Leptospirosis with hypokalemic nonoliguric AKI and hepatic injury

Question

A 25-year-old previously healthy female veterinary student presents for worsening malaise, fever, myalgias, headache, and skin discoloration over the last 2 weeks. Medications include as-needed ibuprofen, which she has used sparingly, and a multivitamin. Social history is significant for two alcoholic drinks weekly; she does not use tobacco, inhaled nicotine, or recreational drugs. On examination, BP is 98/46 mm Hg, heart rate is 110/min, and temperature is 39°C. Eye examination is significant for scleral icterus and subconjunctival hemorrhages without purulent exudate. Abdominal examination reveals splenomegaly. Musculoskeletal examination reveals tenderness to palpation of the lower back and both calves. She is jaundiced, but there is no rash. Laboratory data: WBC count 16,000/μL (reference 4000–11,000); hemoglobin 12 g/dL (12–16); platelets 45,000/μL (150,000–450,000); sodium 138 mEq/L (136–145); potassium 2.9 mEq/L (3.5–5.0); total CO₂ 18 mEq/L (23–28); BUN 55 mg/dL (8–20); creatinine 4.0 mg/dL (0.5–1.1); total bilirubin 14 mg/dL (0.3–1.0); direct bilirubin 12 mg/dL (0.1–0.3); aspartate aminotransferase 300 U/L (10–40); alanine aminotransferase 150 U/L (10–40). Peripheral blood smear shows rare schistocytes. Urinalysis shows dark yellow urine with 1+ blood, 8–10 isomorphic RBCs/HPF, and 1–2 granular casts/LPF. Which of the following is the MOST LIKELY diagnosis?

Accepted Answer

C. Leptospirosis — The most likely diagnosis in this patient with AKI, acute liver injury, and hypokalemia is leptospirosis.

Leptospirosis is a zoonotic disease caused by the spirochete Leptospira interrogans via an infected reservoir, which includes the brown rat, Rattus norvegicus. Infection leads to nonoliguric AKI and acute liver injury. Pathogenic Leptospira are shed from host urine and may contaminate water and soil, leading to environmental spread. This patient is at risk because of her veterinary exposure to rats; other exposure would be those living in hot, urban, unsanitary conditions. Hematogenous spread with accumulation in the tubulointerstitium leads to AKI, which appears as acute tubular necrosis (ATN) or acute interstitial nephritis (AIN) on kidney biopsy. Leptospirosis is also associated with potassium wasting caused by impaired sodium and potassium absorption in the thick ascending limb of the loop of Henle. Muscle pain and tenderness are common and characteristically involve the calves and lower back. Ophthalmologic findings include conjunctival suffusion, dilation of conjunctival vessels without purulent exudate, and subconjunctival hemorrhages and icterus. Hemorrhagic complications are also common and may include life-threatening alveolar hemorrhage associated with coagulation abnormalities.

NSAID-associated AKI, including prerenal AKI, ATN, and glomerular disease, is unlikely, as ibuprofen use was minimal. ATN may be a concurrent finding with leptospirosis in patients with prolonged hypovolemia from diarrhea, and NSAIDs might exacerbate this situation. In this case, NSAID toxicity would not explain the myriad findings.

Although thrombotic thrombocytopenic purpura (TTP) must be considered in the presence of fever, thrombocytopenia, AKI, and anemia, it is not the most likely diagnosis in this case, as features of microangiopathic hemolysis are limited on the peripheral smear, and most of the bilirubin is conjugated, reflecting (with the elevated liver enzymes) hepatocellular injury and biliary stasis rather than intravascular hemolysis.

Catastrophic antiphospholipid antibody syndrome may cause simultaneous liver and kidney disease as a consequence of diffuse thrombosis but would not explain the clinical manifestations present in this case, including eye findings and hypokalemia.

Leptospirosis with hypokalemic nonoliguric AKI and hepatic injury

Explanation

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