Present study aimed to estimate the incidence of recurrent SARS-CoV-2 RNA positivity after recovery from COVID-19 and to determine the factors associated with recurrent positivity. We searched the PubMed, MedRxiv, BioRxiv, the Cochrane Library, ClinicalTrials.gov, and the World Health Organization International Clinical Trials Registry for studies published to June 12, 2020. Studies were reviewed to determine the risk of bias. A random-effects model was used to pool results. Heterogeneity was assessed using I2. Fourteen studies of 2568 individuals were included. The incidence of recurrent SARS-CoV-2 positivity was 14.8% (95% confidence interval [CI] 11.44–18.19%). The pooled estimate of the interval from disease onset to recurrence was 35.4 days (95% CI 32.65–38.24 days), and from the last negative to the recurrent positive result was 9.8 days (95% CI 7.31–12.22 days). Patients with younger age and a longer initial illness were more likely to experience recurrent SARS-CoV-2 positivity, while patients with diabetes, severe disease, and a low lymphocyte count were less likely to experience. Present study concluded that the incidence of recurrent SARS-CoV-2 positivity was 14.8% suggesting further studies must be conducted to elucidate the possibility of infectious individuals with prolonged or recurrent RNA positivity.

Background. The nephroprotective effect of vitamins E and C or losartan against cisplatin (CP)- induced nephrotoxicity when they are accompanied by estrogen was investigated. Methods. The ovariectomized rats received estradiol valerate for two weeks. At the end of the first week, a single dose of CP (7 mg/kg, IP) was also administered, and they received placebo (group 1), vitamin E (group 2), vitamin C (group 3), or losartan (group 4) every day during the second week, and they were compared with another three control groups. Results. CP alone increased the serum levels of blood urea nitrogen (BUN), creatinine (Cr), and kidney tissue damage score (KTDS), significantly (P < 0.05), however at the presence of estradiol and CP, vitamin C, vitamin E, or losartan not only did not decrease these parameters, but also increased them significantly (P < 0.05). The serum level of superoxidase dismutase (SOD) was reduced by CP (P < 0.05), but it was increased when estradiol or estradiol plus vitamin C or losartan were added (P < 0.05). Conclusion. The particular pharmacological dose of estrogen used in this study abolish the nephroprotective effects vitamins C and E or losartan against CP-induced nephrotoxicity.

Introduction. Nephrotoxicity is one the side effect of cisplatin therapy and erythropoietin has been candidate as a nephroprotectant agent. However, its nephroprotective effect when it is accompained with estrogen has not been studied in female. Methods. 27 ovariectomized female Wistar rats divided into five groups. Groups 1 & 2 received estradiol valerate (0.5 mg/kg/week) for four weeks, and single dose of cisplatin (7 mg/kg, ip) was administrated at the end of week 3. Then the group 1 was treated with erythropoietin (100 U/kg/day), and the group 2 received vehicle during week 4. Groups 3 and 4 were treated similar to group 1 and 2, except for placebo instead estradiol valerate. Group5 (negative control) received placebo during the study. Animals were killed at the end of week 4. Results. In non-erythropoietin treated rats, cisplatin significantly increased the serum levels of blood urea nitrogen and creatinine (P < 0.05). However, these biomarkers significantly decreased by erythropoietin (P < 0.05). The weight loss, kidney weight, and kidney tissue damage score in rats treated with cisplatin but without estradiol were significantly less than the values in similar group when estradiol was present (P < 0.05). Conclusion. It seems that erythropoietin could protect the kidney against cisplatin-induced nephrotoxicity. This protective effect was not observed when estrogen was present.

Background. The role of gender for nephroprotectant agent such as vitamin E in cisplatin- (CP-) induced nephrotoxicity has not been documented yet. Methods. One group from each gender of Wistar rats received a single dose of CP (7 mg/kg; i.p) and was treated with vitamin E (1 g/kg/day) for 7 days, and they were compared with similar gender in the control group. Results. The serum levels of blood urea nitrogen (BUN) and creatinine (Cr) in male animals treated with CP was not different from the control group, but it was significantly different in the female rats (P < 0.05). The CP-induced damage intensity in male kidney tissue was not significantly different between the CP-treated and control groups, but this was not the case in female, indicating that the tissue damage in female is significantly different from the control group (P < 0.05). No significant difference in serum levels of magnesium (Mg), nitrite, malondialdehyde (MDA), and lactate dehydrogenase (LDH) was seen between the genders. Kidney weight and body weight changes were statistically significant in both genders (P < 0.05). Significant difference was observed in uterus weight between the two groups of female (P < 0.05). Conclusion. Vitamin E may prevent CP-induced nephrotoxicity in male, but possibly it has not such nephroprotectant effect in female.

Objective. Nitric oxide (NO) has numerous important functions in the kidney. The role of NO in cisplatin (CP)-induced nephrotoxicity is not completely understood. This study was designed to determine the role of NO synthase inhibitor (L-NAME) on the severity of CP-induced nephrotoxicity in rats. Methods. Sixty four male (M) and female (F) Wistar rats were randomly divided into eight groups. The sham groups (group 1, male, n = 6 and group 2, female, n = 6) received saline. Groups 3 (male, n = 8) and 4 (female, n = 8) were treated with L-NAME (4 mg/kg, i.p.), and groups 5 (male, n = 8) and 6 (female, n = 8) received CP (3 mg/kg) for 7 days. Groups 7 (male, n = 8) and 8 (female, n = 8) were treated with L-NAME and CP for 7 days. Results. The CP-alone treated rats showed weight loss and increase in serum levels of blood urea nitrogen (BUN) and creatinine (Cr). Coadministration of L-NAME and CP did not improve weight loss, and it increased the levels of BUN and Cr in male but not in female rats (P < 0.05). CP alone increased kidney damage significantly (P < 0.05 ), however, the damage induced by combination of CP and L-NAME was gender-related. Conclusion. NOS inhibition by L-NAME increased CP-induced nephrotoxicity, which was gender-related.