. 36 (1992) (Suppl. 11) 91-95. 4. M6rien, F., Amouriaux, P., Perolat, P., Baranton, G., Saint-Girons, I.: Polymerase chain reaction for detection of Leptospira spp. in clin- ical samples. J. Ctin. Microbiol. 30 (1992) 2219-2224. 5. Seguro, A. C., Lomar, A. V., Rocha, A. S.: Acute renal failure of lep- tospirosis: nonoliguric and hypokalemic forms. Nephron 55 (1990) 146-151. 6. Lai, K. N., Aarons, L, Woodroffe, A. J., Clarkson, A. R.: Renal le- sions in leptospirosis. Aust. NZ J. IVied. 12 (1982) 276279. 7. SitPrija, V., Pipatmaagul, V., Mertowidjojo, K., Boonpneknavig, V., Boonpueknavig, S.: Pathogenesis of renal disease in leptospirosis: clinical and experimental studies. Kidney Int. 17 (1980) 827-836. T. Bergan (ed.) lnfectiology, Vol. 1 Urinary Tract Infections 142 pages, 23 figures, 34 tables Karger, Basel 1997 Price: DM 134,- Urinary tract infection is one of the most frequent bacterial in- fections in humans. Knowledge of its pathogenesis and optimal modes of treatment have advanced rapidly within the recent de- cade. Books describing the latest developments in research in this field are of particular interest for physicians dealing with uri- nary tract infections. This well-structured book comprises contributions to a session held by the International Society of Chemotherapy Commission of Urinary Tract Infections presented at their 19th International Congress in Montreal. In 22 articles (an average of 6 pages each) authors from research groups from Canada, Germany, Hungary, Japan, New Zealand, the Slovak Republic, Sweden, Netherlands and the U S A  present short reviews or results in selected research fields. The topics are the treatment of uncomplicated and complicated urinary tract infections (i.e. renal transplant recipients, patients with HIV or on anticancer drugs and on glucocorticosteroid ther- apy), acute and chronic prostatitis (clinical studies, experimental work, animal models), pathogenesis of UTI  (adherence, tropism, antibacterial factors, virulence profiles of Escherichia coli). The series of articles concludes with future considerations on re- search priorities. Each section is followed by 4-48 references with the most recent dating back to 1996. The strength of the book is the large number of highly qualified articles in a very confined space, but this is its weakness as well: the authors could not go into detail. Although the title implies comprehensive information concerning urinary tract infection, many of its main clinical aspects (UTI in children and in the el- derly, diagnostic evaluation in patients with UTI, congenital anomalies of the urinary tract such as vesicorenal reflux, UTI in voiding disorders, prophylaxis, vaccination, etc.) are not dealt with. Finally, the book can be recommended for physicians who want a quick overview of some of the modern clinical aspects and re- search fields in urinary tract infection. It is the encouraging first volume of a series of books named Infectiology focussing on new and improved knowledge in this field of medicine. R. Beetz Mainz 56 / 380 Infection 25 (1997) No. 6 © MMV Medizin Verlag GmbH Mtinchen, M~nchen 1997 

