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homemaker with seven children and no exposure to Introduction tobacco or alcohol use. Family history was positive for diabetes with kidney problems. Initially she was Quinine induced haemolytic uraemic syndrome is a thought to have viral gastroenteritis. However, during well described clinical entity consisting of microangithe following 48 h she developed oliguric renal failure opathic haemolytic anaemia, thrombocytopenia, and with an increase in serum creatinine from 1.5 to acute renal injury that occurs following exposure to 5.9 mg/dl, microscopic haematuria, a decrease in platequinine in any of its forms. Patients will usually present let count from 179 000 to 60 000/mm3, and a decrease with a history of fever, chills, nausea, vomiting, abdomin haematocrit from 43 to 33%. Serum LDH was 5166 inal pain, diarrhoea and oliguria that begins within U/l. Because of worsening renal failure she was transhours following quinine ingestion. Serologic evaluferred to University Hospital. ation, when done, has demonstrated antibodies against On arrival, physical exam disclosed a pulse rate of any or all of the haematopoietic cell lines including 72 beats/min (BPM ), blood pressure 176/106 mmHg, platelets, erythrocytes and granulocytes. Treatment has temperature 36.7°C, and a respiratory rate of 20 included supportive care, haemodialysis, steroids, cytobreaths/min. Physical examination was remarkable for toxic medication, plasmapheresis, and splenectomy. bilateral costovertebral angle tenderness and bilateral Plasmapheresis has been very effective in most of the lower extremity oedema. Laboratory studies revealed patients studied but has not always resulted in complete a serum creatinine of 5.9 mg/dl, a BUN of 56 mg/dl, recovery. In this ‘Teaching Point’ two cases of HUS LDH of 4734 U/l, with an AST of 762 U/l, a serum are described with documentation of quinine dependent bilirubin of 1 mg/dl, white blood cell count 8300/mm3, antibodies. a haematocrit of 33%, and a platelet count of 47 000/mm3. A urinalysis showed multiple dysmorphic Case report red cells with red blood cell and granular casts. Further workup showed a normal renal ultrasound, negative anti-nuclear antibody, and anti glomerular basement A 50-year-old female was admitted to another hospital membrane antibodies, normal C3 and C4, with negaon April 4, 1992, because of 2 days of nausea, vomiting, tive serologics for hepatitis A, B, and C, and negative abdominal and bilateral flank pain, as well as headurine culture. A blood smear showed signs of active aches and decreased urine output. Prior to this admission she had been well. Her past medical history was haemolysis with schistocytes, a white cell left shift, and remarkable for long-standing essential hypertension a decrease of platelets. A diagnosis of idiopathic haeand recurrent uncomplicated urinary tract infections. molytic uraemic syndrome was made. The patient was Medications at the time of admission included clonidtreated with plasmapheresis for seven consecutive days, ine 0.3 mg three times a day, and for the week prior then every other day for a total of eleven treatments to admission amoxicillin and ibuprofen after a tooth with fresh frozen plasma as the replacement fluid. She extraction. also received high dose solumedrol 500 mg intravenThe evening before admission she took one tablet ously for three consecutive days, then oral prednisone of 260 mg quinine for leg cramps. She was a married 100 mg/day. She required seven red blood cell transfusions and haemodialysis throughout her hospital stay. Her platelets gradually increased to 400 000/mm3, her Correspondence and offprint requests to: Dr Gary Rabetoy, University haematocrit stabilized, and her LDH returned to of Utah, Division of Nephrology, 50 North Medical Drive, Front Dumke Building, #535 Salt Lake City, UT 84112, USA. normal. After hospital discharge she slowly regained

The lady who had muscle cramps and developed thrombotic microangiopathy