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Original

DIARRHEA ASSOCIATED ACUTE RENAL FAILURE IN A PATIENT WITH SALMONELLA ENTERITIDIS SEPSIS

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Pages 535-538 | Published online: 07 Jul 2009

Abstract

Salmonella enteritidis infection occurs primarily in animals and often results in self-limited gastroenteritis in accidental cross contamination in human. However, the acute renal failure could be a rare but serious complication of the S. enteritidis infection. We report one case of acute renal failure from severe dehydration caused by S. enteritidis food poisoning. The acute renal failure completely recovered after hydration and antibiotic treatment.

INTRODUCTION

Salmonella enteritidis food poisoning has become a worldwide epidemiological phenomenon. In many countries, it is the number one cause of food-borne illness.Citation[[1]], Citation[[2]] The spectrum of clinical illness ranges from acute gastroenteritis to death. Acute renal failure was a rare but fatal complication of S. enteritidis infection.Citation[[3]] There were only one case report in Asia and few case reports in Western countries about this rare complication.Citation[[4]], Citation[[5]] The causes of acute renal failure are often associated with rhabdomyolysis and severe dehydration.Citation[[6]], Citation[[7]] However, we report a female of acute renal failure from severe dehydration without clinical presentation of rhabdomyolysis caused by S. enteritidis food poisoning. The cause of renal failure was prerenal azotemia induced by severe diarrhea. Her acute renal failure completely recovered after treatment with antibiotics and supportive care. To our knowledge, no such case has been previously reported.

CASE REPORT

A 69-year-old woman was presented with a 3 days watery yellowish odorous diarrhea and low abdominal pain. She also had mild fever (37–38°C) anorexia, nausea and vomiting during these days. The frequency of watery diarrhea was more than ten times a day and resulted in severe dehydration and body weight loss about 10 kg. She also had progressive decreased urine amount in these days. She had a history of mild hypertension without medical treatment before and she did not have renal disease history previously. Her family history was unremarkable.

Physical examination revealed a distressed woman with severe dehydration and general weakness. Her body temperature was 36.5°C, pulse rate was 116 b.p.m, and blood pressure was 87/73 mmHg. She had low abdominal cramping pain and tenderness without rebounding pain. There was no limb weakness, no muscle tenderness and no general edema. Her urine color is transparent and yellowish. The initial laboratory studies disclosed the following data: Hematicrit: 40.8%, hemoglobin: 13.1 g/dL, WBC: 8600/iL, (90% of neutrophil), platelet: 313 000/iL, BUN 96 mg/dL, serum creatinine 5.3 mg/dL, uric acid 4.1 mg/dL, sodium 144 meq/L, potassium 4 meq/L calcium 4.2 meq/L and phosphate 4.0 meq/L. Her serum GOT was 11 U/L, GPT 5 U/L. Urinalysis revealed urine protein 1+ and negative occult blood. Urine sediment showed RBC 3–5/HPF, WBC 2–3/HPF and negative urine cast. Stool analysis presented watery brown stool with occult blood 3+ without ova and ameba.

The patient was treated initially with Cefazolin and conservative treatment with saline hydration. However, the renal function was downhill in the first week in hospital. The worst data were BUN132 mg/dL, serum creatinine 9.7 mg/dL three days after admission. The blood culture and stool culture all yielded S. enteritidis. Due to persistent diarrhea with worsening renal function central venous catheter was inserted into right internal jugular vein with CVP level only 1 cm below sternal notch. We shifted antibiotics from Cefazolin to Ceftriaxone according to the sensitivity test and large amount fluid supply guided by CVP level. After adequate antibiotics and aggressive hydration treatment, the renal function recovered. The patient was discharged two weeks later with the normal renal function (serum creatinine 0.7 mg/dL).

DISCUSSION

S. enteritidis has broad host ranges and may produce colonization or gastroenteritis in humans, mice and fowl.Citation[[8]] In humans, S. enteritidis is often associated with gastroenteritis because of the large reservoirs of bacteria in domestic animals.Citation[[9]] The gastroenteritis caused by S. enteritidis is often self-limited after adequate supportive care and antibiotics treatment. However, it could be fatal especially with acute renal failure.Citation[[3]] Scarce reports have emerged from across the continent (mainly Spain and France) of rhabdomyolysis and acute renal failure complicating S. enteritidis infection.Citation[[4]], Citation[[5]], Citation[[6]] In the previous case reports, the cause of acute renal failure is associated with rhabdomyolysis caused by S. enteritidis infection. Cause of rhabdomyolysis is unknown but animal study suggests that bacteria may cause muscle damage by direct invasion or by activating muscle lysosome enzyme.Citation[[10]] However, in our case, there was no obvious evidence of rhabdomyolysis. First, she did not have limbs muscle swelling or pain. Second, she did not have red-color urine and myoglobin in urine. Third, her AST 11 U/L was normal and no hypokalemia with hyperphosphatemia noted. According to the patient history and physical examination, she lost body weight about 10 kg in one week, the oral mucous membrane and skin was dry. Hypotension with tachycardia was also noted in the admission day. Her CVP were −1 cm after hydration. We thought that volume depletion from severe gastroenteritis maybe the cause of her acute renal failure. It is a pity that we did not check the CPK level of this patient at first admission because no clinical clue can be found. Primarily, the elevated serum creatinine phosphokinase level established the diagnosis of rhabdomyolysis. The absence of myoglobinuria with a normal muscle biopsy does not exclude this diagnosis.Citation[[5]] However, we believe that she did not have severe rhabdomyolysis according to her clinical condition. After aggressive hydration and antibiotic therapy her renal function improved gradually. Her acute renal failure was purely pre-renal azotemia induced by S. enteritidis associated massive diarrhea.

In conclusion S. enteritidis associated acute renal failure is a rare entity most often cause by rhabdomyolysis. To our knowledge acute prerenal azotemia caused by S. enteritidis associated diarrhea has never been reported in literature. Adequate fluid supply and appropriate antibiotic treatment would be the best policy for treatment.

REFERENCES

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