English

Acute Renal Failure due to Leptospirosis grippotyphosa

Erasmus University Digital Repository

Correspondence Acute Renal Failure due to Leptospirosis grippotyphosa Introduction In a minority of previously healthy patients presenting with acute renal failure, infectious agents are responsible for renal deterio- ration. Isolation of microorganisms is often unsuccessful and therefore a nosological diagnosis difficult. We describe two pa- tients with reversible acute renal failure, which by serological methods proved to be due to infection with Leptospira grippo- typhosa. It is considered unusual for this microorganism to raise severe symptoms in humans. Case I: A 71-year-old farmer was admitted to our hospital be- cause of a high fever (39.5°C) for 3 days. The patient was in stable health until 5 days before admission, when fever developed. Two weeks before he had supervised the cleaning of ditches on his farmland. On examination he appeared moderately ill. Body temperature was 39.4-C, pulse 78 bpm and blood pressure 110/70 mmHg. No rash or lymphadenopathy was noted. He had a mild conjunctivitis and was not icteric. Examination of lungs, heart, abdomen and neurological examination was normal. Laboratory data showed renal failure (blood urea 41 mmol/1, creatinine 787 Ixmol/1). Bilirubin was normal and liver enzymes were only marginally elevated (ASAT 31 U/l, ALAT  38 U/l, nor- mal both < 30 U/l). Proteinuria of 5.6 g/1 was found. The sediment contained no cylinders or leucocytes and only a few red cells were seen. An ultrasound examination of the abdomen was nor- mal. X-ray films of the chest were also normal. Blood and urine cultures were negative. On the first hospital day the patient be- came anuric. The anuria did not respond to intravenous infusion of 3 litres of saline 0.9%. A Swan-Ganz pulmonary artery cathe- ter was inserted and adequate left ventricular filling pressures were found. On the second hospital day haemodialysis was start- ed. At the fourth hospital day he became polyuric (>6 1/24h) and dialysis was discontinued. During the following days renal func- tion improved. After 12 days he was discharged from the hospi- tal with serum creatinine of 159 t~mol/l. Renal function gradual- ly reverted to normal in the following weeks. Serum antibodies against L. grippotyphosa were demonstrated on the 15th day af- ter hospitalisation (IgM 1:320, IgG 1:1,280), and on day 21 after hospitalisation IgM antibodies were negative, while IgG titre amounted to 1:5,120. Leptospira ntibodies were detected at the K.I.T. Reference Laboratory for Leptospirosis, Amsterdam, The Netherlands (using ELISA for IgM antibodies, combined with a micro-agglutination test for specific IgG antibodies). Serum an- tibodies against hantaviruses remained negative. Case 2: A 47-year-old gardener was admitted to our hospital be- cause of suspected pyelonephritis. He was previously in good health until 4 days before admission When abrupt high fever of 40.5°C developed. Cold chills and bilateral flank pain occurred. On examination he was ill, blood pressure 140/80 mmHg, pulse 100 bpm, temperature 39.6°C. Examination of the chest and ab- domen were normal except for renal lodge pain bilateral on pal- pation. There was no edema. Laboratory data: urea 18.5 mmol/1, creatinine 418 ixmol/t, K 4.7 mmol/1, Na 135 mmol/1, Ca 2.13 retool/l, P 1.33 mmol/1, bilirubin <17 retool/l, direct <5 mmot/1, AF  47 U/l, ASAT 14 U/l, ALAT 19 U/l, LDH 303 U/l, gammaGT •30 U/l, CK 140 U/l, albumin 40 g/1. Urinalysis: 0-10 erythro- cytes/ixl, no leucocytes, no cell cylinders. Proteinuria: 6.9 g/24 h. X-ray of thorax and ECG and ultrasonography showed no ab- normalities. The patient recovered completely and renal rune- tion was restored, while proteinuria disappeared after 3 days. Serologic data for L. grippotyphosa antibodies: 8 days after hos- pitalization, no antibodies could be detected, after 18 days IgM titre was 1:320 and IgG titre 1:1,280. Fifty days after hospitaliza- tion IgM titre amounted to 1:80, while IgG titre rose to 1:5,120. Serum antibodies against hantaviruses remained negative. Discussion Both patients presented with acute renal failure due to L. grip- potyphosa. No signs of Well's syndrome were present in our pa- tients (clinical syndrome of jaundice, thrombopenia and acute renal failure after infection with leptospirae). Anicteric lepto- spirosis is considered to be mild and without concurrent mortal- ity [1], however, our two patients presented with severe acute re- nal failure. Both patients presented with symptoms and signs of acute renal failure suggestive for hantavirus infection (serotype Puumala). It has been encountered several times in our region of the country and also in Germany, in Northrhine-Westphalia, which apparently forms a continuum with the Twente area [2]. In fact, our first impression of the clinical picture was hantavirus nephropathy and therefore we did not perform renal biopsy. In L. grippotyphosa field-mice are the main reservoir and inhala- tion of aerosols, or direct contact with urine, probably causes in- fection. Diagnosis is primarily serologic; however, diagnosis can also be made by recently developed PCR assays in body secre- tions [3, 4]. Acute renal failure in leptospirosis may be oliguric or non-oliguric [5]. Acute tubular necrosis is also described, either caused by hypoxemia or as a direct