A total of 1056 patients were admitted in this specified period. 427 patients were confirmed by RT-PCR. 104 of the PCR confirmed COVID-19 patients experienced AKI (24,3%). 89 patients who developed AKI with an eGFR of over 60 ml/min/1.73 m2 were included in the final analysis (Figure-1). Patients who were 62,4 ± 14,2 years old and there was a male predominance (67 males, 75%).
Twenty-nine (32%) of the patients had AKI on admission. 33 of them (37%) developed AKI during the first week of admission and 27 patients (30%) developed AKI after the 1st week. For patients who developed AKI later than hospital admission date, AKI developed on the 6.7th ± 5.4th day of the admission.
Urine analysis was available in a total of 35 patients. Hematuria was the most prominent finding, which was seen in 21 of them. Proteinuria was documented in 9 patients and they were all 1+ semiquantitavely. Proteinuria was going along with hematuria in 7 patients while two patients had isolated proteinuria.
Electrolyte and acid/base disturbances
Hypochloremia and hyponatremia were the most common electrolyte abnormalities. 65 of the 89 patients (73%) had hypochloremia and 50 (56.1%) of the patients had hyponatremia. Hypernatremia and hyperchloremia was seen in 22 (24.7%) and 18 (20.2%) of the patients respectively. Among potassium abnormalities, hyperkalemia developed in 35 (39.3%) of the patients, while hypokalemia was seen in 16 (17.9%) of them. Among patients for whom phosphorus levels were evaluated (79 patients); 22 had hypophosphatemia (27.8%) and 20 patients (25.3%) had hyperphosphatemia. Acidosis (respiratory and/or metabolic) developed in 23 (25.8%) of the patients and respiratory alkalosis was seen in 38 (42.6%) of them.
Although there is no specific validated treatment for COVID-19 yet, some antiviral therapies were applied in accordance with the ministry of health (MoH) treatment guidelines. These include different combinations of hydroxychloroquine, favipiravir and lopinavir. Anti IL-6 receptor antibody tocilizumab or steroids were used in patients who had high inflammatory response. Low-molecular-weight heparin were prescribed for all patients in line with the MoH guidelines . Continuous renal replacement therapy (CRRT) in ICU setting was performed with Prismaflex® system in a citrate anti-coagulated circuit, aiming a blood flow of around 20 mL/kg/hour.
Comparison according to the timing of AKI
Patients of the three groups (AKI on admission, AKI in the 1st week, AKI after the 1st week) were in similar age and had similar baseline mean arterial pressure, creatinine and hemoglobin levels. Co-morbidities such as diabetes, hypertension, malignancies and ischemic heart diseases/heart failure were also similar between three groups. CRP and D-dimer levels on admission didn’t differ between the groups. Patients who had AKI on admission day had higher initial uric acid levels. All initial laboratory values of the patients can be found in table-1.
Duration of hospital stay, intensive care unit (ICU) requirement and mortality was higher when AKI developed later in the disease course, especially after 7th day. Patients who develop later AKIs had lower serum albumin levels as well as lower arterial O2 pressure and lower oxygen saturation levels. Pre-dominant stage of AKI was stage 1; however, stage 2 & 3 AKIs, which have worse prognosis tend to increase with AKIs that occurred later. Similarly COVID-19 was more severe in patients who had later AKIs (table-2).
While there were no significant differences between the initial inflammatory markers of the three groups, comparison of changes put forth significant differences. Nadir lymphocyte counts were significantly lower while peak CRP and peak D-dimer levels were significantly higher for patients who developed AKI later in the disease course (Table-3). Although it couldn’t reach the statistical significance, peak ferritin levels were also higher for patients who developed AKI later.
Sodium, chlorine and potassium abnormalities were more common in patients who developed AKI later (Table-3).
Treatment modalities were similar for all groups. RRT had to be performed in 6 patients who developed AKI later (2 among the 1st week AKIs and 4 among the AKIs developed after the 1st week) but none of the patients who had AKI on admission needed RRT.
Comparison between survivors and non-survivors
Duration of hospital stay was not different for survivors and non-survivors. Those who died were older. Patients who survived and who didn’t had similar rates of diabetes or hypertension, while concomitant malignancies were more frequent in patients who died (Table-4).
AKI had 24.7% mortality in our patients who had eGFRs above 60 ml/min/1.73 m2. AKI developed later in non-survivors and it lasted longer. Non-survivors had significantly higher initial CRP, LDH, ferritin and D-dimer levels while their hemoglobin and lymphocyte counts were significantly lower (Table-4).
Patients who died had lower serum albumin levels than those who survived. Hematuria or proteinuria (p=0.001; OR: 2.4; 95% CI: 1.4 – 3.8 and p=0.015; OR: 4.34; 95% CI: 1.3 – 14.3 respectively) were more common in patients who died.
Among electrolyte disturbances hyponatremia and hypochloremia were similar between survivors and non-survivors. On the other hand, hypernatremia (p=0.000, OR: 6.5; 95% CI: 3.0 – 13.9) and hyperchloremia (p=0.002, OR:3.8; 95%CI: 1.7 – 8.4) were more common in patients who died. Comparison of other electrolytes can be found in table-4.
Patients who died had more secondary bacterial infections (OR: 3.5 ; 95%CI: 1.9 – 6.4). However, ferritin levels, as a marker of inflammation, were similar in patients who had secondary bacterial infections and in those who hadn’t (n=24; 1120 ±691 vs n=62; 976 ± 109; p=0.548). Urea-to-creatinine ratios checked both on the day of AKI and on the day of worst kidney function, were higher in patients who died (p=0,02 and p=0,000 respectively).