T-Minus 2 days to the Nephrology Boards exams! For any of you out there studying, one useful resource is ASN’s “NephSAP Core Knowledge Questions“, which can be easily reached via the ASN web page. Unlike the main NephSAP questions which tend to ask for very specific details about the content of the NephSAP text (which often involves specific articles or newfangled molecular mechanisms which are unlikely to be tested in the Boards), the Core Knowledge Questions are more general and therefore more Boards-relevant.
Today’s topic is leptospirosis, a zoonotic infection caused by the spirochete Leptospira interrogans. Leptospirosis is spread via exposure to contaminated tissue from a variety of mammalian hosts, often rodents (but can also include cattle, pigs, goats, horses, even dogs). While leptospirosis is most commonly found in tropical areas, it nonetheless has a worldwide distribution and can certainly be found within the United States, as evidenced by this outbreak of participants in an Illinois triathlon, who were presumably exposed while swimming in lakewater.
Up to 10% of individuals with leptospirosis will develop acute kidney injury. The mechanism of AKI is still under debate. Some have suggested that Leptospira endotoxin simply results in an inflammatory response, much like gram-negative LPS; usually, AKI occurs in the setting of multi-organ failure and critical illness. Others have suggested that Leptospira endotoxin has tubular toxicity, as evidenced by a high frequency of renal potassium-wasting and hypokalemia noted in these patients. Still others have stated that tubulointerstitial nephritis is the main mechanism of kidney injury in Leptospirosis. In some instances, rhabdomyolysis can be the main cause of Leptospirosis-associated AKI.
Treatment of Leptospirosis-associated AKI includes standard supportive measures, along with the use of antibiotics (either penicillins or tetracyclines are typically used).