oxic effect of leptospirae. In- flammatory changes in the kidney may be seen in the later stag- es, and in one patient deposition of complement components a d electron dense bodies in glomeruli, suggesting immune complex glomerulonephritis, are described [6]. The mechanisms of dete- rioration of renal function and transient proteinuria have not been elucidated [7]. In this report we present wo patients with symptoms and clinical course compatible with hantavirus infec- tion, who were found to be infected by L. grippotyphosa. Zoo- logic field studies may be needed in the future to investigate ro- dent reservoirs of leptospirae and hantaviruses, as severe renal failure can occur in humans. M. N. Gerding, J. Groen, R. L. M. Brouwer, J. G. M. Jordans, A. D. M. E. Osterhaus References Kennedy, N. D., Rainford, D. J., Pusey, C. D., Higginson, A.: Lep- tospirosis and acute renal failure - clinical experiences and a review of the literature. Postgrad, Med. J. 55 (1979) 176--179. Received: 24 June 1997/Revision accepted: 15 September 1997 M. N. Gerding, M. D., R. L. M. Brouwer, M. D., J. G. M. Jordans, M. D., Medical Spectrum Twente, Dept. of Internal Medicine, P. O. Box 50000, NL-7500 KA Enschede; J. Groen, Ph. D., Center for Exotic Virus Infec- tions, Dept. of Clinical Virology, University Hospital Rotterdam: A. D. M. E. Osterhaus, Ph.D., Center for Exotic Virus Infections, Dept. of Clinical Virology, University Hospital Rotterdam and Institute of Virol- ogy, Erasmus University Rotterdam, The Netherlands. Correspondence to:M. N. Gerding, M. D., Academic Medical Center, FS-171, Meibergdreef 9, NL-1105 AZ Amsterdam, The Netherlands. Infection 25 (1997) No. 6 © MMV Medizin Verlag GmbH Mtinchen, M0nchen 1997 379/55  M. N. Gerding et al.: A Serious Zoonic Infection 2. Gerding, M. N., Groen, J., Jordans, J. G. M., Osterhaus, A. D. M. E.: Hantavirus nephropathy in the Netherlands: clinical, histopatholog- ical and epidemiological findings. Neth. J. Med. 47 (1995) 106-112. 3. Terpstra, W. J.: Serodiagnosis of bacterial diseases: problems and de- velopments. Scand. J. Immunol. 36 (1992) (Suppl. 11) 91-95. 4. M6rien, F., Amouriaux, P., Perolat, P., Baranton, G., Saint-Girons, I.: Polymerase chain reaction for detection of Leptospira spp. in clin- ical samples. J. Ctin. Microbiol. 30 (1992) 2219-2224. 5. Seguro, A. C., Lomar, A. V., Rocha, A. S.: Acute renal failure of lep- tospirosis: nonoliguric and hypokalemic forms. Nephron 55 (1990) 146-151. 6. Lai, K. N., Aarons, L, Woodroffe, A. J., Clarkson, A. R.: Renal e- sions in leptospirosis. Aust. NZ J. IVied. 12 (1982) 276279. 7. SitPrija, V., Pipatmaagul, V., Mertowidjojo, K., Boonpneknavig, V., Boonpueknavig, S.: Pathogenesis of renal disease in leptospirosis: clinical and experimental studies. Kidney Int. 17 (1980) 827-836. T. Bergan (ed.) lnfectiology, Vol. 1 Urinary Tract Infections 142 pages, 23 figures, 34 tables Karger, Basel 1997 Price: DM 134,- Urinary tract infection is one of the most frequent bacterial in- fections in humans. Knowledge of its pathogenesis and optimal modes of treatment have advanced rapidly within the recent de- cade. Books describing the latest developments in research in this field are of particular interest for physicians dealing with uri- nary tract infections. This well-structured book comprises contributions to a session held by the International Society of Chemotherapy Commission of Urinary Tract Infections presented at their 19th International Congress in Montreal. In 22 articles (an average of 6 pages each) authors from research groups from Canada, Germany, Hungary, Japan, New Zealand, the Slovak Republic, Sweden, Netherlands and the USA present short reviews or results in selected research fields. The topics are the treatment of uncomplicated and complicated urinary tract infections (i.e. renal transplant recipients, patients with HIV or on anticancer drugs and on glucocorticosteroid ther- apy), acute and chronic prostatitis (clinical studies, experimental work, animal models), pathogenesis of UTI (adherence, tropism, antibacterial factors, virulence profiles of Escherichia coli). The series of articles concludes with future considerations on re- search priorities. Each section is followed by 4-48 references with the most recent dating back to 1996. The strength of the book is the large number of highly qualified articles in a very confined space, but this is its weakness as well: the authors could not go into detail. Although the title implies comprehensive information concerning urinary tract infection, many of its main clinical aspects (UTI in children and in the el- derly, diagnostic evaluation in patients with UTI, congenital anomalies of the urinary tract such as vesicorenal reflux, UTI in voiding disorders, prophylaxis, vaccination, etc.) are not dealt with. Finally, the book can be recommended for physicians who want a quick overview of some of the modern clinical aspects and re- search fields in urinary tract infection. It is the encouraging first volume of a series of books named Infectiology f cussing on new and improved knowledge in this field of medicine. R. Beetz Mainz 56 / 380 Infection 25 (1997) No. 6 © MMV Medizin Verlag GmbH Mtinchen, M~nchen 1997 

Acute renal failure due to Leptospirosis grippotyphosa.

Acute renal failure due to Leptospirosis grippotyphosa.

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