Pablo, a 2 year male neutered Labrador Retriever, presented to us as an out of hours emergency in November 2022.
He had initially presented with a 2-day history of acute onset anorexia and vomiting, possibly associated with a recent abrupt diet change. In this time, Pablo had also been noted to not be drinking normally.
The referring veterinary practice had found Pablo to be markedly azotaemic and hyperbilirubinaemic on in-house laboratory work, with increased ALT and ALP activity. He was also suspected to be severely thrombocytopaenic. He was started on intravenous fluid therapy but was urgently transferred to Cave’s internal medicine team owing to concerns regarding his reduced urine output. Pablo had no other significant medical history, was up to date with core vaccinations (including the Lepto L4 vaccine), routine anti-parasite treatment and had not travelled outside the UK.
On presentation Pablo was quiet but responsive. His sclera were icteric, hydration was deemed adequate and he was uncomfortable on cranial abdominal palpation. Physical examination was otherwise unremarkable. Pablo underwent emergency assessment. Venous blood gas analysis confirmed increased creatinine (296 umol/L, RI <159) and urea (16.1 mmol/L, RI 2.5-9.6) concentration; his acid-base status was normal and electrolytes were within normal limits. He was prehypertensive (156/99 mmHg, MAP 111mmHg). Patient-side emergency ultrasound of the thorax and abdomen revealed no evidence of effusions, the urinary bladder was present and no significant pyelectasia or ureteric dilation was visible.
Pablo was initially started on 4mL/kg/h of Hartmann’s intravenous fluids. An indwelling urinary catheter with closed collection system was placed. Pablo’s urine output overnight measured 0.8mL/kg/h. A sterile urine sample was obtained via the catheter prior to starting any antibiosis. Pablo was also prescribed intravenous methadone and maropitant for his abdominal discomfort, vomiting and anorexia.
Further investigations demonstrated a marked thrombocytopaenia (30×10^9/L, RI 140-700), confirmed a moderate azotaemia (creatinine 263 umol/L, RI 40-125; urea 19.5 mmol/, RI 2.5-9.0) and also mild hyperphosphataemia (2.1 mmol/L, RI 0.8-2.0). Serum biochemistry showed a cholestatic hepathopathy with increased hepatic enzyme activity (ALP 701 u/L, RI <120; ALT 209 u/L, RI<65), hyperbilirubinaemia (110 umol/L, RI<9) and hypercholesterolaemia (7.9 mmol/L, RI 3.8-7.0); Pablo also had a moderately increased CK activity (7101 u/L, RI<350). Urinalysis was consistent with a renal tubulopathy given his mild proteinuria (UPC 0.82, RI <0.5) with glucosuria despite a normal blood glucose level; urine culture was negative. His coagulation status (PT and aPTT) was normal, not consistent with a consumptive caoguloapthy or disseminated intra-vascular coagulation (DIC). Basal cortisol excluded hypoadrenocorticism and SNAP 4Dx excluded Borrelia burgdoferi. Abdominal ultrasound demonstrated a subjectively thickened urinary bladder wall but was deemed insignificant given the small volume of urine secondary to the indwelling urinary catheter.
The liver was of normal size but hypoechogenic and the gallbladder wall was thickened but with normal content. Pablo was likely mildly volume overloaded owing to the presence of small volume ascites. Fine needle aspirates to assess for infiltrative neoplasia could not be obtained owing to his severe thrombocytopaenia. Leptospirosis and Toxoplasma serology were negative. Blood and urine PCR however was positive for Leptospirosis.
Pablo was diagnosed with Leptospirosis. He remained hospitalised and nursed using personal protective equipment to protect all carers from this zoonotic bacterial infection. Pablo was maintained on intravenous fluid therapy, with the rates adjusted to match his input to urine output, and monitoring his hydration status and weight carefully. His urine output increased within 48 hours, indicative of a positive response to treatment and resulted in post-AKI polyuria, requiring markedly increased intravenous fluid administration to help maintain his hydration. Given his new polyuria, in addition to his persistent anorexia, Pablo became hypokalaemic requiring intravenous potassium supplementation. Venous blood gas analysis was re-assessed every 24 hours and demonstrated an improvement in his acute kidney injury within 10 days (creatinine 134 umol/L and urea 11.4 mmol/L).
His thrombocytopaenia also resolved during this time. Despite this, Pablo remained anorexic and continued vomiting, most likely secondary to his worsened hyperbilirubinaemia (236 umol/L). He was prescribed intravenous ondansetron, a continuous rate infusion of metoclopramide and a nasoesophageal feeding tube was placed allowing the administration a liquid diet; he was started on 1/3 of his resting energy requirements which was gradually increased to a full RER ration over the next 3 days.
Pablo remained hospitalised at for 10 days. Happily, his condition gradually improved over this time and he slowly regained his appetite. Once eating, his nasoesophageal feeding tube was removed and he was transitioned onto oral doxycycline 10mg/kg once daily for 14 days to ensure complete eradication of the bacteria from the kidneys. Pablo’s intravenous fluid therapy was also titrated down as he became better able to tolerate his polydipsia and polyuria to maintain adequate hydration. Pablo was re-assessed by his referring veterinary practice 2 weeks after discharge and continues to do well at home. Repeat analysis of his serum biochemistry demonstrated resolution of his azotaemia (creatinine 94 umol/L; urea 7.6 mmol/L), normalisation of his hepatic enzyme activities and significant improvement of his hyperbilirubinaemia (11.9 umol/L, RI <5.1).