hrvatski

Korelacija kliničkih i laboratorijskih parametara u bolesnika s hemoragijskom vrućicom s bubrežnim sindromom / Correlation between clinical and laboratory findings among patients with haemorrhagic fever with renal syndrome

Haemorrhagic fever with renal syndrome (HFRS) is a group of clinically similar illnesses caused by hantaviruses from the family Bunyaviridae. In a retrospective study we described the clinical characteristics of patients from 2012 HFRS epidemics treated in UHID, and evaluated the laboratory findings for early prediction and risk stratification of acute kidney injury (AKI). 81 patients with proven Puumala and 4 with Dobrava infection, 68 (80%) males, median age of 38 (IQR 31–48) years, were admitted to the hospital 5 days (IQR 4–6 days) after the onset of clinical symptoms. The most common clinical findings were fever (100%), chills/rigors (94.1%), headache (92.9%), muscle aches or back pain (75.3%). Thrombocytopenia was an early laboratory finding and 35 (41.2%) patients had severe thrombocytopenia (thrombocyte count <50x109/L). Platelet counts reached their nadirs on the 5th day of disease (IQR 5–7), followed by consistent rises in the levels of blood urea nitrogen (BUN) and serum creatinine on the 9th day (IQR 7–10). Leukocyte count and CRP, reflecting the inflammatory process, peaked at the same time as thrombocytopenia (7th day ; IQR 5–8 and 5th ; IQR 4–7, respectively). The nadir platelet count correlated inversely with the peak BUN (r=-0.24, p=0.001), creatinine (r=-0.28, p=0.004), leukocyte count (r=-0.35, p<0.001), while leukocytosis positively correlated with urea (r=0.6, p<0.001) and creatinine (r=0.58, p<0.001). 23 (27%) patients developed stage 3 AKI (according to AKIN criteria: creatinine ≥354μmol/L or urine output <500mL/24h). Nadir platelets were significantly lower (41x109/L, IQR 36–41, p=0.012) and leukocyte count higher (13.7x109/L, IQR 8.8–18.7x109/L, p=0.04) in patients with severe AKI. By multivariate analysis, nadir platelet count <41x109/L (OR 4.19 ; 95%CI, 1.02–17.24 ; p=0.013), hematuria (OR 8.91, 95%CI 1.9–41.7, p=0.005), hemoglobin on admission <130 g/L (OR 20.67, 95%CI 2.1–203.6, p= 0.009), leukocyte count >12x109/L (OR 5.54, 95%CI 1.43–21.42, p=0.013) were independently associated with the development of severe AKI. In conclusion, our study identified clinical and biochemical factors as possible predictors of severe AKI.

AKI; DOBV; HFRS; leukocyte count; PUUV; thrombocytopenia

nije evidentirano

engleski

Korelacija kliničkih i laboratorijskih parametara u bolesnika s hemoragijskom vrućicom s bubrežnim sindromom / Correlation between clinical and laboratory findings among patients with haemorrhagic fever with renal syndrome

Haemorrhagic fever with renal syndrome (HFRS) is a group of clinically similar illnesses caused by hantaviruses from the family Bunyaviridae. In a retrospective study we described the clinical characteristics of patients from 2012 HFRS epidemics treated in UHID, and evaluated the laboratory findings for early prediction and risk stratification of acute kidney injury (AKI). 81 patients with proven Puumala and 4 with Dobrava infection, 68 (80%) males, median age of 38 (IQR 31–48) years, were admitted to the hospital 5 days (IQR 4–6 days) after the onset of clinical symptoms. The most common clinical findings were fever (100%), chills/rigors (94.1%), headache (92.9%), muscle aches or back pain (75.3%). Thrombocytopenia was an early laboratory finding and 35 (41.2%) patients had severe thrombocytopenia (thrombocyte count <50x109/L). Platelet counts reached their nadirs on the 5th day of disease (IQR 5–7), followed by consistent rises in the levels of blood urea nitrogen (BUN) and serum creatinine on the 9th day (IQR 7–10). Leukocyte count and CRP, reflecting the inflammatory process, peaked at the same time as thrombocytopenia (7th day ; IQR 5–8 and 5th ; IQR 4–7, respectively). The nadir platelet count correlated inversely with the peak BUN (r=-0.24, p=0.001), creatinine (r=-0.28, p=0.004), leukocyte count (r=-0.35, p<0.001), while leukocytosis positively correlated with urea (r=0.6, p<0.001) and creatinine (r=0.58, p<0.001). 23 (27%) patients developed stage 3 AKI (according to AKIN criteria: creatinine ≥354μmol/L or urine output <500mL/24h). Nadir platelets were significantly lower (41x109/L, IQR 36–41, p=0.012) and leukocyte count higher (13.7x109/L, IQR 8.8–18.7x109/L, p=0.04) in patients with severe AKI. By multivariate analysis, nadir platelet count <41x109/L (OR 4.19 ; 95%CI, 1.02–17.24 ; p=0.013), hematuria (OR 8.91, 95%CI 1.9–41.7, p=0.005), hemoglobin on admission <130 g/L (OR 20.67, 95%CI 2.1–203.6, p= 0.009), leukocyte count >12x109/L (OR 5.54, 95%CI 1.43–21.42, p=0.013) were independently associated with the development of severe AKI. In conclusion, our study identified clinical and biochemical factors as possible predictors of severe AKI.

AKI; DOBV; HFRS; leukocyte count; PUUV; thrombocytopenia

nije evidentirano